REGURGITANT LESIONS

Brook Alemayehu, R3
Moderator: Dr. Dejuma Yadeta
Consultant Internist & Cardiologist
OUTLINE

 Mitral Regurgitation

 Aortic Regurgitation
MITRAL REGURGITATION
 Mitral Regurgitation

Acute Chronic

See below

Primary Secondary/ Functional

See below
•Ischemic heart disease.
•LV systolic dysfunction
• Hypertrophic CM.
FIGURE 14-41 Functional/ischemic MR. Mitral tethering forces are increased because of both annular dilation
and papillary muscle traction, which occur as a result of LV remodeling. Closing forces are reduced because of
impaired LV systolic function. The end result is apical displacement of leaflet coaptation, which creates a
“hockey stick” configuration of one or both leaflets as shown in the apical four-chamber view on the left.
PATHOPHYSIOLOGY
 As the regurgitant mitral orifice is functionally
in parallel with the aortic valve Low
impendance to ventricular emptying.

 Thus, almost 50% of the regurgitant volume

is ejected into the left atrium before the
aortic valve opens.
PATHOPHYSIOLOGY
1. LV empties more completely and by increasing
preload (i.e., by use of the Frank- Starling
principle) EF

2. Acute MR  afterload  late systolic LV

pressure & radius LV wall stress
contractile energy to be expended in
shortening than in tension development
Reciprocal  in the extent and velocity of
myocardial fiber shortening ESV Further
 EF
PATHOPHYSIOLOGY
3. Chronic compensated MR Volume load on
LV EDV and LV mass Wall tension
(Laplace’s)  ESV normalizes
 However, the degree of hypertrophy is often not
proportional to the degree of LV dilation, so the
ratio of LV mass to end-diastolic volume may be less
than normal.
 Left atrial enlargement now accommodates the
regurgitant volume at lower LAP
PATHOPHYSIOLOGY
4.  EDVMitral annular diameter Further
MR (vicious cycle) Eccentric hypertrophy
Chamber stiffness systolic function
TSF & FSV EDV & ESV EF LAP
Decompensation
PATHOPHYSIOLOGY
 The eccentric LV hypertrophy that accompanies
the elevated EDV is secondary to new
sarcomeres laid down in series

 In most patients, compensation is maintained for

years

 Later, the prolonged hemodynamic overload

ultimately leads to myocardial decompensation
 EDV, preload, and afterload all increase, whereas EF
and stroke volume decline.
ASSESSMENT OF CONTRACTILITY
  Ejection phase indices
 i.e.EF, fractional fiber shortening, and velocity of
circumferential fiber shortening (VCF)
 Due to  afterload
 “Normal” LVEF in MR is ~70%.
 LV dysfunction-> LVEF declines towards 60% or ESV
rises towards 40 mm
 Symptoms: LAP & Pulm. Venous pressure; often no
change in these ejection phase indices, which remain
elevated
 In some patients, major symptoms reflect serious
contractile dysfunction
ASSESSMENT OF CONTRACTILITY
 Low normal levels: may actually reflect impaired
myocardial function

 Moderately reduced (EF: 40-50%)

 Generallysignify severe, often irreversible,
impairment of contractility, identifying patients who
may do poorly after surgical correction of the MR

 Severely reduced (EF < 35%)

 Advanced myocardial dysfunction
 High operative risks and may not experience
satisfactory improvement after mitral valve
replacement.
PATHOPHYSIOLOGY
 A brief early diastolic gradient
 As a result of the rapid flow of blood across a normal-sized
mitral orifice early in diastole
 Accompanied by an early diastolic murmur at the apex

 LA compliance is an important determinant of

the hemodynamic and clinical picture in patients
with severe MR
1. Normal or reduced compliance
2. Markedly increased compliance
3. Moderately increased compliance
CLINICAL FEATURES
SYMPTOMS
 Symptoms may herald
 Due to raised Pulm. venous pressure despite preserved
EF
 LV decompensation

