Echocardiography

BVCCT-304

UNIT I

In echocardiogram is a non-invasive (the skin is not pierced) procedure used to assess the heart's function and
structures. During the procedure, a transducer (like a microphone) sends out sound waves at a frequency too high to
be heard. When the transducer is placed on the chest at certain locations and angles, the sound waves move through
the skin and other body tissues to the heart tissues, where the waves bounce or "echo" off of the heart structures.
These sound waves are sent to a computer that can create moving images of the heart walls and valves.

An echocardiogram may use several special types of echocardiography, as listed below:

 M-mode echocardiography. This, the simplest type of echocardiography, produces an image that is similar
to a tracing rather than an actual picture of heart structures. M-mode echo is useful for measuring or viewing
heart structures, such as the heart's pumping chambers, the size of the heart itself, and the thickness of the
heart walls.
 Doppler echocardiography. This Doppler technique is used to measure and assess the flow of blood
through the heart's chambers and valves. The amount of blood pumped out with each beat is an indication of
the heart's functioning. Also, Doppler can detect abnormal blood flow within the heart, which can indicate a
problem with one or more of the heart's four valves, or with the heart's walls.
 Color Doppler. Color Doppler is an enhanced form of Doppler echocardiography. With color Doppler,
different colors are used to designate the direction of blood flow. This simplifies the interpretation of the
Doppler technique.
 2-D (two-dimensional) echocardiography. This technique is used to "see" the actual motion of the heart
structures. A 2-D echo view appears cone-shaped on the monitor, and the real-time motion of the heart's
structures can be observed. This enables the doctor to see the various heart structures at work and evaluate
them.
 3-D (three-dimensional) echocardiography. 3-D echo technique captures three-dimensional views of the
heart structures with greater detail than 2-D echo. The live or "real time" images allow for a more accurate
assessment of heart function by using measurements taken while the heart is beating. 3-D echo shows
enhanced views of the heart's anatomy and can be used to determine the appropriate plan of treatment for a
person with heart disease.

Imaging Modes
There are three basic "modes" used to image the heart:
 Two-dimensional (2D) imaging
 M-mode imaging
 Doppler imaging

Two-dimensional imaging
2D imaging is the mainstay of echo imaging and allows structures to be viewed moving in real time in a cross-
section of the heart (two dimensions). It is used for detecting abnormal anatomy or abnormal movement of
structures. The most common cross-sectional views are the parasternal long axis, the parasternal short axis, and the
apical view (see Figure 1). The gastric or subcostal and suprasternal views are also commonly used.

Figure 1: The most common two-dimensional imaging echo views. The first line illustrates the three planes (think of
them as three plates of glass intersecting at 90°), the second line shows these three planes separated, and the third
line shows the accompanying echo views. (a) Parasternal long axis; (b) parasternal short axis; (c) apical 4-chamber
view (note, in the UK, the 4-chamber view is shown upside down). AV: aortic valve; LA: left atrium; LV: left
ventricle; RA: right atrium; RV: right ventricle.
M Mode

Like the other modes, M mode has operator-controlled parameters to optimize images. Of most importance are
overall gain, TGC, and sweep speed. These M-mode parameters work in a manner similar to spectral Doppler and B
mode. A primary value of M mode is its superior time resolution, which enhances display of rapidly moving objects.
Therefore, using rapid sweep speeds of 100 to 200 mm/sec is advantageous for making the most accurate time-
related measurements. Other physiologic conditions that require observation of multiple beats may benefit from a
slow sweep speed. Specific M-mode motion patterns may define certain pathology better than any other modality.
Similarly, the timing of movement of certain structures within the cardiac cycle is sometimes best delineated with M
mode.

1. Color M Mode. Color M mode integrates the color Doppler image with the M-mode tracing. It may be used to
assist with timing of certain color-flow events within the cardiac cycle by markedly increasing the temporal
resolution of a flow event. Examples in which this technology can be useful are timing of insufficiency jets in the
cardiac cycle and the evaluation of LV inflow propagation velocity.

2. Steerable M Mode. Linear measurements are overestimated when obtained obliquely to the structure of interest.
In some patients (e.g., those with ‘‘steep’’ hearts), it may not be possible to orient the M mode cursor perpendicular
to walls and chambers. Steerable M mode permits the M-mode cursor to be rotated, rather than maintaining a fixed
origin at the narrow point of the 2D image sector. This allows the M-mode cursor to be directed perpendicular to a
structure of interest, improving the accuracy of linear M-mode measurements in patients with steep hearts or off-axis
views. Note that the image is created from selective display of a part of the 2D image. Therefore, temporal and range
resolution are no better than the 2D image parameters, much inferior to directly obtained M-mode images.

Fig 2: M-mode image of (a) the aorta/left atrium and (b) the mitral valve, both in a healthy heart.

Doppler imaging
The concept of Doppler imaging is familiar to all those who have heard the note of a police siren change as it moves
past them – as the police siren travels towards you, the frequency of the wave (pitch) appears to be higher than if it
was stationary; as the siren travels away, the pitch appears to be lower.
Estimates of blood-flow velocity can be made by comparing the frequency change between the transmitted and
reflected sound waves. In cardiac ultrasound, Doppler is used in three ways:
 continuous-wave (CW) Doppler
 pulsed-wave (PW) Doppler
 color-flow mapping (CFM)

Continuous-wave Doppler
CW Doppler is sensitive, but, because it measures velocity along the entire length of the ultrasound beam and not at
a specific depth, it does not localize velocity measurements of blood flow. It is used to estimate the severity of valve
stenosis or regurgitation by assessing the shape or density of the output (see Figure 3).
Figure 3: Continuous-wave Doppler signal.

Pulsed-wave Doppler
PW Doppler was developed because of the need to make localized velocity measurements of turbulent flow (it
measures the blood-flow velocity within a small area at a specified tissue depth). It is used to assess ventricular in-
flow patterns, intracardiac shunts, and to make precise measurements of blood flow at valve orifices.

Color-flow mapping
CFM uses measurements of the velocity and direction of blood flow to superimpose a color pattern onto a section of
a 2D image (see Figure 4). Traditionally, flow towards the transducer is red, flow away from the transducer is blue,
and higher velocities are shown in lighter shades. To aid observation of turbulent flow there is a threshold velocity,
above which the color changes (in some systems to green). This leads to a "mosaic" pattern at the site of turbulent
flow and enables sensitive screening for regurgitant flow.

Figure 4: Color-flow mapping.

Measurement of cardiac dimensions
LEFT VENTRICLE (LV) SIZE AND FUNCTION: Linear Measurements

LVID Diastole (LVIDD)

 Inner edge to inner edge, perpendicular to the long axis of the LV, at or immediately below the level of the
mitral valve leaflet tips. Perform at end-diastole (defined as the first frame after mitral valve
 closure or the frame with the largest LV dimensions/volume.) Each laboratory should choose one method for
consistency.

Fig 5: 2D guided linear measurement

LVID Systole (LVIDS)

 Inner edge to inner edge, perpendicular to the long axis of the LV, at or immediately below the level of the
mitral valve leaflet tips.
 Perform at end-systole (defined as either as the frame after aortic valve closure or the smallest LV
dimension/volume.) Each laboratory should choose one method for consistency.

LV Volume Measurement : 2D Methods

 Preferred technique is Biplane Method of Discs (modified Simpson’s rule).

 Measured from the apical 4- and 2-chamber views (preferably an LV focused view) tracing the endocardial –
blood pool interface (between the compacted myocardium and the cavity) at end-diastole and endsystole on
images with clear endocardial border definition.
 Papillary muscles should be excluded from the cavity tracing.
 Maximize LV area and avoid foreshortening.
 When approaching the MV plane, the contour is closed by connecting the two opposite sections of the MV
ring with a straight line. The LV length is the bisector between this line and the apical point of the LV
contour distant from it.
 Fig 6: Biplane disk summation

Endocardial Border Enhancement

When ≥ 2 contiguous endocardial segments cannot be visualized in the apical views, contrast should be used. If
employed, the contrast-enhanced images should be used for Biplane tracing

o Avoid acoustic shadowing in the basal segments of the LV when contrast concentration is high.

o Note: Normal reference values for contrast enhanced LV volumes are not well established, however contrast
enhanced images have been demonstrated to provide more reproducible volumetric and therefore ejection fraction
data that correlate better with CMR.

Fig 7: Endocardial Border Enhancement

LV Mass Calculations

Linear Method: LVID, IVS, PW Diastole

 Electronic calipers should be positioned on the interface between myocardial wall and cavity, and the interface
between wall and pericardium.
 Perform at end-diastole (previously defined) perpendicular to the long axis of the LV, at or immediately below the
level of the mitral valve leaflet tips.

LV mass = 0.8x (1.04x [(IVS+LVID+PWT) 3 -LVID3] + 0.6 grams

2D-based formulas

 Infrequently used in most clinical labs

Relative Wall Thickness (RWT)

 RWT= (2x posterior wall thickness)/(LVIDD).

 Useful to categorize LV mass and pattern of remodeling.

Left Ventricular Function Assessment

LV Global Systolic Function Parameters

 Fractional Shortening (use is discouraged)

 o FS = LVIDD – LVIDS / LVIDD (normal > 25%)
o Derived from M-mode or linear 2D measurements

 Ejection Fraction (EF) (see below) is the predominant method for assessing global systolic function and is derived
from the LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV).
 Global Longitudinal Strain is a new parameter to assess LV systolic function.

LV Volumes used to calculate EF

 Volumes can be derived from 2DE or 3DE (see section on LV size for methodology).

o The biplane method of disks is the preferred 2DE method.

o In laboratories with 3D experience, three-dimensional volumes should be utilized.

 Volumes derived from linear measurements should NOT be used.

 Use of contrast is encouraged as detailed in LV Volumetric Measurement

LVEF by Biplane Method of Disks (modified Simpson’s rule) or 3DE

LVEF = LVEDV – LVESV / LVEDV

Normal Ranges for LV Size and Function

Normal values for LV chamber dimensions (linear), volumes and ejection fraction
vary by gender.
A normal ejection fraction is 53-73% (52-72% for men, 54-74% for women).

Global Longitudinal Strain (GLS)

 Defined as the change in length of an object within a certain direction relative to its baseline length.
 A measurement of deformation that is used to assess LV systolic function.
 Strain (%) = (Lt – Lo) / Lo

o Lt is the length at time t, Lo is the length at time 0.

 GLS is assessed by speckle tracking, the specific methodology varies by vendor.

 Peak GLS describes the relative length change between end-diastole and end-systole.
GLS (%) = (MLs-MLd)/MLd
(MLs= myocardial length end-systole, MLd= myocardial length end-diastole)
 Since MLs is smaller than MLd peak GLS is a negative number.
 CW of the aortic valve or PW of the LVOT should be obtained for timing of aortic valve opening and closure.
 The three standard apical views should be acquired in succession as LV focused views optimizing endocardial
borders at a frame rate of 60Hz-90Hz. Heart rate should not vary more than 5bpm.
 Follow the system software prompts for analysis (specific method varies by vendor).
 GLS should be measured in the 3 standard apical views (apical 4 chamber, 2 chamber and long axis) and the
average GLS should be reported.
 Normal values depend on several factors including the vendor and version of software. As a general guide, a peak
GLS of -20% can be considered normal. The smaller the absolute number, the more abnormal is the strain.

LV Regional Function
Segmentation of the LV

 Segmentation schemes should reflect coronary perfusion territories and allow standardized communication within
echocardiography and with other imaging modalities.
 When using this 17-segement model to assess wall motion or regional strain, the 17th segment (the apical cap)
should not be included.
 Although certain variability exists in the coronary artery blood supply to myocardial segments, segments are
usually attributed to the three major coronary arteries.
Visual Assessment
 Semi quantitative wall motion score (1-4) can be assigned to each segment to calculate the LV wall motion
score index (sum score of all segments assessed / # segments assessed).

Regional Wall Motion during Infarction and Ischemia

 Coronary artery distribution varies among patients. Some segments have variable coronary perfusion.
 Echocardiography may over or underestimate the amount of ischemic or infarcted myocardium, depending
on the function of adjacent regions, regional loading conditions, and stunning.

Regional Abnormalities in the Absence of Coronary Artery Disease

 Regional wall motion abnormalities may also occur in the absence of coronary artery disease (examples:
myocarditis, sarcoidosis and takotsubo cardiomyopathy).
 Interventricular septal wall motion abnormalities may be found in:
o Left bundle branch block
o RV pacing
o RV pressure/volume overload
o Post op septal motion
 Wall motion patterns due to conduction delays (abnormal sequence of myocardial activation):
o Septal bounce (“beaking”, “flash”)
o Lateral apical motion during systole (“apical rocking”).

RIGHT VENTRICLE (RV) SIZE AND FUNCTION

In order to assess RV size and function it is important to use all available views. Each view adds complementary
information, permitting a more complete assessment of the different segments of the RV.
The essential views for imaging and assessment of the RV are: Left parasternal long-axis view (PLAX)
 Left parasternal short-axis view (PSAX)
 Left parasternal RV inflow view
 Apical 4-chamber view
 Focused apical 4-chamber RV view
 Modified apical 4-chamber view
 Subcostal views
 Size of right ventricle
RV size should be routinely assessed by conventional 2DE using multiple acoustic windows. All chamber
measurements should be made inner-edge to inner-edge. The report should include both qualitative and
quantitative parameters. Most of the values are not indexed to gender, BSA, or height.

Fig 1: To measure the RV diameter, the RV focused apical 4-chamber view (a dedicated view which keeps the LV
apex in the center and displays the largest basal RV diameter as shown below) should be used. Since RV linear
dimensions are dependent on probe rotation and different RV views, the echocardiographic report should state the
window from which the measurement was obtained. A single measurement may not reflect global RV size. An RV
diameter of >41mm at the base and >35mm at the mid-level is abnormal.

Fig 2: RV wall thickness should be measured by 2DE or M-mode at end-diastole, zoomed on the RV mid- wall
(preferably from the subcostal view). A thickness of >5mm is abnormal.

Fig 3: RV Function
RV systolic function should be assessed by at least one or a combination of the following recommended parameters:
1. TAPSE (Tricuspid Annular Plane Systolic Excursion)
2. DTI-Derived Tricuspid Lateral Annular Systolic Velocity S’
3. FAC (fractional area change)
4. RV longitudinal strain
5. 3D EF
 6. Right Index of Myocardial Performance (RIMP or MPI)

1) TAPSE predominantly reflects RV longitudinal function, but it has shown good correlation with parameters
estimating RV global systolic function. TAPSE may over- or underestimate RV function because of cardiac
translation.

2) DTI -derived tricuspid lateral annular systolic velocity S’ represents basal systolic function, not global RV function.
The velocity may not be accurate in patients who are post thoracotomy, pulmonary thromboendarterectomy or heart
transplantation. It is also angle dependent.

3) FAC reflects both longitudinal and radial components of RV contraction. It does not include the contribution of
RV outflow tract to overall systolic function.

4) RV longitudinal strain is less confounded by overall heart motion, but depends on RV loading conditions as well as
RV size and shape. RV longitudinal strain should be measured in the RV-focused view. A normal value is
approximately -20%, the smaller the absolute number the more abnormal is the strain.
5) RV 3D EF does not directly reflect RV contractile function, but provides an integrated view of the interaction
between RV contractility and load. The limitations of 3D assessment of RV EF are load dependency, interventricular
changes affecting septal motion, poor acoustic windows, and irregular rhythms.

6) RIMP (Right Index of Myocardial performance) assesses global RV function. The measurement requires beats with
similar RR intervals and is unreliable when RA pressure is elevated. The IVCT, IVRT and ET intervals used in the
calculation can be obtained from PW Doppler of the TV inflow and RVOT outflow or from tissue Doppler of the
lateral TV annulus (see figure). Normal values differ depending on the method used. a. RIMP = (TCO – ET)/ET
where TCO is the TV closure to opening time (and equals the IVRT + IVCT).

ATRIA

Left Atrium (LA) Area and Volume Measurements

 Should be measured at end-systole when the LA chamber is at its greatest dimension (prior to MV opening).
 Avoid foreshortening.
 Dedicated acquisition of LA from the apical approach should be obtained to maximize LA length and alignment of
the true long axis of the LA for area and volume measures.
 For LA tracings (area or volume) the confluences of the pulmonary veins and LA appendage should be excluded.
 The atrioventricular interface should be represented by the mitral annulus plane.

LA Anterior-Posterior (AP) dimension

 Should not be used as sole LA measurement (does not represent accurate LA size).
 2D measure is preferred over M-mode.
 Perpendicular to the long axis of the LA posterior wall, leading edge to leading edge
 (M-mode) or inner edge to inner edge (2DE).
 Measured at the level of the aortic sinuses.

LA Area and Volumes (Apical 4 and 2 chambers)

LA Area
 The base of the LA should be at its largest size.
 Trace the LA inner border, excluding the area under the MV annulus, pulmonary veins, and LA appendage

LA Volume (Preferred over linear or area measurements)

 Volume can be calculated by the Area-length method or disk summation technique (modified biplane) which is
preferred.
 Trace the LA inner border, excluding the area under the MV annulus, pulmonary veins, and LA appendage from the
apical 4 and 2 chamber views.
 Area-length technique: the length (L) should be measured from the shorter of the two long axes in the 4C and 2C
views.

Right Atrium (RA) Area & Volume Measurements

RA area
 The RA should be measured at end-ventricular systole when the RA chamber is at its greatest dimension, prior to TV
opening.
 A dedicated right heart view (from an Apical 4 chamber view that includes the entire RA and is not foreshortened)
should be used for acquisition to ensure the RA is not foreshortened.
 The RA length should also be maximized ensuring alignment along the true long axis of the RA.
 The base of the RA should be at its largest size indicating that the imaging plane passes through the maximal short-
axis area.
 When performing planimetry of the RA, trace the RA inner border excluding the area under the TV annulus and the
confluences of the RA appendage.

RA Volume (single plane)

 More robust and accurate when compared with linear measurements.
 Should be performed from an Apical 4 chamber view that includes the entire RA and is not foreshortened (dedicated
right heart view), tracing the RA inner border excluding the area under the TV annulus.
 No standard orthogonal RA view to use for biplane so a single-view area-length and/or disk summation technique
should be used.
 Area-length method: the length should be performed at the center of the area under the TV annulus to the superior
RA wall.

AORTA
Aortic Annulus and Aortic Root
Aortic annulus
 Not a true or distinct anatomic structure but is a virtual ring that may be defined by joining the basal attachments, or
nadirs, of the three aortic leaflets.
 The distal (uppermost) attachments of the leaflets, in the shape of a crown, form a true anatomic ring.

 Measurements of the aortic annulus should be made in the zoom mode using standard electronic calipers in mid-
systole, when the annulus is slightly larger and rounder than in diastole.
 Measurement should be performed between the hinge points of the aortic valve leaflets (usually between the hinge
point of the right coronary cusp and the edge of the sinus at the side of the commissures between the left coronary
cusp and the non-coronary cusp) from inner edge to inner edge.
 As a general rule, calcium protuberances should be considered as part of the lumen, not of the aortic wall, and
therefore excluded from the diameter measurement.

