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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Severe aortic stenosis is defined as an aortic valve effective orifice area (AVA) ≤ 1.0 cm2 or ≤ 0.6 cm2 if indexed for body surface area and a mean transvalvular gradient ≥40 mmHg. Important is to note that gradients are a squared function of flow in the continuity equation. So even a modest decrease in left ventricular ejection fraction (LVEF) may result in a significant reduction in the transvalvular gradient. Low flow state can occur with both reduced LVEF (i.e. “Classical” Low-Flow) or preserved LVEF (“Paradoxical” Low-Flow).
It is estimated that 5% to 10% of the patients with a severe AoS have a low-flow low-gradient (LF-LG) severe aortic stenosis due to a decreased left ventricular ejection fraction. These patients typically have a dilated left ventricle with markedly decreased LVEF, most often due to ischemic heart disease and/or to afterload mismatch.1
A LF-LG severe aortic stenosis is defined as an aortic valve AVA ≤ 1.0 cm2 or indexed ≤ 0.6 cm2/m2, a mean transvalvular gradient < 40 mmHg and a LVEF ≤ 40 %. A low flow state is defined as a cardiac index < 3.0 l/min/m2 or a stroke volume of < 35ml/m2. Because the gradient especially depends on the flow per beat the latter is the most frequent used parameter. The stroke volume can be measured by pulsed wave Doppler in the left ventricular outflow tract.
It is necessary to distinguish between true severe and pseudosevere aortic stenosis (prevalence between 20% and 30% of the patients) since patients with pseudosevere stenosis may not benefit from aortic valve replacement. In a true severe AoS, the aortic valve is the primary culprit and the decreased LVEF is a secondary or concomitant phenomenon. Pseudosevere aortic stenosis is a result of decreased contractility due to myocardial disease whereas a true aortic stenosis is a primary valve problem.
To distinguish between true en pseudosevere aortic stenosis dobutamine stress echocardiography (DSE) may be helpful (Figure 2). A pseudosevere aortic stenosis will show an increase in AVA (peak stress AVA> 1.0-1.2 cm2) with none or relative little increase in transvalvular gradient (peak stress mean gradient
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In cases where DSE is inconclusive (e.g. peak stress AVA1.0 cm2 with a peak gradient >40 mmHg): the calculation of the projected AVA at normal flow rate might be helpful.
In this method, the AVA is plotted against the mean transvalvular flow (Q) at each stage of the DSE, and the AVA at a standardized flow rate of 250 ml/s is projected from the slope of the regression line fitting the plot of AVA vs. Q (projected AVA = AVA at rest + [(ΔAVA/ΔQ) x (250 – Q at rest)], where ΔAVA and ΔQ are, respectively, the increase in AVA and Q during DSE (Figure 4). A projected AVA ≤ 1.0 cm2 is used to discriminate between a true severe AoS and a pseudosevere AoS.2 It has been suggested that higher values of peak stress AVA and projected AVA (i.e. 1.2 vs. 1.0 cm2) should be used to differentiate true vs. pseudo-severe AS based on the fact that moderate-to-severe AS may be equivalent to severe AS for a depressed ventricle (Figure 2).1, 2
DSE is also useful to assess flow reserve. Absence of flow reserve (
An accurate and complementary method to TTE and DSE for the assessment of the severity of aortic stenosis is the measurement of the degree of aortic valve calcification with multislice computed tomography. An Agatston score > 1200 AU in women and >2000 AU in men has been shown to provide a good accuracy to distinguish severe from non-severe AoS.3 This method is particularly helpful in patients with no flow reserve given that, in these patients, stenosis severity often remains indeterminate at the outset of DSE (Figures 2 and 3CD).
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