 Rheumatic MR: the time interval between the

initial attack of RF and symptoms often exceeds
two decades

 Indolent course of MR may be deceptive

 By the time that symptoms happen  serious and
sometimes even irreversible LV dysfunction may have
developed.
CLINICAL FEATURES
SYMPTOMS
 Chronic weakness and fatigue are more
prominent features in chronic compensated MR

 Symptoms of pulmonary congestion- in acute AR

or decompensated chronic MR

 Right-sided HF prominent in acute MR

 Angina pectoris is rare unless CAD coexists

CLINICAL FEATURES
PHYSICAL EXAMINATION
 PMI- brisk and hyperdynamic
 Displaced to the left; palpable LV filling wave

 Late systolic parasternal thrust

 Systolicexpansion of the enlarged LA
 May be confused with RV enlargement
CLINICAL FEATURES
PHYSICAL EXAMINATION
 Auscultation
 Diminished S1, Wide S2 split, P2 accentuation
 S3- not to confuse with HF

 Holosystolic murmur, usually constant in intensity,

blowing, high-pitched, and loudest at the apex, with
frequent radiation to the left axilla and left
infrascapular area

 Radiation towards the sternum or aortic area

 Littlecorrelation has been found between the

intensity of the systolic murmur and severity of MR
CLINICAL FEATURES
PHYSICAL EXAMINATION
 Auscultation
 The murmur may be holosystolic, late systolic, or
early systolic.
 Early systolic murmurs are typical of acute MR.
 Mid-systolic (esp. accompanied by a midsystolic click)- MVP

 Late systolic: MVP or to papillary muscle dysfunction

 The systolic murmur is the most prominent physical

finding; it must be differentiated from the systolic
murmur of AS, TR, and ventricular septal defect.
CLINICAL FEATURES
PHYSICAL EXAMINATION
 Auscultation
 Silent MR:
 LV dilation, Acute MI, or paraprosthetic valvular
regurgitation
 Marked emphysema, obesity, chest deformity, or a

prosthetic heart valve

 As noted, a short, low-pitched diastolic murmur

following S3 may be audible in patients with severe
MR, even without accompanying MS.
CLINICAL FEATURES
PHYSICAL EXAMINATION
 Dynamic auscultation
 No/littlerespiratory variation
 Holosystolic MR murmur
 Standing  Squating 
 MVP
 Standing  Squating 
 Strain phase of Valsalva
 holosystolic MR murmur 
 MVP 

 Isometric exerise
 Increases holosystolic murmur of MR
 Differentiates from AS & HOCM
ECHOCARDIOGRAPHY
 Echocardiography plays a central role in
 Diagnosisof MR,
 Determining its cause and potential for repair,
 Quantifying its severity and
 Determining the presence and severity of associated
AR or TR
ECHOCARDIOGRAPHY
 Severe MR
 2D
 Enlargement of LA and LV, with increased systolic motion
of both chambers.
 LV dysfunction   EDV & ESV;  EF & FS

 Doppler echocardiography
 High velocity jet in the left atrium and Reversal of flow in
the pulmonary veins during systole
 Width of the jet across the valve

 RF, RV & ERO:

 Greater accuracy in comparison with angiography

 And these methods are strongly recommended

 Vena Contracta: also predicts severity of MR

DISEASE COURSE
 Asymptomatic patients with severe MR
 Progression to symptoms, LVD, Phtn or AF: 30-40%
at 5 years.
 Mortality:
 Normal LV function- <1% per year
 Higher rates for LVEF < 60%

 High likelihood of requiring surgery over the next 6

to 10 years
FIGURE e63-5 Survival of patients with severe MR related to flair leaflets after
treatment with early surgery (within 3 months of detection) or with initial medical
management. Outcomes are shown for patients with normal left ventricular ejection
fraction (EF) (A) and for patients with mild (B) and severe (C) left ventricular systolic
dysfunction.
FOLLOW-UP
 TTE is indicated periodically to evaluate for
changes in MR severity.
MEDICAL THERAPY
 The indications for afterload reduction in
patients with chronic primary valvular MR are
much less clear.