Aortic Root
 The diameter of the aortic root (at the maximal diameter of the sinuses of Valsalva) should be obtained from the
parasternal long-axis view, which depicts the aortic root and the proximal ascending aorta.
 The tubular ascending aorta is often not adequately visualized from a standard parasternal window. In these
instances, moving the transducer closer to the sternum and/ or to a higher intercostal space may allow visualization
of a longer portion of the ascending aorta.
 Measurements should be made in the view that depicts the maximum aortic diameter perpendicular to the long axis
of the aorta and at end-diastole.
 An asymmetric closure line, in which the tips of the closed leaflets are closer to one of the hinge points, is an
indication that the cross-section is not encompassing the largest root diameter.
 The leading edge to leading edge convention for measurements of the aortic root and aorta is recommended.
 Two-dimensional echocardiographic aortic diameter measurements are preferable to M-mode measurements,
because cardiac motion may result in changes in the position of the M-mode cursor relative to the maximum
diameter of the sinuses of Valsalva.
 INFERIOR VENA CAVA
 The diameter of the IVC should be measured in the subcostal view with the patient in the supine, using the long-axis
view. For accuracy, this measurement should be made perpendicular to the IVC long axis.
 For simplicity and uniformity of reporting, specific values of RA pressure, rather than ranges, should be used in the
determination of systolic pulmonary artery pressure.
 IVC diameter < 2.1 cm that collapses >50% with a sniff suggests normal RA pressure of 3 mm Hg.
 IVC diameter > 2.1 cm that collapses < 50% with a sniff suggests high RA pressure of 15 mm Hg.
 In indeterminate cases in which the IVC diameter and collapse do not fit this paradigm, an intermediate value of 8
mm Hg (range, 5-10 mm Hg) may be used, or, preferably, secondary indices of elevated RA pressure should be
integrated.

Figure 4: Inferior vena cava (IVC) view. Measurement of the IVC The diameter is measured perpendicular to the
long axis of the IVC at end- expiration, just proximal to the junction of the hepatic veins that lie approximately 0.5
to 3.0 cm proximal to the ostium of the right atrium (RA).

Systolic LV function

Assessment and description of left ventricular function comprises usually its systolic or diastolic, global or regional
aspects. Myocardial function during the whole cardiac cycle is more complex, due to myocardial architecture. Radial
left ventricular function predominates certainly, but longitudinal and torsional function also play a role. Global strain
(e.g. 2D-strain), as well as other parameters, can give an insight in the longitudinal left ventricular function. Radial
LV function can be assessed with the methods presented below.

Qualitative assessment of systolic LV function

 — multiple cross-sectional views

 — endocardial movement and myocardial thickening

 — Assessment:

Quantitative assessment of systolic LV function

 — Calculation of left ventricular ejection fraction, LV-EF

  — Formula: [(EDV - ESV) / EDV] x 100 = EF (%)

 — Assessment of LV volumina with the method of discs (modified Simpson's

rule, biplane)

Regional wall motion assessment

17-segment model: left ventricular wall segments

There are several models to depict left ventricular wall segments, and correspondingly, some confusion. The 16-
segment model, suggested by the American Society of Echocardiography in 1989 has proven its practicability in
clinical work.

Three-chamber view, used regularly in echocardiography examinations in Europe since decades introduced two more
apical segments: anteroseptal apical and posterior apical (18-segment model). In American models, apical segments
remained only 4: apical anterior, apical lateral, apical inferior and apical septal.

A new model was recently proposed, in order to equalize standards in echocardiographic, thallium-scintigraphy,
NMR and PET examinations. The document can be downloaded directly from the ASE: Recommendations for
Chamber Quantification, 2005.

The typical distribution of coronary perfusion and the new 17-segment model from the ASE shown here. Segmental
denomination has change since 2005: there are no more posterior segments, also no pure septal or lateral segments,
but anterior and inferior segments (anteroseptal, anterior and anterolateral, as well as inferoseptal, inferior and
inferolateral).

Diastolic LV function
A prerequisite to assessment of diastolic LV function is the capability of the method to measure pressures, and
Doppler echocardiography is only able to measure velocities. Only through application of formulas, as the modified
Bernoulli equation (V² · 4 = ΔP) it is possible to estimate pressure gradients.

Different alternative possibilities to assess diastolic LV function were developed in the last decades. However, these
tools made diagnosis of global diastolic LV dysfunction not always easy and clear. Sometimes different parameters
just do not match to each other, or can not be correctly interpreted in case of atrial fibrillation or flutter.

A new equation enables non-invasive assessment of PCWP, the Nagueh-Formula: 1,9 + (1,24 · E/E') = PCWP, that
could make estimation of diastolic function in some way easier, since PCPW ≈ mLAP ≈ LVEDP. Here an online
calculator from the Canadian Society of Echocardiography, to calculate PCWP.

Mitral inflow velocities examination

Pulsed wave Doppler (PW-Doppler) allows the measurement of velocities at the level of the sample volume. Two
flow velocity envelopes can be seen during diastole in persons with sinus rhythm: the E-wave, representing the early,
passive filling of the left ventricle, and the A-wave, that happens late in diastole, representing the active filling, the
atrial contraction.

Figure: Left: PW-Doppler sample volume is placed at the tips of the mitral valve in the left ventricle.

Figure: Left: pulsed wave (PW) Doppler spectral display shows an E-wave with higher velocities, as well as an end-
diatolic A-wave with lower velocities.
Right: an A-wave twice as large as the E-wave indicates impaired LV relaxation.

Mitral annular velocities examination

Slow wall velocities can be assessed with Tissue Doppler Imaging (TDI). The sample volume, when placed at the
medial mitral annulus, shows slower velocities as when placed at the lateral annulus. The E/E' relationship will be
different according to each case, making more difficult the interpretation of results.
Left: PW-TDI sample volume is place at the level of the lateral mitral annulus.

Left: spectral tissue Doppler (TDI) display shows an antegrade sys- tolic, and two retrograde waves, E' (passive LV
filling) and A'-wave (atrial contraction

Left: PW Doppler spectral display shows a larger systolic (S), a diastolic (D) and a smaller end- diastolic wave (AR), the atria
Right: the shift towards diastole, with a predominant diastolic wave (D) speak for an increase of LA pressure. This can be doc
case of impairment of LV compliance (restrictive pattern).

Velocity of flow progression (Vp)

Velocity of flow progression (Vp) during diastole can be assessed with color Doppler M-mode. A Vp > 50 cm/s can
be considered as normal. A E/Vp ≥ 2.5 in a patient with impaired systolic left ventricular can predict a PCWP > 15
mmHg.

Left: a narrow color Doppler sector is placed between mitral valve and LV apex. The M-mode examination line is
place through the center of the LV entrance flow.

Right: here a normal case. The Nyquist-limit should be reduced if no spontaneous aliasing is ob- served. The first
aliasing velocity front should be measured

Left: higher velocities at the A- wave can be seen at impairment of LV relaxation, even without changing the
Nyquist-limit.
Right: here an example of a restrictive pattern. The Vp is 27 cm/s and hence clearly under the limit of 45 cm/s.

Echocardiographic parameters to assess diastolic LV function

A patient with dyspnea, preserved systolic LV function, dilated left atrium and elevated pulmonary artery systolic
pressure, without any significant mitral valve disease that could explain these findings, is the patient that requires an
intensified search for diastolic LV dysfunction.

I: impaired relaxation, II: moderate diastolic dysfunction (pseudonormal), III: restrictive left ventricular filling

(impaired LV compliance), ECG: electrocardiogram, MI: mitral inflow, MA: mitral annular
velocities, PVF: pulmonary venous flow, Vp: velocity of flow progression, LA: left atrium, PASP: pulmonary artery
systolic pressure.

NYHA: New York Heart Association classification to stages of heart failure, LV-EF: left ventricular ejection
fraction, E/E': relationship between maximal values of passive mitral inflow (E, PW-Doppler) and lateral early
diastolic mitral annular velocities (E', TDI), LV-EDP: end-diastolic LV pressure, PASP: pulmonary artery systolic
pressure.

Right ventricular function

The assessment of the right ventricle (RV) is in a continuos state of "work in progress". Parameters, values and
algorithm presented here may be interpreted differently in the future.

Due to complex RV morphology, a quantitative assessment of systolic RV function is not possible with established
methods, since a required cylindrical form is not available. Therefore, systolic RV function is assessed only
qualitatively. A regional or global RV dilatation must be documented, as well as the diameter and respiratory
behavior of the inferior vena cava.

It is not known if available parameters to assess diastolic LV function would have the same value when assessing
diastolic RV function. However, other have found its place, e.g. parameters for assessment of global function (Tei-
index) or longitudinal systolic function (TAPSE, TASV, RV-strain). A review can be found at Advances in
Pulmonary Hypertension.

Parameters for quantitative assessment: TAPSE, TASV, Tei-Index, LV-EI

For normal values see Table 4 on Guidelines for the Echocardiographic Assessment of the Right Heart in Adults.
Following values can provide fast orientation in the diagnosis of a right ventricular dysfunction.

TAPSE (tricuspid annular plane systolic excursion)   < 2 cm

TASV (tricuspid annular systolic velocity)  < 15 cm/s

Tei-Index (myocardial performance index)   > 0,50

 LV-EI (LV eccentricity index)  >1

Left: TAPSE can be assessed with M-mode, measuring the distance of tricuspid annular movement between end-
diastole to end- systole.
Right: the velocity of this move- ment can be measured with TDI.

Right: Tei-index, also known as "myocardial performance index" (MPI) can be assessed with PW-Doppler in RVOT
and RV inflow, and also with TDI, with the formula (a-b)/b.
Right: eccentricity index (Lei), systolic and diastolic, is an im- portant parameter that can be determined with the
formula: Lei = D1/D2. Normal value = 1.

Assessment of RV function with 3D-echo

RV function can accurately be assessed with three-dimensional echocardiography. Requirements are: a matrix-array
ultrasound probe and a current software for offline analysis of 3D data.

Assessment of pulmonary artery pressure (PA pressure)

The systolic PA-pressure (PASP) is an indicator of cardiac hemodynamic status and can be quiet accurately non-
invasively assessed with echocardiography. There are several pitfalls that may produce over- and underestimation.

Pulmonary artery (PA) pressure estimation

Assessment of PA-pressure is an important part of a correctly and comprehensive conducted echocardiographic

examination. Assessment of pulmonary artery systolic pressure (PASP) can be carried out by measuring maximal
tricuspid regurgitation velocity, and applying the modified Bernoulli equation to convert this value into pressure
values. Estimated right atrial pressure (RAP) must be added to this obtained value. Mean (PAMP) and diastolic PA-
pressures (PADP) can be estimated by assessment of the pulmonary regurgitation.

systolic PA-pressure (PASP)

PASP = tricuspid regurgitation gradient + RA-pressure (RAP)

PASP = (Vmax² x 4) + RAP

Normal values: rest up to 30 mmHg, during exercise up to 40 mmHg.

Mean PA-pressure (PAMP)

PAMP = pulmonary regurgitation gradient (M)

Normal values: rest up to 25 mmHg, during exercise up to 30 mmHg.

Diastolic PA-pressure (PADP)

PADP = pulmonary regurgitation gradient (D) + RAP

Unit II

ANATOMY AND PATHOPHYSIOLOGY OF THE MYOCARDIAL BLOOD SUPPLY

Coronary Anatomy
The myocardium has its own independent blood supply and drainage (Fig.1). Two coronary arteries originate from
the aortic root: The left main coronary artery from above the left coronary cusp of the aortic valve and the right
coronary artery (RCA) from above the right coronary cusp of the aortic valve.
The left main coronary artery bifurcates at around 10 mm into the left anterior descending (LAD) and the left
circumflex (LCX) coronary arteries. The LAD runs along the anterior interventricular sulcus passing the ventricular
apex to reach the posterior interventricular sulcus. On its way to the apex, it gives rise to the diagonal branches and
septal arteries. It thereby supplies the left ventricular (LV) anterior wall, the apex, and the anterior part of the
interventricular septum.
The LCX runs along the left atrioventricular sulcus and gives rise to a large marginal branch and the posterolateral
branches supplying the lateral wall. In patients with left dominant coronary distribution, the distal LCX extends as a
posterolateral branch to supply part of the inferior LV wall.
The RCA runs along the right atrioventricular sulcus, where its middle section gives off the right ventricular (RV)
acute marginal branches. These acute marginal branches supply the RV free wall and the conduction system
including the sinus and atrioventricular node. The RCA bifurcates into the posterior descending artery and the right
posterolateral branch. Their supply territory is the inferolateral RV wall, the inferior part of the interventricular
septum, and the inferior wall of the LV.

  Figure 1. Anatomy of the coronary arteries of the heart.

Figure 2. The 17-segment model of the left ventricle (inner ring) as demonstrated in the transgastric short axis views.
The outer ring shows the common (solid line) and variant (dash line) coronary artery distributions. RCA, right
coronary artery; LAD, left anterior descending artery; LCX, left circumflex artery.

Variations in Coronary Anatomy and Main Distribution Types

There are three major variations of coronary distribution. These distribution types affect the posterior descending
artery and posterolateral branch which supply the inferior septum and inferior wall of the LV ( Figs1–Figs.5). The
right dominant coronary distribution type is the most common (80% to 85%), where supply originates from the RCA.
In left dominant systems supply is via the LCX artery. A balanced or co-dominant type is present in about 5% of
individuals, where the posterior descending artery and posterolateral branch receive supply from both the RCA and
from the LCX. Recent imaging studies, however, have altered traditional concepts of coronary perfusion zones as
well as reveal the significant individual variation in coronary supply to the myocardial segments. For example, the
apical segments are now understood in the majority of cases to be supplied by the LAD with the LCX and RCA seen
in a minority of individuals. The greatest overlap in coronary artery distribution occurs in the inferolateral region
corresponding either to RCA or LCX territories, as well as the inferoseptal region that may be supplied by the LAD
artery, RCA, or even a left-dominant LCX artery. Figure 2. incorporates these recent findings and emphasizes the
large amount of myocardium supplied by the LAD artery and potential for substantial infarct size with LAD
occlusion. The coronary distribution can be defined by cardiac catheterization and this information is valuable when
communicating regional wall contraction abnormalities (RWCAs) to the surgeon.

Figure 3. Segmental anatomy of the left ventricle in the midesophageal 4 chamber view and corresponding coronary
perfusion (common solid color, variant dashed color). LAD, left anterior descending; LCX, left circumflex; RCA,
right coronary arteries.

Figure 4. Segmental anatomy of the left ventricle in the midesophageal 2 chamber view and corresponding coronary
perfusion. LAD, left anterior descending; RCA, right coronary arteries.

Echocardiographic Assessment of Coronary Arteries

Two-dimensional Visualization of Coronary Artery Anatomy

Coronary ostia: From the midesophageal (ME) AV SAX view, the coronary ostia can be visualized by a small
degree of anteflexion or withdrawal of the probe (Fig.6). The left coronary ostium and the full length of the left main
coronary artery to its bifurcation into the LAD and LCX are visible in the middle of the left coronary cusp at the 1- to
2-o’clock positions. The right coronary ostium is visible in the middle of the right coronary cusp at the 6- to 7-
o’clock positions.
Figure 5. Segmental anatomy of the left ventricle in the midesophageal long axis view and corresponding coronary
perfusion (common solid color, variant dashed color). LAD, left anterior descending; LCX, left circumflex; RCA,
right coronary arteries.

Figure 6. The left and the right coronary ostia in the two-dimensional aortic short-axis view (A) and with added color
flow Doppler (B). The left coronary ostium is visible in the middle of the left coronary cusp at the 1- to 2-o’clock
positions. The right coronary ostium is visible in the middle of the right coronary cusp at the 6-o’clock position.

Left coronary artery: The LAD is visualized by further rotation to ~120 to 130 degrees and a slight turn of the probe
to the left. To follow the LCX from the left main bifurcation ME AV SAX view, the probe is turned leftward and
advanced slightly while following the LCX on its way around the atrioventricular groove.

Right coronary artery: The proximal RCA can also be imaged from the ME AV SAX view supported by slight
anteflexion. In addition, the ostium and proximal parts of the RCA can be imaged in a modified ME AV LAX view
at 120 to 160 degrees.

Doppler Evaluation of Coronary Artery Blood Flow

For color flow Doppler assessment of coronary blood flow, it is recommended to initially set the Nyquist limit to 50
cm/s for examination of the left coronary artery and to 20 cm/s for the RCA. Further reduction in the Nyquist limit is
often required to obtain an adequate signal. The angle of incidence has to be taken into account when interpreting the
results, as the angle may continuously change for neighboring sections of the same vessel due to the curved course of
the coronary arteries. Normal coronary arterial blood flow shows a biphasic, laminar pattern with a short systolic
wave of slower velocity and a longer diastolic wave of higher velocity with a deceleration slope. This can be
measured using pulse wave Doppler (Fig.9). Reported normal mean peak coronary flow velocities are in the range of
30 to 35 cm/s during systole and 70 to 75 cm/s during diastole for the left coronary artery, and approximately 25
cm/s during systole and 40 cm/s during diastole for the RCA. Visualization of the coronary ostia and arteries, and of
intracoronary flow may be of importance in situations with acute new segmental wall motion abnormalities, for
example, during separation from cardiopulmonary bypass (CPB) after mitral valve surgery in patients with aortic
dissection or during transcatheter aortic valve implantation.
 .
Figure 7. The left circumflex coronary artery (arrow) in long axis.

Detection of Coronary Artery Pathology

Although echocardiographic diagnosis of coronary artery stenosis is not a daily practice, it can be clinically valuable
for assessing proximal vessel disease when coronary angiography is not practical (i.e., during emergent cardiac
surgery). Indicators are increased echo density, suggesting calcification of the vascular intima, and turbulent color
Doppler flow signals. The following velocities have been published as threshold for hemodynamically relevant
stenosis (>50%): Left main coronary artery >140 cm/s, LAD >90 cm/s, LCX >110 cm/s. The percentage reduction in
vessel diameter or diastolic velocity–time integral at the site of stenosis compared to the normal segment proximal to
the stenosis correlates well with the degree of stenosis diagnosed by coronary angiography.

Figure 8. The right coronary ostium and proximal RCA (arrow) in a modified ME AV
LAX view

Figure 9. Pulsed wave Doppler recording of coronary flow. Normal coronary arterial blood flow shows a biphasic,
laminar pattern with a short systolic wave of slower velocity and a longer diastolic wave of higher velocity.

PHYSIOLOGIC BASIS FOR THE DETECTION OF ISCHEMIA

Segmental endocardial motion and myocardial thickening are the foundations for echocardiographic detection of
myocardial ischemia. As first observed by Tennant and Wiggers in 1937, occlusion of a coronary artery results in
severe regional wall motion abnormality (RWMA) in the corresponding myocardium. Decades later, Pandian et al.
established the value of echocardiography for detecting ischemic RWWAs. Since then, multiple human studies have
shown that RWCA (i.e., reductions in systolic wall motion and/or thickening) detected by echocardiography are an
earlier and more sensitive indicator of ischemia than electrocardiography (ECG).
The progression in wall dysfunction from hypokinesia to dyskinesia correlates to the progression in degree of
perfusion abnormalities which has been established in dog studies. Reductions in systolic wall thickening reflect
subendocardial ischemia, while akinesia reflects ischemia sparing the subepicardial myocardial layer only, and
dyskinesia plus acute wall thinning are seen in the setting of transmural ischemia. An echocardiographic dog study
has found that segmental contraction abnormalities are induced only when myocardial perfusion is less than 25% of
control. Although human data on the possible quantitative relationship between myocardial perfusion and segmental
wall contraction are missing, from a clinical point of view acute changes in segmental function are highly indicative
of acute ischemia.
Prolonged reduction or cessation of coronary flow leads to infarction. By echocardiography, acutely infarcted
myocardium may look similar to acutely ischemic myocardium. In contrast, scar tissue presents
echocardiographically as a thin, dense, and permanently akinetic or dyskinetic wall.
Although reduced or absent wall thickening may be the most sensitive indicator of ischemia, reduced endocardial
motion may be the more conspicuous echocardiographic sign of severe ischemia. However, adjacent nonischemic
regions may pull the endocardium of an ischemic area inward; this points out the importance of also considering wall
thickening that will still indicate ischemia. Quite typically, unaffected, nonischemic regions develop exaggerated
inward movement (termed compensatory hyperkinesis) that partially offsets the adverse effects of akinesis or
dyskinesis in other regions on cardiac stroke volume. This is the principal reason why hemodynamic instability is a
late and ominous sign of ischemia and usually only occurs with very severe regional or global ischemia.

