Hemodynamic Rounds Series II
Hemodynamic Rounds Series II
Hemodynamic Rounds Series II
Hemodynamic Rounds
Fig. 1. Aortic (Ao) pressure (femoral artery) and left ventricular (LV) pressure at baseline
(control, top) and after dobutamine 10 µg intravenous for 3 min (bottom). Scale, 0–200 mm Hg.
Fig. 2. Aortic (Ao) pressure (femoral artery), left ventricular (LV) pressure, and pulmonary
artery (PA) pressure at baseline (control, left) and after dobutamine 10 µg intravenous for 3 min
(right). Scale, 0–200 mm Hg.
increased to 4.2 l/min. Valve resistance was calculated at pulmonary artery (Fig. 2) and left ventricular end-
178 units. Figure 2 shows aortic, left ventricular, and diastolic pressures (Fig. 1, bottom). Based on these data
pulmonary artery pressures before (control) and after (Table I), a recommendation for continued medical
dobutamine infusion. Note the mild decline in systolic therapy without surgery was made.
Low-Gradient Aortic Valve Stenosis 203
contributing to pressure loss in the poststenotic region. operative death and prosthetic valve-related complica-
Pliable valves may have an artificial increase in the valve tions is inherent in the procedure, the risk-benefit ratio is
orifice area with such a catheter. Discrepancies between not favorable to the asymptomatic patient.
measurements may be due to the catheter placed across The study of Otto et al. [13] reinforces the concept that
the aortic valve, contributing to an already diminished no single discrete valve area defining the critical valve
orifice area and leading to overestimation of the transval- exists, but that this area varies from patient to patient
vular gradient. Alternatively, the catheter may contribute depending on cardiac output and problems of the calcula-
to prying open one of the cusps, thereby increasing the tion of valve area. Patients may become symptomatic in
effective valve area, reducing the transvalvular gradient. the range of 0.6–0.8 cm2, whereas asymptomatic patients
This finding is in agreement with that of Carabello et may reside comfortably with valve areas of 0.8–1.0 cm2.
al. [12], where a .5-mm Hg increase in peripheral In general, patients with valve areas .1.0 cm2 are often
arterial pressure could be observed during left ventricular symptomatic due to other noncardiac sources, especially
catheter withdrawal in patients with severe aortic steno- if the mean transvalvular gradient is ,30 mm Hg.
sis, postulated to be due to catheter cross-sectional area.
In most patients, the presence of a catheter across the
stenotic aortic valve does result in a significant increase in CONCLUSIONS
measured transvalvular pressure gradients, and the cath-
eter effect is proportional to the severity of the underlying Before accepting hemodynamic data indicating the
aortic stenosis. Systematic over- or underestimation of critical severity of aortic stenosis in individuals with left
the actual transvalvular gradient should always be consid- ventricular dysfunction and low cardiac output, evalua-
ered. tion of valve function with inotropic agents or vasodila-
tors [6] and their effect on aortic valve area and resistance
should be considered.
ASYMPTOMATIC AORTIC STENOSIS
Otto et al. [13] examined the prospective outcomes of
patients with valvular aortic stenosis who were asymptom- ACKNOWLEDGMENTS
atic. One hundred twenty-three patients with asymptom- The author thanks the J.G. Mudd Cardiac Catheteriza-
atic aortic stenosis were followed on an annual basis for tion Laboratory Team for technical support, and Donna
2.5 6 1.4 yr. Doppler aortic jet velocity increased by Sander for manuscript preparation.
0.32 6 0.34 m/sec/yr, with a mean gradient increase of
7 6 7 mm Hg/yr and a valve area decrease of 0.12 6 0.19
cm2/yr. At 3-yr follow-up, survival was 62 6 8%, and REFERENCES
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