 ACEIs: Small studies failed to show benefit

 No long term study or RCT

 Beta blockers:
 Retrospective data: Delay the progression of LVD
and improve patient outcomes
 No definitive RCTs
MEDICAL THERAPY
 Exception:
 Hypertension
 Associated complications
  Transmitral gradient  Worsening MR

 Severe LVD where surgical or transcatheter

treatment is deferred because of age or other
comorbid conditions or contributing factors.
SURGICAL THERAPY: INDICATIONS
 Without surgical treatment, prognosis is poor

 Asymptomatic (NYHA Class I) Patients

1. LV systolic dysfunction (ejection fraction ≤60%
and/or LV end-systolic diameter >40mm)
2. AF or pulmonary hypertension is present.

 Because of the higher operative mortality, older

patients (>75 years) should, in general, undergo
surgery only if they are symptomatic
SURGICAL THERAPY: INDICATIONS
 Symptomatic Patients
 Moderate or severe symptoms (NYHA class II, III,
and IV) should generally be considered for surgery.

 Exception: LVEF < 30% and MVR required

 Medical therapy vs Surgery

 However, when mitral valve repair appears possible, even

patients with serious LV dysfunction may be considered for
operation
SURGICAL THERAPY: MVR VS REPAIR
 Outcomes after mitral valve repair are more
favorable than those with mitral valve
replacement in comparative studies
 However, this benefit has never been subjected to a
prospective randomized trial.

 Mitral valve repair is strongly recommended

whenever possible.
SURGICAL THERAPY: MVR VS REPAIR
 Disadvantages of MVR
1. Post valve replacement deterioration of LV function
2. Inherent problems with the prosthesis itself
 Risks of thromboembolism or hemorrhage associated with
mechanical prostheses,
 Risk of late structural deterioration of bioprostheses, and

 Infective endocarditis with all

 For MVR, a higher threshold for clinical and

hemodynamic impairment should be used than if
mitral valve repair is contemplated
SURGERY: SURVIVAL BENEFIT
 Surgical treatment substantially improves
survival in patients with symptomatic MR.

 Preoperative factors that correlate with

excellent immediate and long-term survival
rates include
 Age younger than 60 years,
 NYHA class I or II,
 Cardiac index exceeding 2.0 liters/min/m2,
 LV end-diastolic pressure less than 12 mm Hg, and
 A normal ejection fraction and end-systolic volume
SURGERY: SYMPTOMATIC BENEFIT
 Improved clinical status, quality of life, and
exercise tolerance after mitral valve repair or
replacement.

 Due to:-
 Severe pulmonary hypertension is reduced,
 LV enddiastolic volume and mass decrease,
 Coronary flow reserve increases and
 Improvement in contractile function improves
SURGERY: OPERATIVE MORTALITY
 Declining threshold for surgery
 Reduced operative mortality
 Improvements in MV repair procedures, and
 Poor outcome when surgery is done after a long
history of symptoms, impaired LV function, AF, or
pulmonary hypertension

 Decision: Progressive nature of MR vs Surgical

complications
SURGERY: OPERATIVE MORTALITY
 Operative mortality rates:3- 9%
 [Pure or predominant MR (NYHA class II or III)]
 Elective isolated mitral valve replacement.

 MV surgery + CABG
 Operative mortality rates: 7- 12% and even higher
(up to 25%) in patients with severe LV dysfunction,
 Especially when pulmonary or renal function is impaired, or
when the operation must be carried out on an emergency
basis.
 Age per se is no barrier to successful surgery
SURGERY FOR CHRONIC SECONDARY
MR
 Prognosis is strongly influenced by the degree of
LV dysfunction

 There are only sparse data to indicate that

correcting MR prolongs life or even improves
symptoms over an extended time.
 Small RCTs have demonstrated that mitral valve
surgery reduces chamber size and improves peak
oxygen consumption in chronic severe secondary MR.