Table.1 characteristics, echocardiographic findings, and clinical implications of myocardial ischemia.

Clinical Syndromes of Myocardial Ischemia

The echocardiographer must be cognizant of the various presentations of ischemic tissue, including myocardial
stunning and hibernation, which complicate the echocardiographic assessment of myocardial viability. Acute
ischemia results from severe reductions in coronary blood flow and is associated reductions in wall thickening and
endocardial inward motion. Stunned myocardium occurs following an acute episode of ischemia when a potentially
reversible RWCA transiently persists despite full restoration of blood flow. Hibernation is a chronic ischemic
condition where RWCAs persist in viable myocardium with marginal resting blood flow. LV function may improve
markedly and mortality may be reduced following successful coronary revascularization. The time course of
recovery is variable.
The echocardiographic appearance of stunning and hibernation during resting conditions is similar to acutely
ischemic myocardium (Table.1) Echocardiography and other imaging techniques can be used in combination with
clinical algorithms for differentiation of myocardial ischemia, hibernation, stunning, and nonviable, infarcted tissue.
Dobutamine stress echocardiography is used for the detection of viable hibernating myocardium. Viable myocardium
shows improved regional contractile function (inotropic reserve) in response to low dose dobutamine administration.
For patients with ischemic heart disease, dobutamine stress echocardiography predicts the likelihood of left
ventricular functional recovery following revascularization. In addition, in patients with left ventricular dysfunction,
caused by myocardial infarction, dobutamine stress echocardiography is useful for evaluating the presence of
hibernating myocardium due to a residual stenosis that warrants intervention. Patients with left ventricular
dysfunction who demonstrate myocardial viability with dobutamine stress echocardiography have a better survival
with revascularization than with medical therapy. A key message is that an RWCA is not always caused by acute
ischemia but may reflect stunning, hibernation, and/or nonviable infarcted tissue.

ECHOCARDIOGRAPHIC ASSESSMENT OF ISCHEMIA

Anatomic Localization of Ischemia: The 17-segment Model

The 17-segment model of LV topographical anatomy (Fig.2) provides a common nomenclature across imaging
specialties to define the LV segmental anatomy. Using the 17-segment model in the setting of perioperative TEE has
the advantage of applying the same topographical concept for describing regional function of the LV as in
transthoracic echocardiography, cardiovascular magnetic resonance imaging, nuclear cardiology, and cardiac
computed tomography. It also serves as the basis for correlating the location of RWCA with coronary perfusion.
Echocardiographic Imaging of the 17 Myocardial Segments
The 17-segment model divides the LV along its longitudinal axis into three levels plus the apical cap (Fig. 4.2). The
basal and mid (midpapillary) levels are subdivided into six segments: The anteroseptal, anterior, anterolateral,
inferolateral (formerly “posterior”), inferior, and inferoseptal segments. The apical level is subdivided into an
anterior, lateral, inferior, and septal segment.
The three standard ME views (ME four-chamber, ME two-chamber, and ME long-axis) (Figs.3–Figs.5) allow
visualization of parts of all 17 segments. Although all the three views theoretically visualize the distant apical slice
(segment 17), often the echo imaging plane transects the ventricle above the true apex and the TEE image is
“foreshortened.” To obtain correct alignment of the imaging plane along the long axis of the LV, the
echocardiographer should focus on obtaining the maximum long-axis dimension in each view. Favorable settings
include a low ultrasound frequency (usually no higher than 6 MHz), because the apex is in the far field of the TEE
image; a focal zone placed in the area of the apex; and optimized gain settings in that field.
The transgastric (TG) short-axis views (basal, mid, and apical) allow visualizing the entire radius of 16 segments
excluding the apical cap. The TG basal and midpapillary short-axis views are unique in that myocardial territories
perfused by all the three main coronary arteries are visualized (Fig.2). Although ischemia monitoring in TG
midpapillary short-axis view is popular, using this view alone is inadequate, because ischemia caused by stenosis in
an artery more distal to this plane will be missed. Repeated assessment of multiple views is essential as limiting the
examination to the TG midpapillary SAX view alone will miss the majority of RWCA. We advise comprehensive
monitoring of all the 17 segments for ischemia utilizing both ME and TG imaging planes.

Coronary Perfusion of LV Segments

The coronary perfusion to the 17 LV segments is shown in figure. Many segments have a consistent coronary artery
perfusion. Recent imaging studies, however, have altered traditional concepts of coronary perfusion zones as well as
reveal the significant individual variation in coronary supply to the myocardial segments. For example, the apical
segments are now understood in the majority of cases to be supplied by the LAD with the LCX and RCA seen in a
minority of individuals. The greatest overlap in coronary artery distribution occurs in the inferolateral region
corresponding either to RCA or LCX territories, as well as the inferoseptal region that may be supplied by the LAD
artery, RCA, or even a left-dominant LCX artery. Figure. 2 incorporates these recent findings and emphasizes the
large amount of myocardium supplied by the LAD artery and potential for substantial infarct size with LAD
occlusion. In those segments with physiologic variability in coronary supply, the culprit coronary artery of an
RWCA can often be identified by examining neighboring segments whose coronary supply is known. For example,
the combination of ischemia in the anterolateral and inferolateral walls is consistent with a left dominant or co-
dominant LCX occlusive disease while the presence of anterolateral ischemia without inferolateral wall ischemia is
specific for a non-dominant LCX occlusion.

Assessment and Grading of Regional Wall Contraction Abnormalities

To grade the severity of ischemia, it is important to analyze both systolic myocardial thickening and endocardial
inward motion (“radial shortening”) (Table. 2). The American Society of Echocardiography/Society of
Cardiovascular Anesthesiologists (ASE/SCA) guidelines for TEE examination classify systolic ventricular
contraction in five grades: Normal contractility, mild hypokinesis, severe hypokinesis, akinesis, and dyskinesis
(Table 2). For systolic myocardial thickening, a 50% increase is regarded as normal, but given substantial
intersegment and intersubject variability, a value of 30% thickening has been defined as the lower normal limit.
Similarly, systolic radial shortening has been defined as normal if it exceeds 30%.

Table.1 : Five-grade scale of segmental wall contraction abnormalities

Figure10. Normal LV M-mode (motion mode) reading. Normal inward endocardial excursion and wall thickening
are illustrated on an M-mode image through the inferior (top) and anterior (bottom) walls in the transgastric short-
axis view (top inset). Systole starts at the onset of the QRS complex and ends near the end of the T wave ( arrows).
M-mode echocardiographic imaging coupled with the electrocardiogram can on occasion provide helpful
information regarding the timing of wall motion.

Assessment of SV, Cardiac Output (CO), and SVR

Measurement of SV of both the right and left ventricles can be performed readily using PW Doppler.These
measurements can be reliably obtained using TTE and TEE. Assessment of CO is important in determining
responses to medical and surgical therapies, such as administration of inotropic agents for the treatment of right and
left heart failure. Using PW Doppler, SV through a site (such as the RV outflow tract [RVOT] or LV outflow tract
[LVOT]) can be calculated using two variables: (1) the velocity-time integral (VTI), or stroke distance, and (2) the
cross sectional area of the site (using the diameter of the RVOT or LVOT). Thus,
Stroke volume (or flow) = Cross sectional area (cm2) x VTI (cm).

Because CO = SV heart rate, both right- and left-sided CO can be serially measured noninvasively before and after
medical therapies. In clinical practice, RV SV is calculated by using the parasternal SAX view. PW Doppler can be
used to acquire the RVOT VTI (in centimeters) in this view. Because of difficulties in measuring the RVOT
diameter, it is recommended that the RVOT VTI be used as a monitor of RV SV. LV SV is calculated on TTE using
the apical five-chamber or LAX view. The deep transgastric LAX view is used in TEE, whereby the PW Doppler
sample volume is placed in LVOT. Gradients across the aortic valve (in the setting of prosthetic valve thrombolysis
monitoring) should be acquired with continuous-wave Doppler monitoring in this location. Measurement of the
baseline LVOT diameter is best accomplished in the ME LAX view. The LVOT diameter can be used to calculate
area, which when combined with the LVOT VTI and heart rate can be used to calculate SVand CO. Using IVC
collapsibility indices to estimate RAP, and arm blood pressure measurements to calculate mean arterial pressure,
SVR (in Wood units) can be calculated as

SVR = MAP - RA pressure (mm Hg) / CO (lit/ min)

To convert this to conventional SVR units (dynes.sec/cm 5), this value should be multiplied by 80. The limitations of
echocardiographic measurements of SV, CO, and time-velocity integrals in the LVOT are that all measurements
require accurate alignment with the LVOT, and consistent sampling should occur just beneath the aortic valve. The
use of an LVOT diameter adds a second potentially more significant error measurement, and it was the
recommendation of the committee that stroke distance (i.e., LVOT and RVOT time velocity integrals) alone be used
for serial measurements, with the assumption that LVOT diameter remains constant.

Transvalvular gradient, Orifice area, continuity equation

The pressure gradient across aortic valve derived from the Bernoulli equation is the peak instantaneous pressure
gradient, and not the peak-to-peak pressure gradient as measured during cardiac  catheterisation. The peak-
instantaneous gradient derived from Doppler measurements across a stenosis will always be higher than the peak-to-
peak gradient. This means that Doppler interrogation systematically overestimates pressure gradients measured
invasively. To overcome this problem, the mean pressure gradient can be calculated by integrating the velocity curve
during ejection, and thus calculating the mean gradient. This is the average of all the instantaneous pressure gradients
throughout ejection.
This is calculated electronically by tracing the Doppler curve. Mean pressure gradients have been shown to correlate
better with gradients obtained during cardiac catheterization, and are generally used to assess the severity of a
stenosis. The hypertrophic response to an obstructed outflow tract, however, is related more to the peak gradient than
to the mean gradient. So, in the decision-making process to judge the severity of a narrowing, both the peak as well
as the mean gradient has to be taken into account, as well as the effect on the ventricular muscle.

Figure 1. The peak and mean gradients of flow across the aortic valve in a patient with aortic stenosis.
Doppler echocardiography permits measurement of transvalvular velocities. These can be employed to derive
gradients (using the Bernoulli equation). As transvalvular velocities usually exceed 1.7 m/sec in mitral stenosis, it is
necessary to use CW Doppler. Accurate measurement of maximal velocities requires that the Doppler sample be
aligned parallel to mitral valve inflow from the apical view (usually on the 4-chamber view) and traverse the vena
contracta. To optimize the spectrum one should use color Doppler for guidance of the Doppler line. Several beats
should be averaged when atrial fibrillation is present.

Maximal inflow velocity should be measured at the peak E-wave (in the presence of sinus rhythm). This velocity
corresponds to the maximal gradient. As this initial velocity is highly variable and depends not only on the severity
of stenosis, it is of minor importance for the quantification of mitral stenosis. The mean gradient is more relevant; it
is calculated from mean velocity by tracing the Doppler spectrum. Mean gradients are easy to obtain and highly
reproducible. However, they are strongly affected by heart rate and stroke volume. Gradients are also higher when
mitral regurgitation is present.
Traditionally, valve area has been considered a "flow-independent" measure of stenosis severity. However, recent
evidence indicates that Gorlin valve areas vary with changes in transvalvular volume flow rate. Although an apparent
increase in calculated valve area may represent a "true" increase in anatomic orifice area caused by flow-mediated
distension of a nonrigid valve, Gorlin valve areas also have been observed to vary in in vitro models using fixed
orifice areas. This phenomenon has been attributed to volume flow-mediated variability of the discharge coefficients
used in the Gorlin equation. Valve areas derived by both Gorlin and continuity equations are based on similar
hydrodynamic principles. However, the continuity equation measures "effective" orifice area: the area of the vena
contracta.

In contrast, the Gorlin equation approximates "anatomic" valve area by assuming a coefficient of orifice contraction
that is constant at varying transvalvular flow rates. In addition, the Gorlin equation assumes a constant coefficient of
velocity, which accounts for energy dissipation caused by frictional loss and turbulence as pressure converts to
velocity across the stenotic valve. Doppler-echo techniques measure transvalvular velocity directly, thus avoiding
this assumption. As well, the mathematical formulation of the Gorlin equation contains a simplification of the
temporal instantaneous pressure-flow relation that is not required with the continuity equation.

Continuity equation valve areas derived from Doppler-echo data are not free of assumptions. Flow in both the left
ventricular outflow tract and the vena contracta are assumed to be laminar with flat velocity profiles. Thus,
prestenotic and transvalvular velocities measured at one point are assumed to represent the mean spatial velocities
across the left ventricular outflow tract and vena contracta, allowing calculation of prestenotic volume flow rate and
vena contracta area. In addition, technical difficulties in accurate Doppler and two-dimensional data collection and
analysis, most importantly, errors related to nonparallel Doppler/blood flow intercept angle and suboptimal imaging
of maximal outflow tract diameter, are assumed to be minimal.

The different assumptions underlying the Gorlin and continuity equations may have potential implications when
valve area measurements are made at different transvalvular volume flow rates. The purpose of this study was to
investigate the effects of changing transvalvular volume flow rate on aortic valve areas derived simultaneously by
both the Gorlin and the continuity equations. A canine model of chronic valvular aortic stenosis, in which anatomy
and hemodynamics are similar to those of degenerative aortic stenosis, was used in which pressure, volume flow
rate, and Doppler-echo data could be acquired simultaneously during controlled variations in transvalvular volume
flow rate.

Calculation of AVA by means of Doppler echocardiography is a widely used standard for evaluation of aortic valve
stenosis in clinical practice. Transthoracic echocardiography (TTE) plays an important role in management decisions
including indications for surgery and scheduling follow ups in individuals with aortic stenosis. TTE is non invasive,
easily to perform, readily available and inexpensive and offers an acceptable intraobserver and interobserver
reproducibility. Therefore, a full hemodynamic study with retrograde catheterisation of the AV is no longer
recommended if non invasive assessment of the severity of AS is adequate to assess valve hemodynamics.

Echocardiographic valve area calculation is based on the continuity equation, which assumes that the flow (F) on
both sides of the aortic valve orifice is equa. Flow is defined as cross sectional area (CSA) multiplied by flow
velocity (V). Across the aortic valve (AV), the flow is equal to stroke volume (SV). Because SV is the product of the
CSA and time velocity integral (VTI), the CE can be arranged to yield:

AVA = (LVOTVTI x LVOTCSA)/AVVTI)

in which LVOTVTI is the velocity time integral at the level of the stenotic valve and CSA is the cross sectional area
of the LVOT.

Echocardiographic assessment of Mitral Stenosis

Mitral valve assessment with echocardiography should include the pattern of valve involvement and calcification,
severity of stenosis, associated mitral regurgitation and other co-existent valve lesions and atrial chamber dilatation
and function. Mitral stenosis can be assessed in parasternal, apical
or subcostal views. As with any stenotic valve the main diagnostic feature in the parasternal long axis view (Fig. 1)
as in rheumatic MS, the anterior mitral leaflet (AMVL) shows diastolic doming or hockey-stick shape. And the
posterior mitral leaflet (PMVL) has restricted motion or is totally immobile. This doming is due to the reduced
mobility of the valve tips compared to the base of the leaflets.

Figure I: Parasternal long axis view in diastole, showing diastolic doming (hockey-stick shape) of anterior mitral
valve leaflet (AMVL) and thickened, restricted posterior mitral valve leaflet (PMVL). RV = right ventricle, LV = left
ventricle, LA = left atrium
Echocardiography can also adequately assess the Subvalvular apparatus changes such as thickening, shortening,
fusion of chordal and calcification (Fig. 1). Color Doppler in this view with diastolic turbulence across the mitral
valve confirms the diagnosis. On the other hand, Parasternal short axis view of the mitral valve is used to assess
the leaflets thickening and fusion of commissures. The parasternal short axis view is also used to assess the mitral
valve orifice area by planimetry of the mitral leaflets at the level of tips (Fig. 2).

Figure 2: Parasternal short axis view of the mitral valve at the level of the tips to measure mitral valve area (MVA)
by planimetry. (A) Prior to percutaneous balloon mitral valvuloplasty (PBMV), showing fused both commissures
with MVA = 1.2 cm2. (B) Same patient after PBMV, showing complete opening of the anterolateral commissure and
partial opening of the posteromedial commissure. MVA = 2.0 cm2.
Indices of stenosis severity
The Following are different means of measurements by echocardiography to assess the severity of MS, which are
mandatory in all patients:
Planimetry of mitral valve at the level of the leaflets tips in parasternal short axis view (Fig. 2). This method is a
very familiar technique by 2D echocardiography. but the same method can also be used in 3D echocardiography en-
face view of mitral valve (Fig. 3). However, newly developed QLAB software in 3D echo is now available for
calculation of mitral valve orifice area which requires further validation (Fig. 4).

Figure 3: 3D TEE zoom-mode of mitral valve with severe rheumatic MS. (A) Left atrial (LA) view or surgical
orientation, as surgeon will see the mitral valve in the operating room after opening the left atrium. Aorta is located
anterior to the MV and left atrial appendage is oriented at the left side of surgeon. (B) LV view of mitral valve
showing fish mouth of mitral orifice. Surgeon will not see this side of mitral valve except opening from aortic root.
Note grid in the screen which can be used for measurements but still should be validated.

Figure 4 : Calculation of mitral valve area (MVA) by QLAB software implemented in the 3D echo machine. (A)
Two orthogonal views of mitral valve are derived from a 3D zoom-mode acquisition of the mitral valve. After proper
alignment of lines representing x, y and z axis, mitral valve orifice will appear and MVA can be traced. (B) MVA
was traced and showed 1.1 cm2. This software still needs validation.
Calculation of mitral valve area (MVA) by pressure half-time (P1/2 t) should be done in an apical four chamber
view using continuous wave Doppler (Fig. 5). Pressure half-time method is not valid immediately after percutaneous
balloon mitral valvuloplasty (PBMV). MVA should be averaged in 3 consecutive beats and in case of atrial
fibrillation in it should 5 beats.
Figure 5. Calculation of the mitral valve area (MVA) by the method of pressure half-time (P1/2t).
Mean pressure gradient across the mitral valve can be measured in apical views. Modal Doppler (most dense
portion of the Doppler curve) should be used for calculation (Fig. 4). The gradient can be measured by tracing the
dense outline of mitral diastolic inflow and the mean pressure gradient is automatically calculated. The severity can
be assessed as mild (<5), moderate (5–10) and severe (>10).

Continuous wave Doppler parallel to the mitral inflow in apical 4 chamber view to measure mean peak gradient
(Mean PG) across the mitral valve. Measurements should be done in 3–5 consecutive beats and averaged.
Estimation of pulmonary artery systolic pressure and the right ventricular systolic pressure (RVSP) is
necessary. It can be measured from tricuspid regurgitation velocity by Bernoulli equation ( Fig. 6). RVSP can also be
assessed during exercise in borderline cases.

