European Heart Journal Advance Access published online on June 26, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn306
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Hypertension in aortic valve stenosis—a Trojan horse
First Department of Medicine (Cardiology), University Hospital Mannheim, University of Heidelberg, Germany
* Corresponding author. Tel: +49 621 383 2204, Fax: +49 621 383 3821, Email: jens.kaden{at}med.ma.uni-heidelberg.de
Aortic valve stenosis (AS) is the most frequent heart valve disease in the elderly population,1 causing a significant economic burden on Western societies. Many studies have addressed the prevalence of various cardiovascular risk factors in patients with AS, some of them suggesting possible therapeutic strategies to slow down disease progression.2 Among others, arterial hypertension has been shown to be more frequent in patients with AS than in the control populations without relevant valve disease.3 There has been discussion on how arterial hypertension might influence the aortic valve area and the transvalvular pressure gradient. Theoretically, an elevated blood pressure might lead to an increase in the peripheral vascular resistance, a decrease of the vascular compliance, and to changes of the transvalvular flow rate.4 The scientific data published so far are contradictory: while some authors demonstrated a direct influence of blood pressure on the indices of AS severity, others could not prove an independent effect.5–7
In their study, Mascherbauer and colleagues have used a well-controlled in vitro circulation model to assess the influence of a wide range of systolic blood pressure on valve area and transvalvular gradients measured by echocardiography and catheter techniques.8 In their model, pressure gradients as well as valve areas did not change when systemic pressure was raised. Neither valve area nor pressure gradient were independently affected by systemic pressure by multivariable analysis. The results were supported by computational fluid dynamics analysis which also did not reveal an independent effect of systemic pressure on transvalvular pressure gradient and valve area. As in all experimental models attempting to resemble the in vivo situation, the model conditions have to be considered carefully when interpreting the results. The rigid walls and boundaries of the model do not reflect the in vivo situation, and some of the used stenoses do not completely resemble the complex three-dimensional structure of a stenotic aortic valve. Nevertheless, the present model allows assessment of the isolated effects of blood pressure, which would not have been possible in an in vivo setting due to the various interdependences of blood pressure, vascular resistance, and transvalvular flow.
The results of Mascherbauer and co-workers are in line with recent experimental and clinical studies on the influence of blood pressure on the indices of AS severity. Kadem and colleagues6 showed in a porcine model of aortic banding that systemic arterial resistance downstream from the stenosis increased greatly during hypertension, as did the maximum systolic left ventricular wall stress. In contrast, total systemic arterial compliance decreased significantly. Hypertension resulted in a moderate increase in the effective orifice area and significant decreases in catheter gradients. By multivariate analysis, maximum and mean catheter gradients were related only to the energy loss coefficient and flow rate. Thus, the data suggest that the severity of AS may be partially masked by the presence of co-existing hypertension.
Little et al.7 used handgrip exercise or phenylephrine infusion to increase blood pressure in patients with AS. While blood pressure and systemic vascular resistance increased at peak intervention, the transvalvular flow rate decreased. The aortic valve area also decreased while the mean transvalvular gradient did not change. The changes in blood pressure and aortic valve area were inversely correlated; however, the only independent predictor of the change in the aortic valve area was the change in cardiac output. Thus, Little and colleagues show that an acute elevation of blood pressure can indeed affect the echocardiographic indices of AS severity, but this effect depends primarily on the associated change in cardiac output rather than on an independent effect of systemic vascular resistance or arterial compliance. Most importantly, the data show that depending on the direction and magnitude of the change in cardiac output, this can result in a valve appearing either more or less stenotic.
If the notion that blood pressure does not directly affect common indices of AS severity is correct, then does it mean that blood pressure has no relevant effects on the clinical assessment of AS at all? The answer is clearly no. All commonly used indices of AS severity are flow dependent. Hence, acute changes in blood pressure can significantly alter these indices as a consequence of concomitant changes in transvalvular flow.4,6,7 Additionally, blood pressure is an important determinant of global left ventricular afterload which seems to be associated with mortality in patients with AS.9 Thus, blood pressure can indirectly affect both the assessment of AS severity and its prognosis. Therefore, we support previous recommendations advocating the routine measurement of blood pressure and transvalvular flow as part of the evaluation of AS.4,7 The clinical importance of these haemodynamic parameters is not limited to the initial assessment of patients with AS. If they remain unrecognized in patients undergoing serial evaluation of AS, changes in indices of AS severity may erroneously be attributed to disease progression rather than to changes in haemodynamics. However, the major drawback of amalgamating blood pressure and indices of AS severity in clinical practice is that the response of these indices to changes in blood pressure in individual patients is both variable and unpredictable. For example, although in the study by Little et al.7 the acute increase in blood pressure led to an average decrease in the aortic valve area, changes from baseline were quite heterogeneous among individual patients and ranged from –0.26 cm2 to +0.11 cm2.
Another important limitation of the current data regarding the impact of blood pressure on the assessment of AS severity is that most studies so far have focused on acute changes in blood pressure. However, as appropriately mentioned by Little et al., haemodynamic changes due to chronic hypertension may be quite different from changes encountered in acute hypertensive states.7 Thus, current research may not appropriately reflect the relationship between blood pressure and assessment of AS in chronic hypertension.
In conclusion, the study by Mascherbauer et al.8 significantly adds to the weight of evidence indicating that blood pressure has no direct effect on common indices of AS severity. However, blood pressure can indirectly affect the assessment of AS severity through concomitant changes in transvalvular flow, although the magnitude and direction of these changes cannot be forecast in individual patients.4 Ideally, AS severity should be assessed in a normotensive state.
Conflict of interest: none declared.
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
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