 The indications for mitral valve surgery are less

clear for secondary MR than for primary MR
SURGERY FOR CHRONIC SECONDARY
MR
 It is not clear if repair is preferred over MVR

 MV repair: often not durable because of

progression of the underlying LV myocardial disease

 So, is MVR better?

1 retrospective study (n=1006): MV repair patients
more likely to require re-operation
 1 prospective study (n=251): Similar rate of reduction in
LV volume with less recurrent MR during the follow-up
period for MVR
 Neither showed survival benefit
ACUTE MR: MEDICAL MANAGEMENT
 Afterload reduction
 Vasodilators like Na nitroprusside
 Permit stabilization of clinical status, thereby
allowing coronary arteriography and surgery to be
performed with the patient in optimal condition.

 Inotropes
 In patients with acute MR who are hypotensive, an
inotropic agent such as dobutamine should be
administered with the nitroprusside.
ACUTE MR: MEDICAL MANAGEMENT
 Intra-aortic balloon counterpulsation
 Can be helpful to treat acute severe MR.

 By lowering systolic aortic pressure, intra-aortic

balloon counterpulsation decreases LV afterload,
increasing forward output while decreasing
regurgitant volume.

 Only a temporizing measure

ACUTE MR: SURGICAL MANAGEMENT
 Emergency surgical treatment may be required
for patients with acute LV failure caused by
acute severe MR.

 Emergency surgery is associated with higher

mortality rates than those for elective surgery
for chronic MR.

 However, unless patients with acute severe MR

and heart failure are treated aggressively, a
fatal outcome is almost certain.
ACUTE MR: SURGICAL MANAGEMENT
 Acute papillary muscle rupture requires
emergency surgery with mitral valve repair or
replacement.

 Acute papillary muscle dysfunction

 Should be initially managed with hemodynamic
stabilization, usually with the aid of an intra-aortic
balloon pump
 Surgery should be considered for those patients who
do not experience improvement with aggressive
medical therapy.
ACUTE MR: SURGICAL MANAGEMENT
 If patients with MR can be stabilized by medical
treatment, it is preferable to defer operation
until 4 to 6 weeks after the infarction if
possible.

 Vasodilator treatment may be useful during this

period.

 However, medical management should not be

prolonged if multisystem (renal and/or
pulmonary) failure develops
AORTIC REGURGITATION
CAUSES
PATHOPHYSIOLOGY
Laplace’s Law
Wall Stress

 LV dilation also increases the LV systolic tension

required to develop any level of systolic
pressure.

 Thus in AR, there is an increase in preload and

afterload
CHRONIC AR: PATHOPHYSIOLOGY
 LV systolic function is maintained through the
combination of chamber dilation and hypertrophy.

 This leads to eccentric hypertrophy, with

replication of sarcomeres in series and elongation
of myocytes and myocardial fibers.

 In compensated AR, sufficient wall thickening has

occurred that the ratio of ventricular wall
thickness to cavity radius remains normal.
 Under these conditions, end-diastolic wall stress is
maintained at or returns to normal levels.
CHRONIC AR: PATHOPHYSIOLOGY
 As AR persists and increases in severity over
time, however, wall thickening fails to keep pace
with the hemodynamic load, and end-systolic wall
stress rises.