Figure 6: Estimation of pulmonary artery systolic pressure (right ventricular systolic pressure) using TR velocity and
gradient in short axis view in a patient with severe MS and severe pulmonary hypertension (B) Calculation of left
atrial volume using method of discs (MOD) in apical 4 chamber view in same patient, showing severe increase of
LA volume.
Consequences of mitral stenosis on other cardiac chambers such as left atrial dilatation, tricuspid regurgitation and
also right ventricular function should be evaluated by echocardiography. Left ventricular function is usually intact in
uncomplicated mitral stenosis.
Grading of mitral stenosis 
In grading the severity of MS based on echocardiographic evaluation, the following recommendations by the
EAE/ASE are the used standards of practice. Please refer to Table 1.

Table 1: EAE/ASE recommendations for classification of mitral stenosis severity.

Echocardiography in the assessment of mitral valve regurgitation

Mitral regurgitation (MR) is one of the most common acquired valvular heart diseases. Echocardiographic
assessment of MR provides insight into the mitral valve (MV) and plays an important role in:

 Assessment of MV anatomy to understand the aetiology and mechanism of MR.

 Assessment of MR severity.
 Detection of impact on LV cavity size and overall function.
 Guiding the selection of therapeutic strategy.

Assessment of mitral valve Anatomy

A detailed anatomical description of the MV is a crucial part of the assessment of MR. All of the components of the
MV apparatus including the leaflets, annulus, chordae, papillary muscles, and left ventricle (LV) have to be
evaluated carefully by echocardiography. Based on this evaluation, it is possible to differentiate between primary and
secondary chronic MR. In chronic primary MR, the involvement of one or more of the components of the valve
(leaflets, chordae tendineae, papillary muscles, annulus) can cause MR. In chronic secondary MR, the MV is usually
normal and the underlying mechanism is severe LV dysfunction that leads to papillary muscle displacement and
leaflet tethering with associated annular dilation that prevents coaptation.
In chronic primary MR, echocardiography helps in:

 Detailed assessment of the MV leaflets to diagnose prolapsed scallop(s), flail leaflet, perforation, vegetation,
etc.
 Detailed assessment of the subvalvular apparatus to diagnose ruptured chordae, ruptured papillary muscle.

In chronic secondary MR, echocardiography helps in:

 Volumetric measurement of LV size and ejection fraction.

 Assessment of global and regional wall motion abnormalities of the LV.
 Tethering of the MV leaflet due to papillary muscle displacement.
 Symmetric or asymmetric mitral annulus dilatation.

Assessment of MR severity

Many parameters (qualitative, semi-quantitative and quantitative) can be used to define the severity of MR. None of
them can be relied on solely for the definition. An integrative approach to include most of them is a must to achieve
accurate diagnosis and overcome the pitfalls and limitations of each parameter.

Qualitative assessment
n addition to the detailed morphologic description of MV apparatus, the following echo findings can identify the
presence of significant MR but not assess its severity.

Density of MR signals
Using continuous wave Doppler, if the signal is similar in density to that of antegrade flow, this suggests significant
MR, whereas a faint signal or an incomplete envelope is typical of mild MR (Figure 1A).

Colour flow jet of MR

A colour Doppler imaging MR jet indicates the presence of MR. Appropriate adjustment of the gain setting is
important to avoid underestimation and overestimation of MR severity. It can help in understanding the mechanism
of MR through the direction of the MR jet. For example, in MR secondary to leaflet tethering, the regurgitant jet
points towards the restricted leaflet, while in MV prolapse the regurgitant jet points away from the prolapsed leaflet.
Measurement of the MR jet area alone or indexed by left atrium area is not valid for the severity because the jet area
is very dependent on the mechanism of MR and usually underestimates the severity with the eccentric jet. In case of
a normal MV structure, normal LV and LA size, a small central jet area of <4.0cm² (or <10% of LA area) in multiple
views is usually mild MR (Figure 1B).
Semi Qualitative assessment

The following echo parameters help to identify the severity of MR but each one has limitations and pitfalls. These
include:

Vena contracta (VC) width

The VC is defined as the smallest, highest-velocity region of a flow jet and is typically located at or just below the
regurgitant orifice. Its width should be measured in a long-axis imaging plane perpendicular to the mitral leaflet
closure. The VC is independent of flow rate and driving pressure. It can be used for central and eccentric jets and is
accurate in acute MR. However, it is not valid for multiple jets. A VC width <0.3 cm denotes mild MR and a VC
width >0.7 cm is specific for severe MR. Intermediate values of VC width (0.3-0.7 cm) do not mean that MR is
moderate; confirmation by other quantitative methods is needed (Figure 1C).

Pulmonary venous flow reversal

Reduced systolic velocity in >1 pulmonary vein and even reverse flow indicates severe MR. However, increased left
atrial pressure of any cause can result in blunted pulmonary venous systolic flow (Figure 1D). Absence of flow
reversal should not be used for exclusion of significant MR. It can be false negative if the jet is directed away from
pulmonary veins, e.g., highly eccentric MR and/or severely dilated left atrium. On the other hand, if the MR jet is
small but eccentric and directed towards the pulmonary vein, blunted or reverse flow can be recorded in this
pulmonary vein (false positive).  

Peak velocity of E-wave of MV inflow

Using pulsed Doppler at the tip of the MV, early filling (E-wave) usually dominant (E velocity >1.5 m/s) indicates
severe MR due to increased forward flow across the MV. If the A-wave is dominant, severe MR can be excluded
(Figure 1E).

Regurgitant index
A non-geometric pulsed Doppler index, namely the mitral to aortic velocity-time integral (VTI), is used for
quantification of pure isolated organic MR. A ratio ≥1.4 defines patients with severe MR with a sensitivity of 87%,
and a specificity of 91%.
Quantitative assessment

These parameters carry more accuracy for the definition of severe MR. They include:

Effective regurgitant orifice area

The flow acceleration proximal to the regurgitant orifice results in a concentric proximal isovelocity surface area
(PISA). PISA is based on the fact that, near the regurgitant orifice, the blood is disposed in hemispheric layers,
having the same velocity at a certain distance from the orifice. Lowering the velocity at which aliasing appears to 15-
40 cm/s, all the “layers” with a higher velocity will have the aliasing phenomenon. Measuring the first aliasing
hemisphere is a marker of regurgitation degree. PISA measurement requires a narrow sector of colour with zoom
mode and a shift of the Nyquist limit to be between 15-40 cm/sec. Four formulas are used for calculation:

 PISA = 2πr2 (assuming that PISA is a hemisphere).

  Regurgitant flow rate (RFR) = PISA x aliasing velocity (which is equal to the Nyquist limit on the colour
scale).
 Regurgitant orifice area (ROA) = RFR/max MR velocity. Effective ROA (EROA) <0.20 cm² indicates mild
MR and ≥0.40 indicates severe MR.
 Regurgitant volume (RV) = ROA x velocity time integral (VTI) of MR. RV <30 ml/beat indicates mild MR
while ≥60 ml/beat indicates severe MR.    

Volumetric measurement
Quantification of RV and regurgitant fraction (RF) is based on calculation of stroke volume (SV) across the MV and
across another non-regurgitant valve (aortic or pulmonic). The formula used for SV calculation is: SV=cross-section
area x VTI. Subtraction of the SV obtained at two sites is used to calculates RV. RF is calculated as a percentage of
RV to SV across the MV. RF <30% indicates mild MR while ≥50% indicates severe MR. ROA can also be obtained
by the formula: ROA= RV/VTI of MR.  To calculate SV across the aortic valve, a parasternal long-axis view is used
to measure LV outflow tract (LVOT) diameter at the level of the aortic valve annulus, just proximal to the cusps, and
an apical 5-chamber view to measure the VTI of the LVOT using pulsed wave Doppler placing the sample volume at
the level of the same point where the LVOT diameter was measured. To calculate SV across the MV, an apical 4-
chamber view is used to measure the MV annulus diameter and to measure the VTI of the MV using pulsed wave
Doppler placing the sample volume at the tip of the leaflet.

 
Figure 1. Methods used for MR quantification. Continuous Doppler tracing showing dense signal with severe MR
and faint with mild MR (A), tracing of MR jet area (B), width of vena contracta (C), reversal of pulmonary venous
flow (D), dominant E-wave of mitral inflow in severe MR (E), calculation of MR using PISA method (F), and
volumetric measurement of stroke volume across the MV (G).

The criteria used to define severe MR using previous parameters are displayed in following table. Considering the
profound deleterious effect of ischaemic MR, the cut-off levels of severity are lower than in organic MR.
Technical considerations
 To optimise the measurement of VC, the view that is perpendicular to the jet width such as parasternal long-axis or
4-chamber views should be used. Using the apical 2-chamber view, which is oriented parallel to the line of leaflet
coaptation, a wide VC may show even in mild MR.
- In ischaemic MR, the assessment of VC width should be carried out in two
orthogonal planes (e.g., parasternal and apical four-chamber) and an average of these two should be
reported due to the elliptical shape of the regurgitant orifice.
- In multiple jets, both VC width and PISA are not additives and cannot be used.
- In eccentric jets, the largest PISA is to be found in the parasternal long-axis view, while in central
jets the apical 4-chamber view should be used.
- If PISA is not a typical hemisphere, the severity of MR can be overestimated (e.g., if it is flattened)
or underestimated (e.g., if it is oval).
- Volumetric quantification by Doppler is used as an additive to PISA and VC
but not as a first-line method because it is time-consuming.   

Mitral valve prolapse

Mitral valve prolapse is defined by displacement and thickening of the mitral valve leaflets.
In patients with classic mitral valve prolapse, or “floppy mitral valve,” myxomatous connective tissue expands the
spongiosa and separates bundles of collagen in the fibrosa, weakening the support of the valve
• Signs, symptoms, and complications often thought to be associated with mitral valve prolapse more likely result
from severe MR or congestive heart failure.
• Echocardiography shows degree of prolapse and of leaflet thickening; 3-dimensional imaging is most specific.
• A “nonclassic” subtype of mitral valve prolapse involves less thickening of leaflets and carries a lower risk of
complications.
• Complications include severe MR, infective endocarditis, and need for valve replacement.
• Sudden death is rare, usually occurring in the context of severe MR and heart failure; no clear evidence links stroke
to mitral valve prolapse.
M-mode echocardiography

In the early 1970s, a series of reports suggested that M-mode echocardiography might offer an ideal noninvasive
method for visualizing the abnormal motion of the prolapsing mitral valve, and a pattern of abrupt late systolic
posterior leaflet displacement was described. These relatively specific criteria, in small groups of severely affected
individuals and often confirmed surgically or angiographically, were soon deemed insufficiently sensitive, and the
echocardiographic criteria for mitral valve prolapse were expanded until up to 21% of the “normal” population were
deemed affected. Subsequent studies demonstrated that the systolic M-mode appearance of prolapse could be
produced in 40%–55% of “normal” subjects if the beam originated from a transducer placed above the apically
moving valve apparatus. Thus, all M-mode studies have a potential acquisition bias, since the appearance of prolapse
can often be produced in subjects in whom it is expected.

Two-dimensional echocardiography

The advent of 2-dimensional echocardiographic imaging made it possible to relate the movement of the mitral
leaflets to surrounding structures (typically the mitral annulus) rather than to the transducer positioned on the chest
wall, and it appeared that more consistent diagnostic criteria for mitral valve prolapse could be established. Initial
criteria relying on displacement of the mitral leaflet above the plane of the mitral annulus in the parasternal, long-
axis view were confirmed bycineventriculography. These criteria were subsequently broadened to facilitate diagnosis
and increase sensitivity by including displacement of the leaflets above the annulus in the orthogonal apical 4-
chamber view. Application of these expanded criteria required the assumptions that the mitral annulus lay in a
Euclidean plane (was flat) and that therefore the relation of the leaflets to the annulus would be similar when imaged
in orthogonal views (apical 4-chamber versus parasternal and apical long-axis views). These expanded criteria (that
is, the use of apical 4-chamber views to diagnose prolapse) led to a reported prevalence for mitral valve prolapse of
up to 35% in adolescent subjects preselected to be normal.

Diagnosis of Mitral Valve Prolapse

Current echocardiographic criteria for mitral valve prolapse. Despite the erratic path of progress, echocardiography
continues to offer an ideal method for diagnosing mitral valve prolapse: It permits noninvasive visualization of both
mitral leaflets in relation to the mitral annulus. Leaflet-annulus relationships can be recorded in a variety of
projections under basal conditions and in response to stress. Figure 1 illustrates the basic echocardiographic criteria
for mitral valve prolapse and groups prolapse into various subtypes.

Figure 1. Echocardiographic criteria for mitral valve prolapse

As illustrated, prolapse is defined as the displacement of 1 or both mitral leaflets by more than 2 mm above the high
points of the mitral annulus, recorded in either the parasternal or the apical long-axis view. The 2-mm cutoff is based
on studies showing that beyond this threshold there was an incremental increase in the prevalence of complications
(i.e., >1+ (on a scale from 1-4+) mitral regurgitation, left atrial enlargement, and leaflet thickening). As with any
such cutoff, there are undoubtedly patients with otherwise normal leaflets that may extend more than 2 mm above the
annular high points. This value, however, has been shown to be best for separating patients with leaflet displacement
associated with complications from those with otherwise normal valves.

Prolapse is further subdivided into classic and nonclassic forms based on leaflet thickness, with 5 mm consid ered the
upper limit of nonclassic. Prolapsing valves with leaflets more than 5 mm thick are considered to have “classic
prolapse,” while those with leaflets less than 5 mm thick are judged to have “nonclassic” prolapse. As described
earlier, leaflet thickening represents myxomatous degeneration of the valve, often associated with redundancy.
Patients with thickened, redundant leaflets (classic mitral valve prolapse) can be further subdivided into those with
symmetric coaptation, in which the leaflet tips meet at a common point, and those with asymmetric coaptation, in
which the tip of 1 leaflet is displaced toward the atrium relative to the other.

Patients with asymmetric prolapse are particularly prone to progressive deterioration of the valve, possibly associated
with chordal rupture, which may lead to a flail leaflet, whose tip everts and becomes concave toward the left atrium
rather than the left ventricle. Flail leaflet is also a spectrum of disorders, ranging from eversion of the tip alone
through complete detachment of chordae with unrestrained motion of the entire leaflet and severe mitral
regurgitation. Recent data allow examination of the prevalence and complications of mitral valve prolapse based on
this diagnostic construct. Significantly, in addition to leaflet thickness, redundancy, and relationship to the mitral
annulus and to each other, echocardiography can detect many of the complications of prolapse, such as the presence
and severity of mitral regurgitation, the presence and degree of left atrial and ventricular dilatation, depression of left
ventricular function, and the presence of valvular vegetations.

Unit III

Echocardiographic assessment of Aortic stenosis

In the case of aortic stenosis, echocardiography is used to define the initial severity of disease, etiology, and monitor
its progression through serial follow up studies. Evaluation of aortic stenosis would be incomplete without a
comprehensive examination of overall left ventricular function and estimation of pulmonary artery pressures.
Transthoracic echocardiography, therefore, can provide important information about the initial diagnosis,
management, and follow-up of adult patients with native aortic valve stenosis.

ETIOLOGY

When considering the etiology of aortic stenosis, it is important to consider the age and the demographics of the
patient (Fig. 1). Rheumatic valvular disease, once the most common form of aortic stenosis, is less common today in
developed countries. Commissural fusion is a hallmark of this disease and often presents with concomitant mitral
stenosis (Fig. 2) Less commonly, the commissures may fuse eccentrically, producing a de facto bicuspid valve. In
this case, differentiation from a congenitally bicuspid valve can be difficult.
Calcific degeneration is currently the most common form of aortic stenosis in the developed world. It generally
presents later in adult life and is sometimes called senile calcific degeneration (Fig. 3). Commissural fusion can
occur, but is not a hallmark of this disease process. Calcification is visualized as “echo bright” reflectivity of the
valve leaflets and the aortic root.

Congenital bicuspid aortic valves may calcify and thicken over time, eventually producing stenotic lesions that
present earlier than other common causes of adult aortic valvular stenosis (Fig. 1). When observed in the parasternal
short-axis view, bicuspid aortic valves exhibit either a vertical or a horizontal commissural orientation in the
parasternal short-axis view. In the vertical orientation, commissures are in the anterior and posterior position with a
right and left cusp. In the horizontal orientation, commissures are in the right and left positions, with anterior and
posterior cusps. Raphes are commonly seen in both of these orientations (Fig. 4)

Fig. 1. The etiology of aortic stenosis by age group.

Figure 2

The appearance of the valve in systole is characteristic of this etiology, and has been referred to as a fish-mouth
appearance, rather than the triangular appearance of normal valves (Fig. 5)

Two-dimensional assessment

Important morphological information can be gained from initial two-dimensional (2D) views of the aortic valve.
Leaflet restriction in the setting of adequate cardiac output is the hallmark of aortic stenosis, which can be readily
discerned in the parasternal long-axis view. Failure of aortic leaflets to open fully with ventricular ejection often
signifies some degree of aortic stenosis (Fig. 6). Eccentric valve opening visualized in the parasternal long views is a
further clue to the presence of a bicuspid aortic valve. Stenotic aortic valves are generally thickened or calcified. This
is easily seen on either 2D or M-mode assessment of the valve (Fig. 7).
Fig. 2. (A–C) Aortic stenosis showing thickened valve leaflets. (C) Commissural fusion (arrows) is a hallmark
feature of rheumatic valvular heart disease.

Fig. 3. Calcific (“senile”) degeneration of aortic valve showing “echo-bright” reflection (arrows).
Therefore, the 2D characteristics of the aortic valve can provide important clues to the etiology of aortic stenosis.

Doppler assessment

Doppler measurements across the aortic valve are essential to the determination of the severity of aortic stenosis. As
the aortic valve narrows, the velocity of blood flow across the valve will generally increase. This velocity is
dependent on the pressure gradient across the valve. Continuous-wave (CW) Doppler measurements across the aortic
valve should be performed where the ultrasound beam is most parallel to the flow of blood across the valve.
Therefore, measurements are best acquired in the apical five-chamber, right parasternal long axis, or suprasternal
views to obtain the highest velocities across the valve. The maximum velocity obtained is highly dependent on
accurate transducer positioning, and will be underestimated when Doppler beam angle deviates from that of blood
flowing through the stenotic valve (Fig. 8). A nonimaging probe can be used if inadequate envelopes are found with
the duplex imaging transducer.

Fig. 4. Sketch showing bicuspid aortic valve variants with different commissural orientations (parasternal short-axis
views [PLAX])

Fig. 5

The calculation of transvalvular pressure gradients is based upon the Bernoulli principle. The modified Bernoulli
principle relates the transaortic pressure gradient to the square of the maximal velocity found on CW Doppler: P =
4V2 , and is used when the velocity of blood proximal to the stenosis is negligible. In significant aortic stenosis, high
gradients across the aortic valve can be seen. The relationship is accurate when the velocity proximal to the stenosis
is less than 1.5 m/s. Should the velocity in the left ventricular outflow tract (LVOT) exceed 1.5 m/s, then the long
version of the Bernoulli equation should be used to calculate the transaortic gradient.
Fig. 5. Bicuspid aortic valve during diastole (A) and systole (B) in parasternal short-axis (PSAX) view. Note
horizontal commissure (arrow) in diastole and “fish mouth” appearance during systole. (C,D) Systolic doming of
bicuspid aortic valve during systole (parasternal long-axis view [PLAX]).

