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Assessment of aortic stenosis severity: check the valve but don’t forget the arteries!
  1. Philippe Pibarot,
  2. Jean G Dumesnil
  1. Laval Hospital Research Center/Québec Heart Institute, Laval University, Québec, Quebec, Canada
  1. Correspondence to:
    Dr P Pibarot
    Laval Hospital Research Center, 2725 Chemin Sainte-Foy, Québec, Quebec, Canada G1V-4G5; philippe.pibarot{at}

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The accurate assessment of the haemodynamic severity of stenosis is crucial for clinical decision making in patients with aortic stenosis (AS).1 Over the past decades, echocardiography has become the clinical standard for the evaluation of AS severity. Several indices have been used for this purpose including transvalvular velocity and gradient, aortic valve area (AVA), valvular resistance, dimensionless velocity index, left ventricular (LV) stroke work loss and the energy loss coefficient. Unfortunately, these indices are all potentially affected by the haemodynamic state of the patient. Numerous studies have shown that changes in transvalvular flow rate may influence the indices of stenosis severity measured by echocardiography or catheter.2–4 Besides flow rate, there are potentially other haemodynamic factors that may affect the stenotic indices. The purpose of the study by Little et al5 (see page 848) reported in this issue of Heart was to examine the effects of systemic arterial hypertension on the Doppler-echocardiographic indices of stenosis severity. This study is of high clinical relevance, since AS and hypertension are the two most frequent cardiovascular diseases after coronary artery disease in the Western world, and 30–40% of patients with AS concomitantly have hypertension.6,7 Several authors have previously reported that the transvalvular gradient may be reduced in patients with concomitant systemic hypertension.8,9,10 It was, however, unclear in these reports: (1) whether this phenomenon was systematic or not; (2) whether it was predictable or not; and (3) whether it was due to a direct effect of increased systemic vascular resistance and/or reduced arterial compliance on the transvalvular gradient, or due to an indirect effect associated with a concomitant reduction in flow rate. The interaction between valvular and arterial haemodynamics therefore needs to be better understood to improve the evaluation of AS severity and the ensuing clinical conduct.10,11

There have, however, been very few studies examining the effect of systemic arterial haemodynamics on the indices of AS severity, and these studies yielded conflicting results.9,11–14 In a catheter study, Laskey et al9 suggested that the gradient may decrease irrespective of flow, as a direct consequence of the increased systemic arterial resistance. Hence, according to this study, hypertension may cause an underestimation of stenosis severity. In contrast to these results, Razzolini et al12 found that, for each flow level, the gradient increases linearly with systemic arterial resistance, thus overestimating the stenosis severity. In a recent in vitro study,14 we observed that, for a given level of flow rate, arterial resistance and compliance had no direct effects on the valvular haemodynamics.


The present study5 is, to our knowledge, the first one to attempt manipulation of the blood pressure in patients with AS, in order to determine the effects of hypertension on the Doppler-echocardiographic indices of stenosis severity. The most important findings of this study are: (1) hypertension may interfere with the Doppler-echocardiographic assessment of stenosis severity; (2) as opposed to what was suggested in some previous reports,9,12 the systemic arterial haemodynamics—that is, resistance, compliance or pressure—have no direct independent effect on the Doppler-echocardiographic indices of stenosis severity; (3) the changes in AVA and gradient that may occur with hypertension are essentially related to the changes in mean flow rate, and, depending on the direction of these changes, the severity of stenosis may be overestimated or underestimated. These findings are consistent with our recent animal study,13 wherein we concluded that the changes in peak and mean gradients occurring with hypertension are due to concomitant changes in AVA and/or flow rate, and that arterial resistance and compliance have no direct effect on the gradients. The only exception is the peak-to-peak gradient measured by catheter, which is strongly dependent on systemic arterial compliance.14 Systemic arterial compliance is reduced in approximately 40% of patients with moderate or severe AS,7 and, in these circumstances, the peak-to-peak gradient tends to be reduced and may markedly underestimate the AS severity.7 This consideration is particularly important to remember when confronting echocardiographic findings with catheterisation data.