 At this point, the afterload mismatch results in

a decline in systolic function, and the ejection
fraction falls
CHRONIC AR: PATHOPHYSIOLOGY
 In AR, LV mass usually is greatly increased,
often to levels even higher than in isolated AS*
 Atautopsy the hearts of these patients may be
among the largest encountered, sometimes weighing
>1000g

 Patients with severe chronic AR have the largest

end-diastolic volumes of those with any form of
heart disease, resulting in so-called cor bovinum.
 However, end-diastolic pressure is not uniformly
elevated (i.e., LV compliance often is increased).
CHRONIC AR: PATHOPHYSIOLOGY
 In more severe cases of AR, the regurgitant
flow may exceed 20 liters/min, so the total LV
output at rest approaches 25 liters/min
A level that can be achieved acutely only by a trained
endurance runner during maximal exercise.
CHRONIC AR: PATHOPHYSIOLOGY
 During exercise, peripheral vascular resistance
declines  Increase in heart rate  Diastole
shortens  Regurgitation per beat decreases,

 This facilitates an increment in effective

(forward) cardiac output without substantial
increases in end-diastolic volume and pressure
CHRONIC AR: PATHOPHYSIOLOGY
 The ejection fraction and related ejection phase
indices are often within normal limits, both at
rest and during exercise
CHRONIC AR: PATHOPHYSIOLOGY
LV FUNCTION
 In advanced stages of decompensation, LA,
pulmonary artery wedge, pulmonary arterial, RV,
and RA and the effective (forward) cardiac
output falls, at first during exercise and then at
rest.

 The normal decline in end-systolic volume or the

rise in ejection fraction fails to occur during
exercise

 Symptoms of heart failure develop, particularly

those secondary to pulmonary congestion
CHRONIC AR: CLINICAL FEATURES
SYMPTOMS
 Asymptomatic for 10-15 years
 Earliest symptoms is Palpitation

 Exertional dyspnea occur after years of having

palpitation and indicate worsening of cardiac
reserve
 Then, orthopnea, PND and excessive diaphoresis
follow
 Signs of congestion like hepatomegaly and
peripheral edema develop late in the course
 Angina: Late in the course
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 The jarring of the entire body and the bobbing
motion of the head with each systole can be
appreciated,
 DeMusset's sign — A head bob occurring with each
heart beat.

 The abrupt distention and collapse of the larger

arteries are easily visible.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Arterial Pulse
 Corrigan's pulse: pulses are of the “water-hammer”
or collapsing type with abrupt distention and quick
collapse
 The arterial pulse is often prominent and can be best
appreciated by palpation of the radial artery with the
patient's arm elevated

 Quincke's pulse (capillary pulsations) — can be

detected by pressing a glass slide on the patient's
lip, by transmitting a light through the patient's
fingertips, or by exerting gentle pressure on the tip
of a fingernail.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Arterial Pulse
 Traube's sign
 also known as “pistol shot sounds” refers to booming
systolic and diastolic sounds heard over the femoral artery

 Duroziez sign — consists of a systolic murmur (bruit)

heard over the femoral artery when it is compressed
proximally and a diastolic murmur when it is
compressed distally.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Arterial Pulse
 Mueller's sign — Systolic pulsations of the uvula
 Gerhard's sign — Systolic pulsations of the spleen
 Rosenbach's sign — Systolic pulsations of the liver
 Becker's sign — Visible pulsations of the retinal
arteries and pupils
 Hill's sign* — Popliteal cuff systolic pressure
exceeding brachial pressure by more than 60 mmHg
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Blood Pressure
 SBP is elevated, and DBP is abnormally low
 Korotkoff sounds often persist to zero even though
the intra-arterial pressure rarely falls below 30 mm
Hg.
 The point of change in Korotkoff sounds (i.e., the
muffling of these sounds in phase IV) correlates
with the diastolic pressure
 As heart failure develops, peripheral
vasoconstriction may occur and arterial diastolic
pressure may rise, even though severe AR is present.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Precordium- Inspection & Palpation
 Shifted AI and PMI
 Systolic retraction may be detected over the
parasternal region.
 Diastolic thrill along LLSB
 A prominent systolic thrill may be palpable at the
base of the heart or in the suprasternal notch and
transmitted upward along the carotid arteries
 Due to the augmented stroke volume
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Auscultation
 A2
 Root d/rs: Normal or accentuated
 Valve d/rs: Soft or absent

 P2 may be obscured by the early diastolic murmur.