Fig. 6. Aortic stenosis showing restricted leaflet opening (arrow) during systole (parasternal long-axis view [PLAX]).
Left ventricular ejection fraction was reduced, hence “low stroke volume-low gradient” aortic stenos is.

Therefore:

Transaortic pressure gradient = 4 (Vmax 2 – VLVOT 2) when VLVOT ≥ 1.5 m/sec

In most cases, the modified Bernoulli equation is an accurate and simple measure of the peak instantaneous
transaortic pressure gradient.

Peak transaortic gradient measured by Doppler should be differentiated from the peak-to-peak gradient obtained at
cardiac catheterization. Hemodynamically, the peak-to-peak gradient measures the difference between the peak left
ventricular pressure and the peak aortic pressure—which are not measured simultaneously. Therefore, peak-to-peak
gradients are not physiological, and no Doppler measurement exactly corresponds to this measurement in the
cathetherization laboratory. However, mean gradients across the aortic valve are similar when measured by Doppler
and by cardiac catheterization.

The Doppler derived mean gradient is the average gradient over the systolic ejection period. This is usually
calculated by tracing the CW envelope obtained across the aortic valve, and the numerical values are automatically
calculated by the machine’s software package (Fig. 9). It is important to ensure that it is actually the aortic envelope
that is traced, as a mitral or tricuspid regurgitant jet may mimic an aortic stenotic envelope.

Fig. 7. M-mode through aortic valve showing characteristic thickening of valve leaflets in aortic stenos is.

Calculation of aortic valve area

The calculation of aortic valve area (AVA) is based on the continuity equation (Fig. 11). This equation relates the
flow proximal to the stenosis and flow through the valve. AreaLVOT × VLVOT = AVA × Vmax Where the AVA is
the aortic valve area and Vmax is the maximal velocity obtained by CW Doppler. VLVOT is the velocity in the
LVOT obtained by pulse wave Doppler usually in the apical five-chamber view. Area LVOT is the area of the
LVOT and is calculated by multiplying π by the square of the radius of the LVOT.

The equation thus becomes: AVA = π(radius of LVOT)2 × VLVOT/Vmax Therefore, the AVA can be easily
calculated using velocities. Alternatively, the velocity time integral (VTI) can also be used instead of velocities to
obtain the AVA.

Fig. 8. (A) Continuous-wave (CW) Doppler of maximum velocity across stenotic aortic valve. (B) Optimal Doppler
alignment for assessment of peak velocities in aortic stenosis.

Fig. 9. Calculation of trans-aortic gradients by continuous-wave Doppler.

Assessment of stenosis severity

The normal aortic valve orifice area in adults ranges from 2 to 4 cm2 . In general terms, severe stenosis is not seen
with an AVA of more than 1.0 cm2 . According to American College of Cardiology/American Heart Association
guidelines, severe aortic stenosis is seen when the AVA is less than 1 cm2 (Table 1).

Table 1: Severity of Aortic Stenosis by Valve Area

Transvalvular gradients should not be ignored when assessing severity of aortic stenosis. Overall, when the mean
transvalvular gradient exceeds 50 mmHg, severe stenosis is usually present. Alternative methods of assessing aortic
stenosis severity exist. The Doppler Velocity index or Dimensionless index is a measure of the ratio of the LVOT
velocity to the AV velocity using CW Doppler across the aortic valve. It is normally higher than 0.28 but decreases
with significant aortic stenosis. An index of less than 0.25 generally correlates with severe aortic stenosis. VTI may
be used instead of velocities. In addition, because peak transvalvular gradients are linearly correlated with mean
gradients, a peak gradient greater than 4.5 m/s is also indicative of severe stenosis.

Therefore, a combination of methods may be used to assess aortic stenosis severity. Nonetheless, symptoms are the
major guide to therapeutic decisions, and no single measurement is used to guide referral for surgical intervention.
Thus, echocardiographic measurements of severe stenosis in conjunction with the wider clinical picture are the
benchmarks for referral for aortic valve replacement.

Low-gradient aortic stenosis

Low-flow, low-gradient, low-LVEF, severe AS: Low-flow, low-gradient, low-LVEF, severe AS (“classical” low-
flow, low-gradient severe AS) is defined as severe AS in the presence of systolic LV dysfunction (LV ejection
fraction < 40%) with a mean transaortic pressure gradient < 40 mmHg if estimated by echocardiography or < 30
mmHg if measured invasively.
To establish a diagnosis of LFLG severe AS with preserved LVEF the following 3 criteria are recommended.
 Confirmation of low-flow states by and indexed stroke volume < 35 mL/m 2.
 Confirmation of increased global LV afterload (ventriculo-arterial impedance) by Zva ≥ 4.5 mmHg/mL per
square meter.
 Confirmation of concentric LV remodeling by the following: (1) relative wall thickness (RWT) ≥ 0.45. RWT
is calculated using the following formula: RWT = (IVS + LVPW)/LVEDD, where IVS is the end-diastolic
ventricular septal thickness; LVPW is the end-diastolic LV posterior wall thickness; and LVEDD is the end-
diastolic LV diameter; (2) end-diastolic LV diameter < 47 mm; and (3) indexed end-diastolic LV volume <
55 mL/m2.
When the calculated AVA is ≤ 1 cm2 in low flow states, one should differentiate whether this is primarily due to the
low flow (pseudo severe AS, where the anatomical AVA is > 1 cm 2) or if there is true severe AS (AVA remains
fixed and ≤ 1 cm2 regardless of flow). Dobutamine stress echocardiography (DSE) is typically performed to
differentiate between the two conditions because it evaluates the response of AVA to increased transaortic flow.
Although planimetry may be used to measure the orifice area by transesophageal echocardiography, it is not
commonly implemented in clinical scenarios, as transvalvular gradients and AVA can be easily applied in most
situations.

Echocardiographic evaluation of Aortic Regurgitation

Echocardiographic assessment of patients with aortic regurgitation involves assessment of valve morphology, the
aortic root, the degree of aortic regurgitation, and assessment of ventricular size and function.
Assessment of aortic valve morphology
To evaluate the patient with aortic regurgitation, it is important to first investigate the morphology of the aortic valve
and adjacent structures (including the aortic root) followed by an assessment of the impact of aortic regurgitation on
left ventricular geometry and function. Doppler measurements provide semiquantitative and quantitative assessment
of the degree of severity of aortic regurgitation. Both transthoracic and transesophageal echocardiography may be
used to evaluate and quantitate the severity of valvular dysfunction.
Echocardiographic evaluation of aortic valve morphology
The parasternal long-axis view is used to measure the left ventricular outflow tract, aortic annulus, and aortic sinuses.
Leaflet thickening and prolapse can be visualized from this imaging window. A congenitally abnormal valve should
be strongly suspected whenever markedly eccentric leaflet coaptation is seen in parasternal views. Color jet width is
also measured in this view. Parasternal short-axis images are the optimal views for identifying leaflet morphology
(tricuspid vs bicuspid or quadricuspid). Vegetations may appear as masses attached to the valve leaflets that may
prolapse into the left ventricular outflow tract. Endocarditis can cause valve leaflets to perforate, becoming evident
as color flow abnormalities that indicate leaflet perforation. In patients with aortic regurgitation, the dimensions of
the aortic annulus, aortic sinuses and sinotubular junction should be recorded, and the presence or absence of valve
thickening and other congenital abnormalities should be noted.
Fig. 1. Anatomical relationships of aortic valve and leaflets on two-dimensional echocardiography.

/
Fig. 2. Sketch illustrating various etiologies of aortic regurgitation
Doppler echocardiographic evaluation of the patient with aortic regurgitation
Color flow Doppler imaging provides a semiquantitative method to evaluate the severity of aortic regurgitation. The
regurgitant jet can be visualized by color flow imaging in multiple views. Color flow Doppler in the parasternal long
axis view provides an estimate of the size of the regurgitant orifice. The color jet diameter (or width) is measured in
diastole immediately below (within 1 cm) the aortic valve. In patients with aortic regurgitation because of trileaflet
aortic valves this jet width is proportional to the size of the aortic valve defect. If the orifice is irregular, as in
bicuspid aortic valve disease, the color jet width is not related to the degree of regurgitation. The ratio of jet diameter
to left ventricular outflow tract diameter can be calculated (Fig. 4). This ratio can provide a semi-quantitative
estimate of the degree of regurgitation: less than 10%, trace; 10–24%, mild; 25–65%, moderate; and greater than
65%, severe.

Fig. 3: Ratio of the aortic jet width (diameter) to left ventricular outflow tract (LVOT) diameter. The diameter of the
color jet is measured immediately beneath the aortic valve is a semi-quantitative index of aortic regurgitation
severity.

Fig. 4. Semi-quantitative assessment of aortic regurgitation severity by the vena contracta width. Note the three
components of the aortic regurgitant flow: the flow convergence—above the orifice, the vena contracta—through the
orifice, and the regurgitant jet—below the orifice.
Fig. 5. Bicuspid aortic valves may have a visible raphe—the fusion ridge of two aortic leaflets. The aortic orifice
often exhibits an ovoid or “fish mouth” appearance during systole. PSAX, parasternal short axis view.

Fig. 6. (A) Left ventricle dimensions (parasternal long-axis [PLAX] measurements). (B) Dimensions of the aorta
(PLAX measurements).

Fig. 7. M-mode showing premature diastolic closure of the mitral valve—a reflection of the hemodynamic impact of
aortic regurgitation on the left ventricle. Other M-mode signs include anterior mitral valve leaflet fluttering (and less
commonly, septal diastolic fluttering).

Fig. 8: Ratio of the aortic jet width (diameter) to left ventricular outflow tract (LVOT) diameter. The diameter of the
color jet is measured immediately beneath the aortic valve is a semi-quantitative index of aortic regurgitation
severity.
Measurement of the vena contracta—the regurgitant jet as it traverses the aortic orifice or the effective regurgitant
area—can also be used to estimate aortic regurgitant severity. Using a Nyquist limit of 50–60 cm/s, a vena contracta
width of less than 0.3 cm correlates with mild aortic regurgitation. A vena contracta width of 0.3–0.6 cm is consistent
with moderate aortic regurgitation, whereas a vena contracta width greater than 0.6 cm indicates severe aortic
regurgitation. Visualization of the color jet of aortic regurgitation on the parasternal short-axis view is another
method for quantitation of the severity of regurgitation. The regurgitant color jet area can be measured and compared
to that of the left ventricular outflow tract with the result expressed as a percentage. Using this simplified area ratio
method, patients with mild aortic regurgitation have ratios of less than 5%. Severe aortic regurgitation occurs when
ratios exceed 60%, with a broad range between 5 and 60% indicative of moderate aortic regurgitation. The color jet
disturbance of aortic regurgitation is also easily visualized from the apical windows (Fig. 11A). The color jet length
and area, however, are less proportional (in these views) to the degree of regurgitation and are more influenced by
the aortic to left ventricular diastolic pressure gradient as well as interactions between the regurgitant jet and the
outflow tract walls (Fig. 11B). The color jet width is occasionally measured from this view but the parasternal
projection provides better axial resolution.

Fig. 9. Semi-quantitative assessment of aortic regurgitation severity by the vena contracta width. Note the three
components of the aortic regurgitant flow: the flow convergence—above the orifice, the vena contracta—through the
orifice, and the regurgitant jet—below the orifice.
Quantitative measures of aortic regurgitation
Continuous-wave Doppler of the aortic regurgitant jet reflects the pressure difference between the aorta and the left
ventricle during diastole. The continuouswave Doppler signal is best measured from the apical windows. For
eccentric jets, better signals may be obtained from the second right intercostal window. The denser the spectral
envelope, the more severe is the regurgitation. The rate of deceleration of the continuous-wave Doppler signal is both
a function of the degree of regurgitation and the ventricular enddiastolic pressure. As the degree of regurgitation
increases, the aortic diastolic pressure decreases and the left ventricular end-diastolic pressure increases. This leads
to a rapid drop-off in pressure (as well as velocity) across the valves—corresponding to the familiar clinical signs of
a widened pulse pressure. A pressure half-time of less than 200 ms is consistent with severe aortic regurgitation.
Moderate aortic regurgitation equates to a pressure half-time of 200–500 ms, whereas mild regurgitation is indicated
by a pressure half-time exceeding 500 ms. Overall, pressure half-times are more accurate measures of acuity of aortic
regurgitation than volumetric measures of aortic regurgitation, as pressure-half time is influenced by chamber
compliance in addition to chamber pressures. Accurate measurement of pressure halftime is also dependent on
obtaining a well-visualized signal from the regurgitant jet. Patients with small volumes of regurgitation or poor
windows may have incomplete spectra making measurement of this measurement difficult. Calculation of regurgitant
volume and regurgitant fraction provides a better quantization of the severity of valve insufficiency. The regurgitant
volume is equal to flow out the aortic valve (aortic stroke volume) minus flow through the mitral valve (mitral stroke
volume). Calculation of regurgitant volume requires measurement of the left ventricular outflow tract and mitral
annular diameters, as well as velocity time integrals (VTI) of flow through the left ventricular outflow tract and the
mitral annulus. Aortic flow is equal to pi (π) multiplied by the square of the radius of the left ventricular outflow
multiplied by the VTI of aortic flow. Mitral flow is calculated as π multiplied by the square of the radius of the mitral
annular diameter multiplied by the VTI of mitral flow. Mild aortic regurgitation is considered when the regurgitant
fraction is less than 30 mL/beat, moderate–between 30 and 60 mL/beat, and severe regurgitation—in excess of 60
mL/beat. The regurgitant fraction is equal to the regurgitant volume divided by the total stroke volume. The total
stroke volume is equivalent to flow out the aortic valve as previously defined. Regurgitant fractions of less than 30%
are consistent with mild regurgitation, 30–50% with moderate regurgitation, and more than 50% with severe
regurgitation. The regurgitant orifice area may be calculated as the regurgitant volume multiplied by the VTI of the
continuouswave Doppler jet. This parameter represents the average size of the defect in the aortic valve during
diastole and is proportional to regurgitant severity. Grading of aortic regurgitation severity using the regurgitant
orifice area is as follows: mild, less than 0.10 cm2 ; moderate, between 0.10 and 0.30 cm2 ; and severe, more than
0.30 cm2 .
Fig.10. (A) The color jet area measured from the parasternal short-axis view (PSAX) is proportional to the
regurgitation orifice area. In these images, color from the aortic regurgitation (blue) is seen centrally, but varies
throughout diastole owing to a changing orifice area (please see the companion CD for the video). (B) Semi-
quantitative assessment of aortic regurgitation severity by color flow Doppler assessment (simplified jet/left
ventricular outflow tract [LVOT] area ratio) using PSAX.
Calculation of the regurgitant volume, fraction, and orifice area is dependent on careful measurement of several
variables. Errors in any one of these variables will lead to further errors in the calculations. Experienced laboratories
should be able to perform these measurements and calculations accurately with careful attention to detail. Aortic
regurgitation can lead to diastolic flow reversal in the aorta. With milder degrees of regurgitation, there is brief
reversal of flow early in diastole. As the degree of regurgitation increases, flow reversal becomes sustained
throughout diastole at velocities exceeding 20 cm/s. Criteria for flow reversal have been established in the distal
aortic arch. Significant sustained reversal in the abdominal aorta is also a sensitive sign of severe aortic regurgitation.
Individuals with severe aortic regurgitation may exhibit altered mitral flow patterns. Because aortic regurgitation
results in elevated diastolic left ventricular pressures and mitral inflow ceases early in diastole, this can lead to
shortened mitral deceleration times. For this reason, the assessment of mitral valve area in a patient with mitral
stenosis can be overestimated in patients with aortic insufficiency.
Fig.11. (A) From the apical windows, the aortic regurgitation jet appears as a diastolic color flow disturbance in the
left ventricular outflow tract. Jet length and jet area are influenced by the aortic driving pressure (aorta-to-left
ventricular pressure) and are therefore less reliable indicators of disease severity. Measuring jet width from the apical
projections is possible, but generally less reliable than parasternal measurements. (B) Continuous-wave (CW)
Doppler assessment of flow across the aortic valve in a patient with aortic regurgitation. Many patients have mixed
aortic valve disease. Increased transvalvular systolic velocities may represent stenosis.

Fig. 12. Signal intensities in aortic regurgitation severity

Fig. 13. Deceleration rate. The rate of deceleration of the continuous-wave Doppler signal reflects both the degree of
regurgitation and the ventricular end-diastolic pressure

Fig. 14. Pressure half times (PHT or P 1/2 t). The pressure half time is the time it takes for peak pressure (mmHg) to
drop to half its initial value. As the degree of regurgitation increases, the aortic diastolic pressure decreases and the
left ventricular end-diastolic pressure increases. This leads to a rapid drop-off in pressure (as well as velocity) across
the aortic valve. The more severe the aortic regurgitation, the greater the slope and the shorter the PHT.

Fig. 15. Aortic regurgitant volume and fraction.

Fig. 16: The regurgitant orifice area or EROA represents the average size of the defect in the aortic valve during
diastole and is proportional to regurgitant severity. The regurgitant volume across the aortic valve may be calculated
as the difference between the LVOT volume and the transmitral volume, assuming there is no significant mitral
regurgitation (see Fig. 15)

Fig. 17.Aortic flow reversal. Diastolic flow reversal can be seen in significant aortic regurgitation by Doppler
interrogation of flow in the aortic arch and descending thoracic aorta. In this pulsed wave Doppler envelope, the
regurgitant flow velocities almost equal those of systolic forward flow—a feature indicative of severe aortic
regurgitation.
Assessment of Aortic Regurgitation Severity by Doppler Echocardiography: A Summary or Semi-
Quantitative Method

Evaluation of prosthetic valve stenosis

• Mechanical valves
• Tissue (biological) valves – Human
• Allografts
• Autografts
– Animal (xenografts)
• Porcine aortic valves
• Bovine pericardial tissue
• Stented or stentless
• Annular rings
• Percutaneous valves/clips
Echocardiographic Approach to Assessment of Prosthetic Heart Valves
 Evaluation similar to that of native valves
 Reverberations and shadowing play a significant role
 Fluid dynamics of each specific valve prosthesis influences the Doppler findings
Valve prostheses may have different sizes, which affects the echocardiographic parameters characterizing the
functioning of the valve. The size of the prosthesis is determined by the outer diameter of its ring and is indicated in
millimeters. Therefore, this diameter is not the diameter of the opening area of an artificial valve, which is usually
smaller.