In our animal model of supravalvular stenosis,13 the average AVA increased significantly with hypertension, and approximately 50% of this AVA augmentation was independent of the change in flow rate, thus suggesting that the rise in systolic aortic pressure could increase the radial force applied against the aortic wall and thereby induce an enlargement of the stenotic orifice. Nonetheless, in light of the results of the present study,5 this phenomenon does not seem to occur in patients with moderate or severe aortic valve stenosis. In these patients, the calcification of the aortic valve annulus may indeed limit the enlargement of the valve orifice under increased pressure. Hence, the changes in AVA observed during hypertension are essentially related to the changes in flow rate. In this context, it must be emphasised that all indices of stenosis severity, including AVA of the valve, transvalvular gradient, valve resistance, LV stroke work loss and energy loss coefficient, vary with flow rate.2–4 Moreover, the direction and magnitude of the changes in transvalvular flow rate associated with hypertension may vary from one patient to another, so that the effect of hypertension on the parameters of AS severity cannot be predicted from blood pressure readings alone, nor is there any easy formula to account for this phenomenon. Little et al5 very appropriately make the point that not taking this factor into consideration when performing serial evaluations of AS severity may result in erroneous conclusions with regard to the progression of disease severity, which in turn may inappropriately influence clinical conduct.

In this context, it would thus seem reasonable to make the following recommendations: (1) blood pressure should be recorded systematically during the echocardiography in patients evaluated for AS; (2) serial evaluations should take into account whether the patient’s blood pressure level is within the same range as in the previous evaluation; and (3) Doppler echocardiographic evaluation should be performed when blood pressure control is optimal. If the blood pressure is elevated at the time of examination, it would seem preferable to repeat the measurements after optimisation of blood pressure treatment.


Notwithstanding the aforementioned considerations, it must nonetheless be remembered that calcific AS cannot be viewed as an isolated disease of the valve, but that it is often one manifestation of an atherosclerotic process involving various components of the vascular system, including the aorta. Hence, in many patients, the increase in global LV afterload is not only because of the valvular stenotic process but also because of a decrease in systemic arterial compliance. Recent studies have shown that global LV afterload is best evaluated by calculating valvulo-arterial impedance using the formula ZVA = (SAP+ΔP)/SVi, where SAP is the systolic arterial pressure measured by sphygmomanometry, ΔP is the mean transvalvular gradient; and SVi is the stroke volume index.7 This index can easily be calculated at the time of the Doppler-echocardiographic examination, and it seems to be superior to the standard indices of AS severity in predicting LV dysfunction and patient outcomes. Indeed, a value of the valvuloarterial impedance >5 mm Hg/ml/m2 is independently associated with a fourfold increase in the risk of LV systolic dysfunction,7 and a value >5.5 mm Hg/ml/m2 is associated with a 2.5-fold increase in the risk of overall mortality in patients with moderate or severe AS.15

These findings thus strengthen the need for a more comprehensive evaluation of AS severity going beyond the classical measurements of stenosis severity, and also emphasise that patients with the combination of AS and systolic hypertension represent both a diagnostic and a therapeutic challenge. Indeed, the presence of symptoms may logically be related to the degree of global afterload, and hence patients with moderate AS may become symptomatic, because of the contribution of concomitant hypertension to an increased afterload. In such patients, the logical first step would be to treat their hypertension and then to re-evaluate the situation. Traditionally, vasodilator therapy has been considered contraindicated in patients with severe AS, because of the potential hypotensive effect of peripheral vasodilation on fixed valvular obstruction. Recent studies, however, suggest that flow rate can increase in response to a decrease in total afterload, except in patients with very severe disease, suggesting that medical treatment of hypertension may be beneficial in patients with AS.1,16 However, caution is needed, especially in patients with severe AS. In these patients, it is preferable to start antihypertensive drugs at very low doses and then progressively increase the dosage to a therapeutic level.

Further studies will, however, be necessary to determine whether, in patients with symptoms of AS with concomitant hypertension, significant improvement in symptomatic status and outcome can be achieved with the intensification of medical treatment alone. Indeed, optimisation of blood pressure levels may have its limitations, since patients with AS often have reduced arterial compliance, which may not be completely normalised by treatment. Likewise, it may be worthwhile to operate on some of these patients, although their criteria for AS severity do not meet the current guidelines for operation. The rationale behind this approach could be that the total afterload of these patients is markedly increased and that any significant decrease in either the arterial load or the valvular load may improve their prognosis and well-being. If the surgical option was contemplated, one would, however, have to ensure that the projected operation would achieve an optimal reduction in the valvular load. To this effect, particular attention should be paid to avoid patient–prosthesis mismatch, as suggested previously.17


PP holds the Canada Research Chair in Valvular Heart Diseases, Canadian Institutes of Health Research, Ottawa, Ontario, Canada.

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  • Competing interests: None declared.

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