 Thus S2 may be absent or single or exhibit narrow or
paradoxical splitting.

 S3 correlates with an increased LV enddiastolic

volume
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Aortic regurgitant murmur
 High frequency and begins immediately after A2.
 Blowing, decrescendo diastolic
 Best heard: 3rd intercostal space along left sternal
border
 Mild AR: brief
 Severe AR: Louder and longer, indeed holo-diastolic

 When the murmur is soft, it can be heard best with the

diaphragm of the stethoscope and with the patient
sitting up, leaning forward, and with the breath held in
forced expiration
 vs PR
 Earlier onset (i.e., immediately after A2 rather than after P2)
 Presence of a widened pulse pressure.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Aortic regurgitant murmur
 The severity of AR correlates better with the
duration than with the intensity of the murmur
 Mild AR: Limited to early diastole and typically is high-
pitched and blowing.
 Severe AR: Holodiastolic and may have a rough quality.

 When the murmur is musical (cooing dove murmur),

it usually signifies eversion or perforation of an
aortic cusp.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Aortic regurgitant Murmur
 In patients in whom the AR is caused by primary
valvular disease, the diastolic murmur is usually
louder along the left than the right sternal border.

 However, when the murmur is heard best along the

right sternal border, it suggests that the AR is
caused by aneurysmal dilation of the aortic root.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Other findings: Systolic murmur
 Many patients with chronic AR have a harsh systolic
outflow murmur caused by the increased total LV
stroke volume and ejection rate, which often
radiates to the carotid vessels.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 Other findings: Austin Flint murmur
A mid-diastolic and late diastolic apical rumble

 Common in severe AR and may occur in the presence

of a normal mitral valve.

 Due to the severe aortic reflux impinging on the

anterior leaflet of the mitral valve or the free LV
wall
 Convincing evidence for obstruction to mitral inflow in
these patients is lacking.
CHRONIC AR: CLINICAL FEATURES
PHYSICAL EXAMINATION
 The auscultatory features of AR are intensified
by strenuous and sustained handgrip, which
augments systemic vascular resistance
CHRONIC AR: ECHOCARDIOGRAPHY
 Determines cause of AR (valve vs root disease)
 Assesses LV size

 Assesses LV function

 Assess severity of AR

 Doppler echocardiography and color flow Doppler

imaging is the most sensitive and accurate noninvasive
techniques for the diagnosis and evaluation of AR.
CHRONIC AR: ECHOCARDIOGRAPHY
 Aortic regurgitant orifice size and aortic regurgitant
flow
 Can be estimated quantitatively and such determinations
are strongly recommended
 These quantitative data provide the basis for the
definitions of mild, moderate, and severe AR

 Severe AR,
 The central jet width assessed by color flow Doppler
imaging exceeds 65% of the left ventricular outflow tract,
 The regurgitant volume is > 60mL/beat,
 The regurgitant fraction is > 50%, and
 There is diastolic flow reversal in the proximal descending
thoracic aorta.
CHRONIC AR: OTHER TESTS
 Cardiac catheterization
 Invasive assessment is indicated when CMR is not
available or there are contraindications for CMR,
such as implanted devices

 For assessment of hemodynamics, coronary artery

anatomy and severity in symptomatic patients with
equivocal echocardiographic evidence

 Exercise Testing
 Exercise stress testing can be used to assess
symptomatic status and functional capacity in
patients with AR.
CHRONIC AR: CLINICAL FEATURES
CHRONIC AR: CLINICAL FEATURES
DISEASE COURSE
 Once the patient becomes symptomatic, the
downhill course becomes rapidly progressive.
 Congestive heart failure, punctuated by episodes of
acute pulmonary edema, and sudden death may occur,
usually in previously symptomatic patients who have
considerable LV dilation.
 Old reports: Death within 4 years after the
development of angina pectoris and within 2 years
after the onset of heart failure.
 Recent reports: 4-year survival without surgery in
patients with NYHA class III or IV symptoms is only
approximately 30%
DISEASE COURSE
 LV dysfunction is more likely to be reversible if
detected early,
 Before ejection fraction becomes severely
depressed,
 Before the left ventricle becomes markedly dilated,
and
 Before significant symptoms develop.