Fig. 1. Transesophageal visualization of prosthetic bileaflet valve opening. Clearly seeing two disks in opened
position as a parallel lines with intensive shadowing down. It is also visible three parts of prosthetic orifice: the
smallest one at the center between the two opened cusps (long arrow) and two bigger orifices laterally (short arrows).
Dysfunction of the valve prosthesis is a specific pathology that requires a special knowledge regarding the
functioning of prosthetic valves, methods of their examination and the causes of prosthetic function disorders.
Thrombosis is the main cause of prosthetic heart valve dysfunction. According to various data it occurs in 0.1 – 5.7%
of patients per year. In addition, disorders of the prosthetic functioning may occur due to the vegetation growth, the
development of ring abscess or pannus formation. A reverse flow (regurgitation) through the prosthetic orifice or
outside the valve ring (paravalvular regurgitation) could be detected. Extremely rarely a deformation of the closing
disk may occur with a violation of its operation.
Because a clinical examination is not sufficient to evaluate a prosthetic valve, several diagnostic methods have been
proposed to assess its functional status. The main echocardiographic characteristics of the prosthetic valve
functioning are the pressure gradient and the effective orifice area determined by the Doppler method. The pressure
gradient depends not only on the normal leaflet or disc opening but also on other factors, in particular hemodynamic
situation. Therefore, it is necessary to take into account without excessive anxiety the elevated gradient numbers in a
patient with no complains and symptoms of heart function worsening. Flow velocities through prosthetic valves and
calculated gradients usually are significantly higher than through healthy native valves. These parameters also
depend on the blood flow volume, cardiac output, heart rate, the presence of concomitant regurgitation, the size and
type of prosthesis, the size of a chamber or vessel the prosthesis is opening in. Even "normal" numbers should be
treated with some caution. The best approach to avoid serious mistakes is to compare the obtained numbers with the
results of previous examinations. It is important for all patients to have measured prosthetic valve function
parameters immediately after implantation and before their discharge from the hospital indicated in the medical
records.
In practice, the mean pressure gradient is more useful than peak valve gradient, which is more hemodynamically
dependent. The mean Doppler pressure gradient obtained by echocardiographic examination correlates closely with
the mean gradient obtained by the direct measurement during heart catheterization. This applies to both mitral and
aortic valve prostheses.
One more quantitative parameter used for prosthetic valve evaluation is DVI which is the ratio between the velocity
time integral (VTI) of the prosthetic transvalvular flow and the VTI of the left ventricular outflow tract (LVOT):
DVI =VTIPrV / VTILVOT. Prosthetic valve dysfunction is suspected when the DVI ratio is reduced (less than 0.3)
in a case of prosthetic aortic valve, or increased (greater than 2.2 m/s) in a case of prosthetic mitral valve.
The mitral prosthetic opening area is obtained calculating the pressure half-time by the same way as mitral stenosis
evaluation. It is called the "effective orifice area" because it reflects the true prosthetic lumen taking into account that
opened closing disks and supporting hinges create a certain obstacle to the blood flow. The prosthetic mitral valve
effective orifice area should be not less than 2.0 cm2 . Bileaflet mechanical valves have a larger area than single-
tilting disk valves. As a rule the biological prostheses have a larger open area than mechanical prostheses. The
prosthetic aortic valve orifice area calculated by continuity equation method should not be less than 1 cm2 The main
echocardiographic sings indicating mitral valve prosthetic obstruction are listed in the Table 1.

The main cause of prosthetic valve thrombosis is insufficient anticoagulant administration. Instrumental diagnostic
criteria of the mechanical valve thrombosis include: 1) limited opening or completely blocked disc movement on the
fluoroscopic examination; 2) elevated Doppler gradients on the prosthetic valve on transthoracic echocardiography
(TTE); 3) detection of the thrombus during transesophageal echocardiography (TEE). A thrombus on a prosthetic
valve could be rarely visualized during transthoracic examination due to the presence of intense artifacts and
ultrasound signal reverberation. In most cases prosthetic thrombosis develops rapidly with a dramatic increasing of
heart failure manifestations.
TTE examination in these patients reveals an elevated pressure gradient on the prosthesis and a reduced effective
orifice area, and occluding clots should be detected using transesophageal examination. Prosthetic mitral
insufficiency (regurgitation) is often difficult to diagnose during a transthoracic echocardiography because the
ultrasound beams pass through a prosthetic metal structures and discs giving intensive artifacts. There is need to use
non-standard scanning planes. Performing TTE examination the clinically significant mitral prosthetic regurgitation
could be suspected in the presence of next findings: a dilated and hyperkinetic LV; systolic flow convergence on the
ventricular side of the prosthesis; increased mitral diastolic E wave velocity (≥2 m/s); mean pressure gradient >6 mm
Hg; DVI >2.2; unexplained and/or increasing pulmonary arterial hypertension.

Fig. 2. Transesophageal echocardiography of thrombus obstructing the orifice of mitral valve prosthesis (long
arrow). At the same time the thrombus in left atrial appendix is visualized (short arrow).
In cases of technically difficult transthoracic examination it is useful to perform TEE. It is possible to identify by
TEE the origin and underlying mechanism of the regurgitant jets, such as prosthesis dehiscence, pannus formation,
thrombus, vegetations, abscess formation or paraprosthetic fistula. Color Doppler allows to detect a reverse flow on
mitral valve prosthesis at the parasternal left ventricle long-axis view. Continuous wave Doppler (CW) can give an
idea of the presence of a reverse flow, but one must be careful not to confuse it with the flow through the aortic
valve. Color Doppler allows detecting whether the reverse flow occurs on the prosthetic valve itself or outside its
ring (paraprosthetic regurgitation). Semi-quantitative way of the estimation of the mitral prosthetic or paraprosthetic
regurgitation degree is to measure the ratio of maximum area of the regurgitation jet in the left atrium to the left
atrium cross-sectional area: the mild degree is less than 20%; moderate degree - 20-40%; severe degree - more than
40%. It is simple but often not accurate. Generally, the estimation of the severity of prosthetic valve regurgitation can
be performed similarly to native valve. The main Doppler parameters of prosthetic mitral valve regurgitation are
presented in Table 2.

However, limited data exist on the validation and application of different quantitative echo-parameters such as the
effective regurgitant orifice area, width of the regurgitant jet or the vena contracta and calculated regurgitant volumes
in the context of valvular prosthesis. That is why a multiparametric echocardiographic approach should be
reasonable in connection with clinical presentation.
There are many observations that 3D-Echo is superior to two-dimensional TEE in the assessment of mitral
paravalvular fistulas and regurgitant jets providing detailed visual information regarding precise localization and
analysis of the leak size and shape. The main echocardiographic parameters indicating the severe aortic valve
prosthetic obstruction are listed in the Table 3.
Aortic prosthetic regurgitation could also be evaluated by the ratio of the proximal jet width to the LVOT diameter at
the same level: a mild degree - 1-24%; moderate degree - 25-46%; moderate-to-severe degree - 47-64%; severe
degree - over 65%. The reverse flow through the aortic valve prosthesis can be clearly seen in color Doppler mode
on a short-axis plane at the level of the left ventricular outflow tract. The neck of the jet visualization in a short-axis
view allows determination of the circumferential extent of paravalvular regurgitation. A regurgitant jet area
occupying less than 10% of the sewing ring or stent circumference corresponds to mild, 10-20% - moderate, and
more than 20% suggests severe reverse flow. Prosthetic rocking visible on biplane image is usually associated with
dehiscence more than 40%. In a case of multiple jets, the estimation of regurgitation severity becomes a difficult
task. The recommended Doppler parameters for evaluation of the severity of prosthetic aortic valve regurgitation are
presented in Table 4.

The most common drawback of the transcatheter implanted prosthetic aortic valve is regurgitant flow. First of all
paravalvular leakage could be a consequence of incomplete apposition of the valvular prosthesis to the aortic
annulus. Transvalvular regurgitation occurs as a result of restricted leaflet motion or leaflet destruction and improper
sizing or overdilatation of the valve during the implantation. If the prosthesis has been implanted too low in the
aortic position a special form of regurgitation termed supraskirtal could develop.
Infective endocarditis could be a cause of prosthetic valve dysfunction (Fig. 3). Its main echocardiographic
manifestations include vegetation, thrombi on the replaced valve structures, dehiscence of the prosthetic ring,
abscesses, pseudoaneurysms, fistulas and paravalvular regurgitation. It should be kept in mind that insignificant
paravalvular jets often happen even in the absence of endocarditis. The sensitivity of TEE in the detection of thrombi
and vegetation in prosthetic valve infective endocarditis is much more higher (almost 90%) than transthoracic
method (not more than 40%).
Fig. 3: A long vegetation (arrow) attached to the atrial surface of mitral valve prosthesis visible by transesophageal
echocardiography
One more cause of prosthetic valve dysfunction is pannus formation. Pannus is a connective tissue progressively
growing into the orifice of the prosthesis and gradually obstructing it. The pathophysiology seems to be explained by
a chronic inflammation that results in the gradual and late clinical presentation looking like a thrombosis. But the
correct diagnosis of pannus is critically important for choosing a treatment method since fibrinolytic agents could
resolve thrombosis and have no effect on pannus. Cases of pannus are possible to diagnose mostly by TEE (Fig. 4).
According to the published data, the incidence of this complication is 1.6%-2% in the different series and occurs
exclusively in mechanical prostheses more often in the aortic position. A tricuspid valve prosthetic stenosis may be
suspected in the presence of abnormal morphology and limited mobility of the leaflets in combination with a
transvalvular peak velocity greater than 1.7 m/sec, mean gradient exceeding 6 mm Hg and a pressure halftime more
than 230 msec.
Mostly prosthetic pulmonary valves have been implanted in pediatric patients with congenital heart disease. Usually
for this purpose surgeons use different homo- and heterografts. When a prosthetic stenosis develops marked
thickening or immobility of the cusps, high transvalvular peak velocity, the presence of a depressed right ventricular
function or elevated right ventricular systolic pressure could be revealed by echocardiographic examination. In the
presence of severe pulmonary prosthetic valve insufficiency, it is possible to identify a right ventricle volume
overload signs.

Fig.4. Pannus formation from the atrial side of mitral valve prosthesis (short arrows) visualized by transesophageal
echocardiography. Partially opened prosthetic disk is limited in its movement by thrombus (long arrow).
In a patient with a prosthetic aortic valve, a high peak systolic pressure gradient on it may also indicate that the size
of the prosthesis is not consistent with the cardiac output (too small diameter of the prosthesis – patient-prosthesis
mismatch – PPM). In these cases, TEE allows to find out that the prosthesis itself operates normally and there are no
signs of thrombosis, pannus growing or infectious lesions. The widely used parameter for PPM identification is the
indexed effective orifice area (calculated prosthetic EOA divided by the patient's body surface area). A value of
indexed EOA eft atrium thrombosis and fluid in the pericardial cavity. In all cases suspicious for prosthetic valve
dysfunction the transesophageal echocardiography is indicated. This method is highly sensitive in detecting of small
clots and vegetations, in addition, it helps to localize regurgitation jets properly and assess the severity of
regurgitation more precisely.
Therefore, the complete echocardiographic evaluation of prosthetic valves includes: 1) a two-dimensional
examination, which does not provide enough information, but can show clear a prosthetic dehiscence; 2) spectral
Doppler examination allowing to calculate the pressure gradients in cases of prosthetic obstruction (thrombus,
pannus, large vegetations) and calculate the effective orifice area; 3) color Doppler helping in detection of valvular
and paravalvular regurgitation; 4) transesophageal echocardiography as a particularly valuable and sensitive method
allowing the visualization of thrombi, vegetations, pannus and regurgitant jets.

Echocardiographic features of dilated cardiomyopathy

Contractile dysfunction and impaired left ventricular ejection fraction are hallmarks of dilated cardiomyopathy.
Dilatation of the ventricle is a compensatory mechanism to maintain an adequate stroke volume. Aside from the
above mentioned features, patients with dilated cardiomyopathy may have several other abnormalities.

A) Contractile dysfunction

By definition, the ejection fraction is below 55%. Typically the ventricle is globally hypocontractile. However, there
may be certain variations in the degree of regional dysfunction. Such differences may be partly explained by the
geometry of the heart, myocardial mechanics, or regional variations in myocardial damage (i.e. myocarditis).
Contractility is quite commonly better in the posterolateral region. Such variations in contractility make it difficult to
distinguish between ischemic and dilated cardiomyopathy.

In subtle and incipient forms of dilated cardiomyopathy, contractile dysfunction may be limited to the longitudinal
component (see myocardial mechanics). As the disease progresses, other deformation parameters as well as torsion
and diastolic untwisting will be affected.

Assessment of left ventricular function should include visual estimation of ejection fraction and, whenever possible,
calculation of ejection fraction (biplane Simpson or 3D methods). Other parameters that may be used are fractional
shortening (M-mode), calculation of contractility (dP/dt), or the Tei index.

B) Dilated left ventricle

The degree of left ventricular dilatation is highly variable and depends on the stage of disease as well as the severity
of left ventricular dysfunction. In the acute phase, the ventricle is just mildly dilated or may even be normal in size
because compensatory dilatation has not yet developed. Patients with additional volume overload (mitral or aortic
regurgitation) tend to have larger ventricles. With progressive dilatation the ventricle assumes a more spherical
shape.

Spherical geometry of the left ventricle in a patient with a severely dilated left ventricle. Note that septal motion is
biphasic (dyssynchrony).

C) Thin myocardial wall

The left ventricular wall in typical dilated cardiomyopathy is rather thin. However, as the left ventricle is enlarged,
the total left ventricular mass may be increased. The thickness of the septum may be increased in patients with left
ventricular hypertrophy who develop dilated cardiomyopathy.

D) Dyssynchrony

When individual myocardial segments contract at different points in time, the condition is referred to as an abnormal
contraction pattern or left ventricular dyssynchrony. Dyssynchrony may not be limited to the ventricle
(intraventricular dyssynchrony), but may also occur between the right and left ventricle (interventricular
dyssynchrony). In this case, blood is ejected from the left ventricle (aortic flow) much later than it is from the right
ventricle (pulmonary flow). There is overwhelming evidence for the damaging effects of dyssynchrony on the heart.
Dyssynchronous contraction is inefficient in respect of hemodynamics as well as "energy expenditure". It results in
further deterioration of cardiac function. Detection and assessment of dyssynchrony in patients with heart failure is
very important because these patients may benefit to a great degree from cardiac resynchronization therapy (CRT).

Specific pacemakers with placement of an additional lead into the coronary sinus permit cardiac resynchronization
(CRT) in patients with dyssynchrony. Dyssynchrony is caused by delayed electrical conduction. This may occur in
various situations:

 Bundle branch block

 Right ventricular (or single chamber) pacing or
 During ectopic ventricular beats.
 E) Dyssynchrony and bundle branch block

By far the most common cause of dyssynchrony is complete left bundle branch block.

Dyssynchrony occurs less frequently in right than in left bundle branch block.
Left bundle branch block is a common finding in patients with dilated cardiomyopathy. It is present in approximately
one third of patients. The likelihood of developing a left bundle branch block increases with the severity of left
ventricular dysfunction. More than one half of patients with severely reduced left ventricular function have a left
bundle branch block.
The wider the QRS complex, the more frequent and severe is dyssynchrony.

There are several ways to detect dyssynchrony on the echocardiogram. Experienced investigators can detect
abnormal contraction patterns simply by observing the motion of the left ventricle on the two-dimensional image. On
a four-chamber view the ventricle will show a "hula hoop" or rocking motion.

The delay between contraction of the septum and the posterolateral wall (SPWMD) is also seen in the M-mode.

Figure 1: M-mode tracing showing dyssynchrony between the septum and the posterolateral wall (septal to posterior
wall motion delay = SPWMD). The inward motion of the septum occurs long before that of the posterolateral wall

A very simple way of assessing dyssynchrony is to measure electromechanical delay: one measures the delay
between the onset of the QRS complex and the start of the LVOT signal on a PW spectral Doppler tracing.
Significant dyssynchrony is present when the interval is longer than 140 ms. Several other echo modalities permit
detection and quantification of dyssynchrony.

Echocardiographic features of HCM- Echocardiographic features of HCM are foundational to our understanding
of the disease. Current American College of Cardiology and American Heart Association diagnostic criteria include
the identification of a hypertrophied left ventricle (LV) of wall thickness typically ≥15 mm in adults without another
underlying cause.1 Asymmetric septal hypertrophy has long been recognized as a common and distinctive feature of
HCM. In the past, a ratio of septal-to-posterior (inferolateral) wall thickness of 1.3 was used as a diagnostic criterion
for HCM, but this finding has severely limited sensitivity and specificity and fails to exclude alternate causes of
asymmetric septal enlargement and to include other morphologic variants of HCM.2 These include global/concentric
hypertrophy, mid-ventricular hypertrophy with or without apical aneurysm, apical hypertrophy, and focal
hypertrophy (Figure 1).

Figure 1: Apical Variant HCM

Echocardiography, including M-mode, has brought to light several distinct features of HCM, including mitral valve
systolic anterior motion (SAM) and LV outflow tract (LVOT) obstruction (Figure 2). SAM and LVOT obstruction
remain an essential imaging dyad with important prognostic implications. SAM causes LVOT obstruction via a
confluence of hemodynamic perturbations attendant to HCM. HCM alters the valve spatial orientation such that the
mitral coaptation point is anteriorly displaced at baseline. The hypertrophic, bulging septum redirects LV outflow
more obliquely along a posterior-to-anterior course, a trajectory that enhances anterior drag on the mitral
valve.2 Finally, higher velocities through a narrowed LVOT are thought to exert Venturi forces on the anterior mitral
leaflet, pulling it into the LVOT from above as it is pushed in the same direction from the apex.1 These elements can
vary significantly according to rhythm, heart rate, pre-load, and afterload, leading to dynamic changes in the severity
of LVOT obstruction. Thus, provocative testing can be helpful in assessing the degree of LVOT obstruction,
particularly in individuals with symptoms but no evidence of resting LVOT obstruction.

Figure 2: SAM of the mitral valve anterior leaflet as seen on (A) M-mode and (B) two-dimensional
echocardiography.

The implications of SAM and LVOT obstruction are manifold. In addition to premature aortic valve closure and
reduced cardiac output, the process often distorts the mitral apparatus enough to affect competency and induce mitral
regurgitation (MR). The combination of mid-systolic LVOT flow acceleration and mitral regurgitant flow (typically
via a posterolaterally directed jet) is described as the "V sign," often best appreciated in the parasternal long axis
views (Figure 3). Most important, however, is the quantification of LVOT pressure gradient. An LVOT gradient
greater than 30 mmHg marks the diagnosis of obstructive HCM and carries an increased risk of sudden cardiac
death.2 For this reason, extensive pulsed Doppler interrogation of the LVOT gradient in the apical views is essential
to identify any significant gradients. Careful examination of the Doppler envelope is critical as well because these
velocity jets are often situated close to MR jets, and the two can be easily confused. A true intra-cavitary gradient
typically demonstrates late peaking of velocities and a dagger-shaped appearance (Figure 4).

Figure 3: Concomitant systolic flow acceleration through the LVOT and MR, leading to the "V-sign."

Figure 4: Doppler tracing of true LV outflow trace velocities (left) compared with a hybrid envelope contaminated
by an MR jet (right) in the same patient.
Echocardiographic predictors of unfavourable outcome
Several echocardiographic parameters given below, are also important for prediction of unfavourable outcome in
HCM patients.

 Sudden death: Maximal wall thickness >30mm

 HCM related death: LVOT gradient at rest >30mmHg, EF <50%
 All-cause mortality: Left atrial diameter >48mm
 Heart failure development: LA volume >27ml/m2 at baseline of during follow up
 Intraventricular dyssynchrony: >45

Echocardiographic criteria of constrictive pericarditis

Constrictive pericarditis is a potentially curable condition caused by a variety of situations which result in inflamed,
scarred, thickened, or calcified pericardium. When the abnormal pericardium limits diastolic filling, there are a series
of hemodynamic consequences which manifest as fatigue, dyspnea, abdominal bloating, peripheral edema, or right
heart failure. These clinical manifestations of constrictive pericarditis are similar to those due to a cardiomyopathy.
Since their hemodynamic and clinical features are similar, it is often challenging to distinguish constrictive
pericarditis from a myocardial disease. Even the traditional invasive hemodynamic criteria of "equalization of end-
diastolic pressures" is not specific for constrictive pericarditis. Despite many similarities between myocardial and
pericardial diseases, there are several unique features of constriction that allow a reliable diagnosis. Those features
are 1. Respiratory variation in ventricular filling 2. Interventricular dependence and 3. Augmented longitudinal
motion of the heart.
Respiratory variation in ventricular filling arises from the dissociation of intrathoracic and intracardiac pressure
change and enhanced ventricular interaction in constrictive pericarditis. Inspiration reduces intrathoracic pressure
which usually is fully transmitted to intracardiac pressures, but in constriction, the intracardiac pressures falls much
less than intrathoracic pressure because of pericardial constraint. This difference in pressure change with inspiration
results in reduced filling to left side of the heart. The reduction in left heart filling during inspiration causes a
reduction in mitral inflow velocity and a shift of the interventricular septum toward the left ventricle. With
expiration, left heart filling increases which shifts the interventricular septum back toward the right ventricle, leading
to reduced filling to right side of the heart and a late-diastolic reversal of flow in the hepatic veins.
The advent of tissue Doppler imaging has provided increased diagnostic confidence to separate constriction from a
myocardial disease. Tissue Doppler measures myocardial tissue velocity and provides a non-invasive evaluation of
myocardial relaxation. The early diastolic mitral annular velocity (e') which reflects the status of LV myocardial
relaxation is reduced in most forms of heart failure related to myocardial disease, including restrictive
cardiomyopathy. The normal e' velocity from the medial mitral annulus is 9 cm/sec or greater, and it is usually
6cm/sec or less in patients with a myopathy. In contrast, e' is usually preserved or even increased in constrictive
pericarditis since the lateral motion of the heart is limited by the constrictive pericardium. Furthermore, the medial
mitral annular e' velocity is usually greater than the lateral mitral annular e'. This again stands in contrast to what is
expected in other forms of heart failure, and may reflect tethering of the lateral annulus by the constrictive process.

Figure 1
Two other echocardiographic findings are expected in constrictive pericarditis as well as in restrictive
cardiomyopathy. The first is a plethoric inferior vena cava, which may appear dilated or collapse insufficiently
during inspiration. This is the echocardiographic marker for increased venous pressure. The second is a relatively
"flat" Doppler profile of the systolic component of the superior vena cava. In contrast to normal patients and those
with obstructive lung physiology, patients with constrictive pericarditis have restricted cardiac filling and exhibit
little variation in the superior vena caval inflow velocity during the respiratory cycle. This finding is clinically useful
because severe obstructive lung disease or other conditions associated with exaggerated respiratory effort may
sometimes cause echocardiographic findings that mimic those of constrictive pericarditis.
In summary, constrictive pericarditis should be considered in patients presenting with heart failure symptoms and
preserved ejection fraction. Since echocardiography is usually an initial diagnostic test to evaluate such patients, the
following features can aid in the diagnosis of constrictive pericarditis:
1. Ventricular septal motion abnormality (from ventricular interdependence)
2. Medial mitral annulus e' velocity ≥ 9 cm/sec
3. Hepatic vein expiratory diastolic reversal ratio ≥ 0.79 (Figure) in addition to restrictive mitral inflow velocity (E/A
ratio > 0.8) and plethoric inferior vena cava.

Echocardiography of restrictive cardiomyopathy (RCM)

Echocardiography is the first imaging modality for the assessment of patients with dyspnea and/or heart failure. In
patients with RCM, it usually discloses nonspecific findings such as normal (not dilated) ventricles with normal or
increased wall thickness (Figures 1(a) and 1(b)) although it can occasionally give specific clues to the diagnosis.
Transmitral spectral Doppler often shows restrictive filling pattern (accentuated early diastolic velocity with low or
absent late filling velocity with E/A ratio > 2, E wave deceleration time < 150 ms, and short isovolumic relaxation
time < 60 ms, Figure 1(c)) although this is commonly a sign of advanced myocardial involvement. There is marked
left or biatrial dilatation usually as a consequence of chronically elevated filling pressures (Figures  1(a) and 1(b)).
Although classically systolic function as expressed by means of ejection fraction (EF) is normal or near normal,
novel techniques like tissue Doppler and speckle tracking echocardiography (STE) reveal the presence of latent
systolic myocardial impairment which may be specific to the disease state. Tissue Doppler of the mitral annulus
shows reduced systolic waves (s wave), blunted early diastolic waves, and preserved or blunted late diastolic waves,
depending on the degree of atrial involvement in the myopathic process(Figures 1(d) and 1(e)).

Figure 1: Echocardiographic images from a patient with restrictive cardiomyopathy. Two-dimensional 4-chamber
view in diastole (a) and systole (b), showing normal left ventricular volume, wall thickness, and systolic function (EF
62%). There is marked biatrial enlargement. Pulse wave Doppler from the left ventricular inflow (c) showing
restrictive filling pattern with an E wave velocity of 1 m/sec, an A wave velocity of 0.4 m/sec, and an E wave
deceleration time of 145 msec. Spectral tissue Doppler from the lateral (d) and septal (e) mitral annulus. There is
marked reduction in systolic annular velocities indicative of latent systolic dysfunction. E/e′ (e′ measured as the
average between the two annular e′ velocities) is 16, indicative of increased left ventricular filling pressure. Note the
marked reduction in lateral a′ velocity (<4 cm/sec) indicative of left atrial systolic dysfunction.

One of the main utilities of echocardiography is the differential diagnosis between constrictive pericarditis (CP) and
RCM. Both present as heart failure with normal-sized ventricles and preserved EF, dilated atria, and Doppler
findings of increased filling pressure (often restrictive filling pattern). Differential diagnosis is important since CP
can be treated by means of anti-inflammatory drugs or surgery while the treatment options of RCM are dictated by
the underlying condition. For the main differences between those disease states, the reader can refer to Table 2 and
recent research findings.
Table 2: Differential diagnosis between restrictive cardiomyopathy and constrictive pericarditis.

UNIT IV
Echocardiographic diagnostic criteria for Pericardial Constriction

Constrictive pericarditis is a potentially curable condition caused by a variety of situations which result in inflamed,
scarred, thickened, or calcified pericardium. When the abnormal pericardium limits diastolic filling, there are a series
of hemodynamic consequences which manifest as fatigue, dyspnea, abdominal bloating, peripheral edema, or right
heart failure. These clinical manifestations of constrictive pericarditis are similar to those due to a cardiomyopathy.
Since their hemodynamic and clinical features are similar, it is often challenging to distinguish constrictive
pericarditis from a myocardial disease. Even the traditional invasive hemodynamic criteria of "equalization of end-
diastolic pressures" is not specific for constrictive pericarditis. Despite many similarities between myocardial and
pericardial diseases, there are several unique features of constriction that allow a reliable diagnosis. Those features
are

1. Respiratory variation in ventricular filling.

2. Interventricular dependence
3. Augmented longitudinal motion of the heart.

Respiratory variation in ventricular filling arises from the dissociation of intrathoracic and intracardiac pressure
change and enhanced ventricular interaction in constrictive pericarditis. Inspiration reduces intrathoracic pressure
which usually is fully transmitted to intracardiac pressures, but in constriction, the intracardiac pressures falls much
less than intrathoracic pressure because of pericardial constraint. This difference in pressure change with inspiration
results in reduced filling to left side of the heart. The reduction in left heart filling during inspiration causes a
reduction in mitral inflow velocity and a shift of the interventricular septum toward the left ventricle. With
expiration, left heart filling increases which shifts the interventricular septum back toward the right ventricle, leading
to reduced filling to right side of the heart and a late-diastolic reversal of flow in the hepatic veins.

The advent of tissue Doppler imaging has provided increased diagnostic confidence to separate constriction from a
myocardial disease. Tissue Doppler measures myocardial tissue velocity and provides a non-invasive evaluation of
myocardial relaxation. The early diastolic mitral annular velocity (e') which reflects the status of LV myocardial
relaxation is reduced in most forms of heart failure related to myocardial disease, including restrictive
cardiomyopathy. The normal e' velocity from the medial mitral annulus is 9 cm/sec or greater, and it is usually
6cm/sec or less in patients with a myopathy. In contrast, e' is usually preserved or even increased in constrictive
pericarditis since the lateral motion of the heart is limited by the constrictive pericardium. Furthermore, the medial
mitral annular e' velocity is usually greater than the lateral mitral annular e'. This again stands in contrast to what is
expected in other forms of heart failure, and may reflect tethering of the lateral annulus by the constrictive process.

Two other echocardiographic findings are expected in constrictive pericarditis as well as in restrictive
cardiomyopathy. The first is a plethoric inferior vena cava, which may appear dilated or collapse insufficiently
during inspiration. This is the echocardiographic marker for increased venous pressure. The second is a relatively
"flat" Doppler profile of the systolic component of the superior vena cava. In contrast to normal patients and those
with obstructive lung physiology, patients with constrictive pericarditis have restricted cardiac filling and exhibit
little variation in the superior vena caval inflow velocity during the respiratory cycle. This finding is clinically useful
because severe obstructive lung disease or other conditions associated with exaggerated respiratory effort may
sometimes cause echocardiographic findings that mimic those of constrictive pericarditis

Figure 1:Showing features of constrictive pericarditis

In summary, constrictive pericarditis should be considered in patients presenting with heart failure symptoms and
preserved ejection fraction. Since echocardiography is usually an initial diagnostic test to evaluate such patients, the
following features can aid in the diagnosis of constrictive pericarditis: 1. Ventricular septal motion abnormality
(from ventricular interdependence) 2. Medial mitral annulus e' velocity ≥ 9 cm/sec 3. Hepatic vein expiratory
diastolic reversal ratio ≥ 0.79 in addition to restrictive mitral inflow velocity (E/A ratio > 0.8) and plethoric inferior
vena cava.

Echocardiographic detection of pericardial effusion

Trans-thoracic echocardiography (TTE) is used to detect and evaluate for pericardial effusion and any concomitant
cardiac disease. Assessment of regional wall motion abnormalities can help differentiate acute pericarditis from
myocardial ischemia. Echocardiography is essential in the presence of hemodynamic abnormalities, history of recent
cardiac surgery, or if there is a clinical suspicion of a large or increasing pericardial effusion.

Pericardial effusion (PEff) is defined by an increase in the physiological amount of fluid within the pericardial space.
It can appear following different medical conditions, mainly related to inflammation and cardiac surgery. Cardiac
tamponade is a critical condition that occurs after sudden and/or excessive accumulation of fluid in the pericardial
space that restricts appropriate filling of the cardiac chambers disturbing normal hemodynamics and ultimately
causing hypotension and cardiac arrest. It is, therefore, a life-threatening condition that must be diagnosed as soon as
possible for correct treatment and management. Echocardiographic evaluation of PEff is paramount for timely and
appropriate diagnosis and management. A structured echocardiographic approach including two-dimensional, M-
mode, and Doppler echocardiographic evaluation assessing (i) quantity and quality of pericardial fluid, (ii) collapse
of cardiac chambers, (iii) respiratory variation of the ventricular diameters, (iv) inferior vena cava collapsibility, and
(v) flow patterns in atrioventricular valves should give the bedside clinician the necessary information to
appropriately manage PEff.

Pericardial effusion appears as an echo-free space between the two layers of the pericardium. Echocardiographic
assessment should be structured and focused to (i) differentiate between global or localized effusion; (ii) quantify the
effusion; (iii) describe fluid appearance; and (iv) analyze hemodynamic compromise. Standard views along with
two-dimensional (2D) echocardiographic, M-Mode, and Doppler analysis used routinely in the assessment of PEff.
Four standard views used for reproducibility [subcostal, four-chamber, and parasternal long and short axis, however,
in emergent situations, a single view usually the subcostal one] is enough to diagnose significant PEff. A
combination of the aforementioned four standard views used to determine whether the effusion is global or localized.

Figure 3: Parasternal long axis (two-dimensional on the left and M-mode on the right) in a patient with pericardial
effusion (PEff). Arrow shows echo-free signal from pericardial fluid. M-mode shows PEff only during systole.

Figure 4: Standard echocardiographic views to assess a pericardial effusion (*). (A) Parasternal short axis; (B) four-
chamber view; and (C) subcostal view.
Table 3: Sizing of Pericardial Effusion by Echocardiography

Quantitative assessment of the PEff can be helpful for diagnosis and follow-up. However, as previously mentioned,
the volume of PEff does not necessarily correlate with the clinical symptoms. PEffs in adults are commonly
classified according to the size including trivial (seen only in systole), mild (<10 mm), moderate (10–20 mm), and
severe (>20 mm) (21). The most common and easy view to reproduce is the parasternal long axis, but it is still
important to compare with other standard views such as the parasternal short axis and the four-chamber view. A
subcostal view is also very commonly used, but it is important to know that depending on the angle of the probe, it is
easy to overestimate the size of the effusion. At end diastole, echo-free space between both pericardial layers can be
measured along the posterior wall of the left ventricle (LV). M-mode echocardiography in the parasternal long axis
shows an echo-free space throughout between the visceral and the parietal pericardium. This sign is only seen in
systole in case of mild effusions and during the complete cycle when the effusion is at least moderate.
Since PEff can be of different etiologies, it is usually difficult to make an appropriate qualitative assessment of fluid
characteristics just by echocardiographic signal. A qualitative assessment can be made by defining whether it is
global or loculated, transudative, exudative, or containing clotted blood or fibrin. Intrapericardial fibrin and pyogenic
exudates can create tabications and loculate the effusion. Particular echogenic densities such as the ones seen in
complex exudates or hemopericardium with the presence of fibrin strands and clots are easily recognized by
echocardiography. On the other hand, transudates will usually show a more echo-free signal giving a characteristic
sinusoid image in M-mode echocardiography that could help differentiate complex exudates from transudates.
Hemopericardium can be differentiated because of the spontaneous contrast signal resulting from the swirling of the
blood within the pericardial space. Nevertheless, a complete clinical assessment complemented by laboratory tests
and imaging studies should always be taken into consideration to find the underlying condition.
Figure 6: Subcostal view showing fibrin strains in a large pericardial effusion.

Echocardiographic detection of pericardial tamponade

Usually, a moderate-size or large pericardial effusion is present and leads to increasing compression and subsequent
diastolic compression of the cardiac chambers, usually in the sequence right atrium, right ventricle, left atrium (with
the lowest pressure chamber being affected first). The most sensitive finding for tamponade physiology on the
echocardiogram is inferior vena cava plethora, with absent inspiratory collapse; however this is not very specific.
Right atrial inversion for >1/3 the cardiac cycle length is the most sensitive and specific sign. Right ventricular
diastolic inversion may also been seen. Other, less-specific findings include excessive respiratory variations across
the mitral valve inflow (>30%), which is analogous to pulsus paradoxus and the tricuspid inflow (>60%). Absent
diastolic flow from the hepatic views suggests tamponade physiology.

On echocardiogram the tamponade will demonstrate the following:

 A large pericardial effusion

 A collapse of the right ventricle during diastole
 Dilation of the inferior vena cava
 Compression of the left atrium and ventricle
This will result in poor left heart filling with a drop in cardiac output and venous stasis in the superior and inferior
vena cava.

Echocardiography should be obtained immediately if cardiac tamponade is suspected. The information obtained from
this study should assess (i) quantity and quality of pericardial fluid; (ii) collapsibility of cardiac chambers; (iii)
diastolic ventricular size variability with respiratory cycle; (iv) septal “bounce”; (v) collapsibility of the inferior vena
cava (IVC); respiratory variation of flow patterns through and semilunar valves; and (vi) hepatic and pulmonary
veins flow patterns. The first five signs are easily obtained with both 2D echocardiography and M-mode. Assessment
of flow pattern variability will require Doppler evaluation.

A common sign of cardiac tamponade with significant hemodynamic compromise is collapse of the right atrium
(RA) and the RV. This happens during their relaxation phase, when intra-chamber pressures are lower than
pericardial pressures. Atrial and ventricular collapses are observed at different points of the cardiac cycle. Atrial
collapse is usually observed before ventricular collapse in the sequence of progressive cardiac tamponade.
Right atrium collapse is commonly observed during systole. In early systole (near the peak of the R wave),
intracavity pressure is lower and the atrial indentation of the thin free wall is seen. Moreover, duration of atrial
collapse (collapse longer than one-third of the cardiac cycle) has been described as an almost 100% sensitive and
specific sign of clinical cardiac tamponade. While isolated RA collapse is frequently observed, collapse of the left
atrium is, although described, rarely observed as a single chamber collapse. It is usually seen in cardiac tamponade
along with collapse of the RA. Collapse of both atria increases the sensitivity and specificity of cardiac tamponade.
 Figure 7: On the left, subcostal view of a patient with significant pericardial effusion and evidence of right
atrium (RA) collapse. On the right, M-mode through RA shows collapse duration over 1/3 of the systole.

Figure 8: Right ventricle (RV) collapse (left) in early diastole (end of T wave) in a
patient with cardiac tamponade. On the right, collapse of both atria in another patient
with signs of tamponade.

Figure 9: Loculated severe post surgical pericardial effusion around the left ventricle
(LV). Fibrin strains are also seen within the fluid.

These echocardiographic signs of cardiac tamponade may not be present in those cases in which right ventricular
diastolic pressures are elevated at baseline such as in pulmonary hypertension, positive pressure ventilation,
severe LV failure, or other cardiac congenital or inherited conditions that would increase RV diastolic pressures.
On the other hand, collapse of the right chambers may occur earlier than expected in those conditions with
reduced baseline intracavitary pressures, such as hypovolemia. Even with these limitations, absence of collapse
of any cardiac chamber has a 90% negative predictive value.
When cardiac tamponade is present, M-mode in both parasternal long and short axes is a useful tool to assess
exaggerated ventricular interdependence with the respiratory cycle. During inspiration, RV filling is increased,
while LV size in diastole decreases. The opposite scenario is present during expiration. This is a physiological
phenomenon that can cause a variation of no more than 5% of the cardiac output in absence of tamponade.

Figure 10: An exaggerated ventricular interdependence following significant pericardial

effusion shows increased right ventricle (RV) diastolic diameter during inspiration with
decreased diameter of the left ventricle (LV), with the opposite changes happening on
expiration.

Assessment of IVC in tamponade: An important sign of tamponade seen in 2D

echocardiography is dilatation of the IVC (>20 mm in an adult size heart) and hepatic
veins. This is known as IVC plethora, and, although not very specific, it is a very sensitive
sign of cardiac tamponade (92%). A decrease of the physiological collapsibility of the
IVC during inspiration is the commonly observed sign. M-mode through the IVC will
 demonstrate a less than a 50% reduction of caliber in most cases of significant PEff

Figure 11: Typical image of inferior vena cava (IVC) plethora (left) in a patient with
significant pericardial effusion. Collapse of IVC during inspiration is less than 50%
(right).

Septal “bounce”: An inspiratory “bounce” of the interventricular septum toward the LV

is a common, but not specific finding in cardiac tamponade. An M-mode through the parasternal long axis will
show this abnormal movement of the interventricular septum. It may not be present in case of LV hypertrophy or
increased LV filling pressures.

Figure 12: Arrow shows paradoxical movement of the interventricular septum in early diastole
suggesting elevated right ventricle filling pressures.

Pulsed-wave Doppler is key in the assessment of respiratory variations of the transvalvular flows in patients with
cardiac tamponade. In spontaneously breathing healthy individuals, Doppler peak velocities in the tricuspid and
pulmonary valves increase during inspiration, while they decrease in the mitral and aortic valves. As previously
mentioned in this review, a physiological variation of the cardiac output of around 5% exists with normal respiratory
cycle, which is reflected in normal peak E-wave variation of up to 10%.
In cardiac tamponade, these variations in the Doppler velocities are larger.
1. Mitral valve: research studies demonstrate an inspiratory reduction in mitral peak E-wave velocity in
cardiac tamponade of at least 25%. The value of the E-wave peak will vary based on the phase of the
respiratory cycle at the time of early diastole (lower filling pressures)

Figure 13: Diagram showing mitral and tricuspid valves inflow patterns variability with the respiratory
cycle in cardiac tamponade physiology. (B) Mitral peak E-wave of 119 cm/s (expiration) and 58 cm/s
(inspiration), 48% drop in mitral E-wave velocity. (C) Doppler through tricuspid valve in the same patient
shows an increase in peak E-wave (>40%) during inspiration.