 It is therefore important to intervene surgically

before these changes have become irreversible
MEDICAL TREATMENT
 General Principles
 Mild or moderate AR, asymptomatic with normal or
only minimally increased cardiac size require no
therapy
 But should be followed clinically and by echocardiography
every 12 or 24 months.

 Severe AR, asymptomatic, normal LV function

Periodic evaluation at intervals of approximately 6
months.
MEDICAL TREATMENT
 General Principles- Activity
 Mild to moderate AR and those with severe AR with
a normal ejection fraction and only mild ventricular
dilation may engage in aerobic forms of exercise.

 However, patients with AR who have limitations of

cardiac reserve and/or evidence of declining LV
function should not engage in vigorous sports or
activities entailing heavy exertion
MEDICAL TREATMENT
 General Principles
 Systemic arterial diastolic hypertension, if present,
should be treated because it increases the
regurgitant flow
 Vasodilating agents such as nifedipine or ACE inhibitors are
preferred, and beta-adrenergic blocking agents should be
used with caution.

 AF and bradyarrhythmias are poorly tolerated and

should be prevented, if possible.
 If these arrhythmias occur, they must be treated promptly
and vigorously
MEDICAL TREATMENT
FOR ASYMPTOMATIC PATIENTS

 No specific therapy to prevent disease

progression in chronic AR is currently available

 ACEIs and Beta blockers: conflicting data

MEDICAL TREATMENT
FOR SYMPTOMATIC PATIENTS
 AVR is the treatment of choice for symptomatic
patients.

 Chronic medical therapy may be necessary for some

patients who refuse surgery or are considered to be
inoperable because of comorbid conditions.
 Aggressive HF regimen with ACEIs, digoxin, diuretics,
and salt restriction; beta blockers may also be beneficial

 Vasodilator therapy may be particularly helpful in

stabilizing patients severe LVD while preparing for
operation
SURGERY
 Patients with chronic AR have excellent
prognosis in the short and medium term

 Therefore, operative correction should be

deferred in patients with
 Chronic severe AR who are asymptomatic, and
 Exhibit good exercise tolerance, and
 Have an EF > 50% without severe LV dilation (i.e.,
end-systolic diameter < 50 mm) or progressive LV
dilation on serial echocardiograms.
SYMPTOMS HERALD
 LVEF IMPLY POOR OUTCOME!
 Postoperative survival is significantly higher in
symptomatic patients with normal LVEF
compared with those with impaired systolic
function

 Such patients often exhibit persistent histologic

changes in the left ventricle, including massive
fiber hypertrophy and increased interstitial
fibrous tissue.
 LVEF IMPLY POOR OUTCOME!
 In a series of 724 patients who underwent AVR
 Long-term survival: LVEF <30% vs >30%
 At 1 year: 81% versus 92%
 At 5 years: 68% versus 81%

 At 10 years: 46% versus 62% at 10 years,

 At 15 years: 26% versus 41%, and

 At 20 years: 12% versus 24%

(p=0.04)

 Therefore it is highly desirable to operate on

patients before irreversible LV changes have
occurred.
Normal at rest but fails to rise with exercise? 
Not considered an indication for surgery per se
But is an early warning sign that portends impaired
function at rest
ESD IMPLY DOWN-HILL COURSE!
 ESD < 40mm almost invariably remain stable and
can be followed without immediate surgery.

 ESD > 50 mm have a 19% likelihood/year of

developing symptoms of LV dysfunction
 7% and 7.6% also reported

 ESD > 55 mm are at increased risk for

development of irreversible LV dysfunction if
they are not operated on.
ESD IMPLY POOR OUTCOME!
 Indexing for body size may be appropriate,
particularly in women or small patients.
 Study of 246 patients: ESD > 25 mm/m2 is
associated with a poor outcome in asymptomatic
patients.

 Other studies- poor outcome with ESD >24 mm/m2 &

>26 mm/m2
SURGERY
 In the absence of contraindications or serious
comorbidity, surgical treatment is advisable for
 Symptomatic patients with severe AR and
 For asymptomatic patients with either
 An EF < 50% or
 Severe LV dilation (end-systolic diameter >50 mm)

 The risk of operation vs the risk associated with

continued fluid overload should be assessed well
SURGERY
 Patients with severely impaired LV function
(ejection fraction <25%) are at high surgical risk
and have a guarded prognosis, even after
successful AVR.

 However, their outlook is also extremely poor

when they receive medical therapy alone, and
their management should be considered on an
individual basis
SURGERY
 Aortic root/Ascending Aorta diseases
 Indications- Similar to primary valvular disease.

 Another indication for repair of aortic sinus,

AVR or replacement of Ascending Aorta
 Progressive expansion of the aortic sinuses and/or
ascending aorta to a diameter > 55 mm with any
degree of regurgitation in patients with a bicuspid
valve (or other connective tissue disorder)
 In patients with risk factors for Aortic dissection:
this threshold is decreased to 50 mm
 i.e. Family history of aortic dissection or rate of increase
in diameter of ≥0.5 cm/year)
SURGERY- TYPES OF OPERATIONS
 Standard: AVR
 Concurrent aortic root replacement is performed when
aortic dilation is the cause of or accompanies valve
dysfunction.

 AV repair?- Durability remains a major concern

 Experience is accumulating with surgical repair
 Torn leaflets by trauma- Repair
 AV leaflet prolapse- Re-suspension procedures
 Leaflet perforation by healed IE- Repair with pericardial
patch

 Transcatheter AVR for AR is under investigation but is

not an established approach.
SURGERY- RISKS
 Depends on
 The general condition of the patient,
 State of LV function, and
 Skill and experience of the surgical team.

 Operative mortality: 3% to 8%
SURGERY- BENEFITS
 After surgery, early rapid and then slower long-
term reductions in
 LV mass,
 Ejection fraction,
 Myocyte hypertrophy, and
 Ventricular fibrous content

 By extending the indications for operation to

symptomatic patients with normal LV function, as
well as to asymptomatic patients with LV
dysfunction, early and late results are improving.
ACUTE AR
 Acute AR may result from
 Abnormalities of the valve, primarily IE, or
 Abnormalities of the aorta, primarily aortic
dissection.

 Acute AR may also occur from iatrogenic

complications
 Following percutaneous aortic balloon dilation or
TAVR or
 Following blunt chest trauma.
ACUTE AR: MANAGEMENT
 Therefore the risk of acute AR is much greater
than that of chronic AR.
 Early death caused by LV failure is frequent

 Despite intensive medical management, prompt

surgical intervention is indicated.

 While the patient is being prepared for surgery,

treatment with an intravenous positive inotropic
agent (dopamine or dobutamine) and/or a
vasodilator (nitroprusside) often is necessary.
ACUTE AR: MANAGEMENT
 Beta blockers and intraaortic balloon
counterpulsation – Contraindicated
 Because either lowering the heart rate or augmenting
peripheral resistance during diastole can lead to rapid
hemodynamic decompensation.

 In hemodynamically stable patients with acute AR

secondary to active infective endocarditis,
operation may be deferred to allow 5 to 7 days of
intensive antibiotic therapy
 However, AVR should be undertaken at the earliest sign
of hemodynamic instability or if echocardiographic
evidence of diastolic closure of the mitral valve develops.
REFERENCES
 Braunwald’s Heart Disease, 10th ed.

 2014 AHA/ACC Guideline for the Management of

Patients With Valvular Heart Disease

 Harrison’s principles of Internal Medicine, 19th

ed.
THANK YOU!