2. Ticuspid valve: peak E-wave tricuspid valve physiological variation is larger than the mitral valve
fluctuations. In cardiac tamponade, the peak E-wave velocity will drop at least 40% in expiration compared
to inspiration (changes seen mainly in first two heart beats of expiration)
Right and left ventricular outflow tracts: physiological variations in aorta and pulmonary trunk are typically less than
10%. In presence of hemodynamically significant PEff, peak velocities in both outflow tracts will show a larger
difference with respiratory cycle. During inspiration a drop of >10% of the peak velocity will be seen in the aorta
while the opposite will happen in the right ventricular outflow tract, where an increase of at least 10% will be
noticed.

Figure 14: Respiratory variability seen with Doppler analysis of the left ventricular
outflow tract, demonstrating decrease of >10% following deep inspiration.

3. Hepatic veins: normal flow pattern shows a biphasic wave followed by a reversal wave corresponding with
atrial contraction. In cardiac tamponade, while venous return will still increase with inspiration, decreased or
even reversal flow will be seen in diastole (before atrial contraction). High positive and negative predictive
values have been reported for changes in Doppler signal in hepatic veins (82 and 88%, respectively).
Nevertheless, this has some limitations since hepatic vein flow is difficult to assess in up to one-third of
patients.

Figure 15: Pulsed-wave Doppler through hepatic veins shows reversal of the normal D wave on
expiration (left). Diagram showing changes of normal pattern in cardiac tamponade (right).
4. Pulmonary veins: pulmonary vein flow shows a biphasic wave with reversal flow during atrial contraction.
During inspiration, D wave is smaller due to reduced left ventricular filling (increased LV filling pressures).
In expiration, S wave is larger following decrease in LV filling pressures (increased flow toward the
ventricle).

ECHOCARDIOGRAPHIC EVALUATION of CHD

Common Hemodynamic features in shunt lesions

Left to right shunts share common haemodynamic features, which should be assessed by 2D imaging, colour flow
Doppler mapping and spectral Doppler.
 Size of the shunt: The size of the shunt is proportional to the size of the defect and the relative resistances of
the systemic and pulmonary vascular beds.
 Direction of flow: This is usually left to right. The flow across the ASD is phasic occurring predominantly
in late ventricular systole and early diastole with augmentation of the shunt during atrial contraction (2). The
shunt across the VSD is present throughout the cardiac cycle and provides increased blood flow to the
pulmonary circulation, resulting in left heart dilatation. Right to left or bidirectional shunt can be seen in the
setting of significant pulmonary hypertension or impaired right ventricular (RV) compliance.
 Chamber dilatation: Left to right shunts lead to volume overload of the cardiac chambers; atrial shunts
cause dilatation of the right atrium (RA) and RV. Shunts at the ventricular level and ducts cause left heart
dilatation.
Guidelines have been published regarding the RV morphometric evaluation for children and adults. In children, this
can be challenging with two-dimensional (2D) echocardiography as measurements are underestimated when
compared with MRI in children as opposed to adults. 3D echocardiography (3DE) offers more reproducible and
comparable measurements. In children, the LV dimensions should be indexed to body surface area.
  Elevated pulmonary arterial pressure: Large left to right shunts result in elevated pulmonary arterial
pressure and resistance. The systolic RV pressure can be estimated by the peak velocity of the tricuspid
regurgitation (TR) or by continuous-wave Doppler interrogation of the flow across the VSD. Diastolic
pulmonary pressure can be calculated from the peak and end-diastolic velocities of pulmonary regurgitation,
if present.
 The shape of the interventricular septum (IVS): In RV volume overload, the IVS is displaced towards the
LV in diastole with subsequent septal flattening. Presence of pulmonary hypertension will lead to systolic
septal flattening.
 Qp:Qs: The left to right shunt can be expressed as pulmonary (Qp) to systemic (Qs) blood flow ratio and
calculated using the continuity equation :
Qp/Qs = RVOT VTI x RVOT area / LVOT VTI x LVOT area
RVOT = right ventricular outflow tract, LVOT = left ventricular outflow tract, VTI = velocity time integral.
Paradoxically, in patients with a persistent duct, the area of the RVOT and corresponding VTI are used to calculate
the systemic blood flow and the pulmonary blood flow is calculated using the LVOT area and VTI. Qp: Qs should be
used cautiously as there are potentially sources of error. The calculation of the RVOT and LVOT area is based on the
measurement of the diameter of these outflow tracts, which is then squared in order to calculate the corresponding
area. This renders the estimation of Qp:Qs highly sensitive to errors as small differences in the measurement will
lead to significant discrepancies in the final result. Moreover, the measurement of the RVOT can be challenging
given the sometimes challenging or inadequate windows.
Ventricular function: RV function can be affected particularly in the context of pulmonary hypertension. Older
patients with significant atrial shunt can have LV diastolic dysfunction that becomes unmasked following closure of
the ASD.
 Effect on outflow tracts: A large shunt can exaggerate the pressure gradient across the outflow tracts e.g. a
large atrial shunt can increase the pressure gradient across the pulmonary outflow tract.
 Secondary effects: For example, a significant VSD might lead to dilatation of the mitral valve annulus and
subsequent mitral regurgitation.
 Association with other congenital cardiac malformations: The echocardiographic investigation should be
thorough, following a sequential segmental approach. Some of those malformations might be unmasked only
after the shunt lesion is closed e.g. the severity of a mitral stenosis may become apparent after closure of a
large ASD.

Figure 1: Parasternal short-axis view showing a perimembranous VSD (*) partially covered by aneurysmal tricuspid
valve tissue in 2D (A) and colour Doppler (B). (C) Shows the Continuous Doppler trace across the defect. The
Bernoulli equation allows the calculation of the pressure gradient (PG) between the right and left ventricles, in this
case PG = 4 × 4.72 = 88.36 mmHg. The left ventricular systolic pressure is assumed to be equal to the cuff-measured
systolic pressure provided, there is no left ventricular outflow tract obstruction. In this case, the systolic blood
pressure of the patient was 115 mmHg. The right ventricular pressure will be the difference of the LV systolic
pressure and the PG between the two ventricles = 115−88.36 = 26.64 mmHg.

Echocardiographic assessment of ASD

The atrial septum should be assessed from subcostal, apical and parasternal views:
Subcostal: The preferred acoustic window. The atrial septum is seen in the anterior-posterior (four-chamber view)
and superior-inferior axis (sagittal view). The latter allows assessment of the margins to the SVC and IVC and is the
optimal window for imaging a sinus venosus defect.The left anterior oblique (LAO) view shows the length of the
atrial septum and demonstrates the ostium primum defect as well as dilatation of the CS if present. Partially or
completely unroofed CS can be seen from this view. Colour Doppler interrogation and contrast studies can be
performed.

Figure 1: Subcostal four-chamber view shows a large ostium secundum ASD on 2D (A) and colour Doppler (B).

Figure 2: Superior sinus venosus defect (*) demonstrated from subcostal sagittal view on 2D (A) and Colour Doppler
(B).

Figure 3: Subcostal view showing a primum atrial septal defect (*). The bridging leaflets of the common valve are
attached to the crest of the septum (**) allowing shunt only at the atrial level. This is a partial AVSD.

Apical four chamber

In this view, the ultrasound beam is parallel to the atrial septum and measurements should be avoided, as there is risk
of an artificial dropout. The four-chamber view allows haemodynamic assessment of the ASD (RA and RV dilation)
and estimation of the RV pressure based on the TR jet velocity.
Figuree 64 Dilated right atrium and right ventricle in an adult with a large secundum ASD (*).

Parasternal short axis (PSAX) : The atrial septum is seen posterior to the aortic root and thus the aortic rim of the
defect can be identified. Sinus venosus and postero-inferior defects can also be seen in this view but measurements
of the defect are not recommended due to the risk of drop out.

Figure 7: Parasternal short-axis view on 2D (A) and colour Doppler (B) showing a large secundum ASD (*). Note
the dilated right atrium (RA).

High right parasternal: The patient is positioned in the right lateral decubitus position with the probe in a superior-
inferior orientation. This view is ideal for detection of sinus venosus defects.
In young children TTE will usually allow a full diagnostic study. In older children and adults, in particular, those
considered for a transcatheter device closure, transoesophageal echocardiography (TOE) offers additional valuable
information.

Echocardiographic evaluation of ventricular septal defect

Echocardiography is valuable not only in diagnosing VSDs but also in the percutaneous and surgical treatment of
these defects. Echocardiographic evaluation of VSDs includes:
 Identification of the location of defects on the septum
 Establishing the number of defects
 Confirm ventricular septal defect (VSD).
 Determine the size and morphological location of VSDs.
 Rule out associated lesions.
 Assessment of chamber size and wall thickness.
 Estimation of shunt size (pulmonary/systemic flow ratio).
 Estimate right ventricular and pulmonary arterial pressures.
Stepwise evaluation for VSD
o Initial indication is the volume overload of the chambers (LA and LV)

o Visualize the defect from all possible windows to look for the defect

o Determine the presence of additional defects (screening the septum – septal sweep in subcostal view,
apical 4c view and parasternal short and long axis sweep in color and 2d)

o Determine the direction of shunting of the defect

o Look for the associated structures particularly outflows

o Look for the pulmonary artery pressures: VSD gradients, TR and PR gradients

o Determine the volume overload of chambers (Z scores of LV, particularly in M mode)

 o Determine suitability for device closure

Classification of VSD: Ventricular septal defects can be classified into following types:
1. Perimembranous ventricular septal defect
2. Muscular ventricular septal defect:
i. muscular inlet
ii. muscular outlet
iii. trabecular defect,
3. Doubly committed ventricular septal defect
4. Inlet ventricular septal defect

Figure 12: Schematic diagram of the interventricular septum with removed RV cavity from the RV side. Various part
of the septum are profiled: blue (muscular septum) this forms the region of the muscular VSD. The muscular septum
can further be classified with respect to the muscular moderator and septal band. Yellow region signifies the
perimembranous region, purple color signifies the inlet septum and green color the outlet septum.

Figure 13: 2d echocardiography with four chamber view with anterior tilt showing the perimembranous VSD defect
getting restricted by septal leaflet of the tricuspid valve in 2d (A) and color Doppler (B).

Figure 14: 2d echocardiography with subcostal coronal view with anterior tilt with opening of the aortic outflow
showing the outlet muscular VSD with left to right shunt in 2d (14A) and color mapping (B).

Figure 15: 2 d echocardiography with parasternal long axis view showing the apical muscular type of trabecular
muscular VSD with left to right shunt in 2d (A) and color mapping (B).
Figure 16: 2d echocardiography with parasternal long axis view showing the doubly committed VSD with left to
right shunt in 2d (A) and color flow mapping (B).

Figure 17: 2d echocardiography shows in 4 chamber view shows the large inlet VSD getting partially restricted by
septal leaflet of tricuspid valve. Such partial closure of VSD is more commonly a feature of perimembranous VSD
and is very rarely seen in the inlet VSD as in the present case.

Figure 18: 2d echocardiography with various view shows the profilation of perimembranous VSD. A: shows the
perimembranous defect with anterior tilt in subcostal coronal view with anterior tilt showing the defect. B: shows the
parasternal short axis view shows the location of the perimembranous defect from 9 o'clock to 11 o'clock position,
C1: shows the location of the perimembranous VSD with slight posterior tilt toward the tricuspid valve in 2d and
color flow mapping (C2).
Figure 19: 2d echocardiography with parasternal long axis view shows the doubly committed VSD getting restricted
with right coronary cusp of the aortic valve with significant prolapse of the right coronary cusp. Though such
prolapse may significantly decrease the left to right shunting and hence volume overload, it by itself because of the
significant prolapse is an indication of surgery to prevent the damage to the aortic valve.

Size of ventricular septal defect

The judgment of size of defect is generally made on hemodynamic grounds (degree of left to right shunt, presence of
volume overload, and pulmonary artery pressure).
Comparative size: According to some authors a VSD size is defined in relation to aortic root size. Small ventricular
septal defect are defined if less than 1/3rd of aortic root diameter, 1/3rd to 2/3rd of aortic root diameter considered as
moderate sized defect, and the lesions that are approximate to the size of aortic root are defined as large VSD. The
disadvantage of the method of classifying defects is that some defects which are anatomically large can be restricted
in terms of shunt and pressure because of reduction in size by tricuspid valve or aortic valve.
Hemodynamic classification uses the pressure differential across the left to right ventricle to classify defects. With
isolated defects, when there is equalization of pressure between two ventricles in absence of pulmonary stenosis,
then it is called as large or nonrestrictive defect. Since right and left ventricles do not contract exactly
simultaneously, there is always some inequality in the ventricular pressures as estimated by Doppler technique since
it measures instantaneous pressure difference. A restrictive defect is one in which right ventricular and pulmonary
artery pressures are lower than left ventricle with pressure gradient of more than 60 mmHg (ventricular septal defect
peak velocity more than 4 m/s), and moderately restrictive ventricular septal defect with pressure difference of 25–
60 mmHg (ventricular septal defect peak velocity 2.5–4 m/s).
The VSD may be associated with anterior or posterior malalignment and these VSDs in the region of the
perimembranous area are generally large VSDs. Those with anterior malalignment may be associated with narrowing
of the anterior outflow tract (generally pulmonary) as in Tetralogy of Fallot. Those VSDs associated with posterior
malalignment are associated with narrowing of the posterior outflow (generally aorta) (Fig. 20 A–C).

Figure 20 : A and B shows a large malaligned ventricular septal defect with anterior malalignment of the septum
leading to associated pulmonary stenosis profiled in parasternal long axis view (A) and subcostal view (B). C shows
the large malaligned VSD with anterior malalignment leading to subaortic narrowing profiled in parasternal long axis
view.

Patterns of shunting across VSD

 Nonrestrictive ventricular septal defect with high pulmonary vascular resistance, direction of flow can be bi-
directional or dominantly right to left depending upon the severity of pulmonary vascular obstructive disease.
 With associated pulmonary stenosis, there may be isolated right to left shunt depending upon the severity of
pulmonary stenosis. With severe right ventricular outflow obstruction, if ventricular septal defect is small, one
can get a turbulent jet of right to left shunt with suprasystemic right ventricle systolic pressure.

Figure 21: 2d echocardiography with parasternal long axis view of a case of doubly committed VSD in a 25-year-old
man with Eisenmenger syndrome showing significant right to left shunt. The LV dimensions were normal in the
present case with Z score of 1.1.
 With the use of color flow mapping with careful interrogation, one should also look for any left ventricle to right
atrial shunt as high velocity of left ventricle to right atrial jet can be misinterpreted as elevated right ventricle
pressure. This can happen particularly with ventricular septal defect which are getting smaller by septal leaflet of
tricuspid valve.

Direction of shunt

 With isolated uncomplicated nonrestrictive VSD, pressure between the two ventricles is similar.
 In patients with low pulmonary vascular resistance, dominant shunt occurs from left to right during systole, and
with increase in left ventricle end diastolic pressure left to right shunt will persist during diastole also.
 A typical ‘M’ shaped flow pattern is being described in patients with nonrestrictive VSD, explanation for which
is– as left ventricle contraction starts early and last longer than right ventricle, so with onset of systole flow occur
from left to right, with decrease in degree of shunt during mid systole as pressure between two ventricles
equalized, and in later part of systole as right ventricle relaxes left to right shunt dominates.
 With restrictive VSD, left to right shunting occurs throughout systole. In some small muscular VSD, left to right
shunt occurs only during a portion of systole, presumably because of closure of muscular ventricular septal
defect in mid systole with ventricular contraction. Bidirectional or right to left shunting can occur with restrictive
and nonrestrictive VSD as described earlier.

 Continuous and pulsed wave Doppler examination

Pulsed and continuous wave Doppler examination is used to assess:
 Direction of shunt across VSD.
 Pressure gradient across the defect (difference of left ventricle–right ventricle systolic pressure).
 Right ventricle pressure (by VSD gradient and peak gradient of tricuspid regurgitation jet).
 Diastolic function of both ventricles.

Pressure gradient across ventricular septal defect

 While taking continuous wave Doppler across VSD, the cursor should be well aligned with VSD jet on color
flow mapping.
 The velocity of the VSD shunt can be determined using the Bernoulli's equation. This will give the difference
between the left and right ventricular systolic pressure.
 The left ventricular systolic pressure is derived from the systolic blood pressure (provided there is no left
ventricular out flow obstruction), which should be recorded at the time of Doppler study using appropriate sized
BP cuffs.
 Right ventricular pressure = Systolic blood pressure VSD jet peak gradient

This equation has been found to have good correlation with cardiac catheterization derived right ventricle systolic
pressure.

 However, sometimes the jet velocity may not reflect the interventricular pressure gradient accurately because
proper alignment of the Doppler beam with the jet is not possible, and that if the defect has some length to it, the
viscous frictional forces make the application of the modified Bernoulli's equation inappropriate.
 Determining the right ventricular pressure from tricuspid insufficiency jet velocity (which may be found in some
cases) is also very useful.

M mode echocardiography
Figure 22: M mode echocardiographic evaluation of a case of VSD taken in parasternal long axis view. The LV end
diastolic dimensions (LVIDd) is compared to expected for the weight of the child and a dilated LV with  Z score of
more than 2 signifies significant left to right shunt (>2:1) and hence an indication for intervention.

 Assess the left atrial and left ventricular size to quantitate shunt across ventricular septal defect.
 Right ventricular size and wall thickness, which will reflect, elevated right ventricular systolic pressure.
 For direction of shunt, this is rarely used in daily practice but depicts best the direction of shunting during the
various phases of a cardiac cycle.

Interrogation of the atrioventricular and semilunar valves for regurgitation and stenosis

 The tricuspid regurgitation velocity should always be obtained to predict the right ventricular systolic pressure
and hence indirectly the pulmonary artery pressure if there is no pulmonary stenosis.
 Presence of pulmonary stenosis, and aortic regurgitation should be evaluated.
 The velocities of both atrioventricular valves and semilunar valves should be taken to rule out any associated
abnormality. The mitral valve gradients may get exaggerated in the presence of VSD.

Figure 23: 2d echocardiography with color compare showing the well open mitral valve in 2d (A) and turbulence
across mitral valve in B. The turbulence in color flow mapping across the mitral valve is essentially because of the
increased flow across the mitral valve because of the associated nonrestricted VSD extending from the
perimembranous to the inlet septum.

 Pulmonary blood flow to systemic blood flow ratio

As regards quantifying pulmonary and systemic shunt flow using Doppler echocardiography several methods
currently exists, although none is widely used due to variable results.

Assessment of suitability for device closure

Percutaneous closure for mid muscular VSD and perimembranous VSD can be done. While assessing the child for
device closure of muscular defect, the defect should be at least 5 mm away from atrioventricular valves and
semilunar valves and there should not be associated other defects requiring cardiopulmonary bypass.

Utility of transesophageal echocardiography

Transesophageal echocardiography has helped in better visualization of VSD, especially when transthoracic window
is poor, like in adolescents and adults. Straddling and overriding of the atrioventricular defect can be better detected
by transesophageal echocardiography.