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• W1978178527 abstract "The combination of aortic stenosis with arterial hypertension is becoming very frequent, in part due to aging of the population in industrialized countries, exposing an increasing number of individuals to age-associated anatomic deterioration of aortic valve [1,2]. Prevalence of arterial hypertension is frequent in clinical series of aortic stenosis (20–68%) [2,3], and is as high as 50% and even more in unselected elderly populations [4]. In contrast, in clinical populations of hypertensive individuals, aortic stenosis is not frequently found (1–2%) and this low prevalence is also confirmed in elderly populations [2,4,5]. This apparent inconsistency may suggest that a number of hypertensive individuals may develop aortic stenosis, whereas the opposite is unlikely, supporting the clue that hypertension might be a risk factor for aortic stenosis, through its atherogenic effect in precipitating or aggravating the age-related degeneration of cardiac valves [1,6] together with other atherogenic risk factors [7,8]. Coexistence of hypertension with aortic stenosis is particularly insidious, because hypertension can alter the clinical presentation of aortic stenosis. In elderly patients with aortic stenosis, clinical presentation of even severe aortic stenosis can be remarkably altered, due to increased characteristic aortic impedance, early wave reflections, and, in general, increased stiffness of the conduit artery system [9–11]. These vascular modifications produced by hypertension can, therefore, abnormally increase the velocity of the carotid upstroke and reduce typical crescendo-decrescendo systolic murmur, making it similar to the frequent murmur heard in aortic valve sclerosis, and causing underestimation of the severity of, or even inability to recognize, this valvular disease [10]. In addition to this diagnostic challenge, the coexistence of hypertension and aortic stenosis generates peculiar features, including the complexity of cardiac loading conditions and the response of left ventricular adaptation and eventually raises questions about the opportunity and the means to aggressively treat arterial hypertension and managing aortic stenosis. Severity of aortic stenosis in the presence of arterial hypertension Much information on the combination of aortic stenosis and arterial hypertension has been obtained in unselected population samples with a broad spectrum of severity of valve disease, often including also symptomatic patients and explaining the inconsistent findings on the effect of hypertension on the LV adaptation occurring in aortic stenosis. However, this might not be the best way to examine the issue, as epidemiological studies suggest that it is the aortic stenosis that develops in the context of arterial hypertension [1,6–8]. In this issue of J Hypertens, Rieck et al. [12] report results from the cohort of the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study, which has the important characteristic of being formed by patients (mainly elderly) with asymptomatic calcified aortic stenosis, thus in a state of good cardiac compensation. The present study, therefore, adds important information on the natural history of aortic stenosis allowing assessment of cardiovascular phenotype in both normotensive and hypertensive individuals, prior to the development of symptoms. Symptoms are very important in the natural history of aortic stenosis and, albeit debated, they remain the main criterion for decision-making and timing for aortic valve replacement, especially in elderly individuals [13,14]. The lack of clinical symptoms attributable to the valve disease is therefore the distinctive characteristic of the SEAS study, exceeding in importance the attempt made by the authors to quantify the severity of aortic stenosis, which might be in fact cumbersome in the presence of arterial hypertension. In an animal experiment, Kadem et al. [15] demonstrated that increased systemic arterial resistance and arterial stiffness caused by hypertension produced a significant increase in the effective orifice area and decrease in both catheter and Doppler gradients resulting in an underestimation of the severity of aortic stenosis. As opposed to the apparent reduction of the severity of aortic stenosis, maximum systolic left ventricular wall stress increased by 43% during the superimposed hypertension. This experiment is consistent with the observation that symptoms of aortic stenosis develop with larger valve area and lower stroke work loss in hypertensive than in normotensive patients [16] and suggest that the traditional Doppler-echocardiographic approach for evaluation of severity of aortic stenosis might yield errors in some circumstances. Possibly the severity of aortic stenosis in the presence of hypertension should be evaluated following criteria different from those used in normotensive populations and never separated from an evaluation of the flow through the valve [17]. Looking at a simplified Gorlin formula for calculation of aortic area [18]: in which EOA is effective orifice area, Q is the flow rate, PGmax is the peak pressure gradient; if PGmax is reduced without consistent changes in the Q, EOA will increase as a result. But, of course, at a constant PGmax, variation of Q can also generate even larger variations of EOA. In arterial hypertension, both increased systemic vascular resistance/arterial stiffness, reducing PGmax, and increased Q might influence the assessment of severity of aortic stenosis. Although an acute increase in systemic vascular resistance and/or arterial stiffness is sufficient to affect the noninvasive evaluation of aortic stenosis severity, the impact of arterial pressure on the assessment of aortic stenosis severity depends primarily on the associated changes of both flow and resistance components and, therefore, can result in more or less severe stenosis, depending on the direction and magnitude of these changes [19]. Interestingly, blood pressure, as a single component of peripheral resistance or arterial compliance, is not sufficient to alter pressure gradient or estimated severity of aortic stenosis [20], indicating that the interplay between pressure and flow components is substantial. In the SEAS cohort, LV diastolic dimension and ejection fraction were on average identical in normotensive and hypertensive groups, indicating that also stroke volume had to be very similar. However, heart rate was significantly greater in hypertensive than in normotensive individuals, also indicating that cardiac output had to be greater, resulting in a larger EOA in the presence of near identical PGmax. The traditional normalization of EOA for body surface area offsets this difference because body mass was greater in hypertensive individuals. However, it should be noted that, albeit commonly adopted, normalization for body size is purely empiric, because it does not fit with fluid dynamics, for which the estimation of the severity of a pipe obstruction is a function of the amount, the velocity and the viscosity of the fluid passing throughout the obstruction. All these variables interact with each other directly without any consideration of the container of the hydraulic system (i.e., body mass). The possibility to estimate with accuracy the severity of aortic stenosis is further complicated in the SEAS cohort because of the frequent coexistence of aortic regurgitation (more than 60% of the population), a potent stimulus for Starling forces recruitment and both consequent alteration of the Q parameter of the Gorlin equation. Loading conditions and left ventricular adaptation Hypertension and aortic stenosis impose a significant overload on the left ventricle (LV), but when these two conditions coexist, the interplay between the two might be difficult to assess. In theory, there are differences between the two conditions, aortic stenosis being a near-pure pressure overload [21], whereas arterial hypertension encompasses a wide range of hemodynamic conditions from a prevalent volume overload to a prevalent pressure overload [22,23]. However, whereas aortic stenosis might be a near-pure pressure overload, arterial hypertension is never a pure volume overload, representing rather in most circumstances a mismatch between minute output and peripheral resistance. Based on Grossman's postulate [24], LV adaptation to aortic stenosis is expected to result in a concentric-type geometry, whereas in arterial hypertension it may assume different characteristics, consistent with the dominant type of overload [22]. Whereas the combination of the two conditions might be simplistically supposed to enhance the concentric pattern of LV remodeling, whether aortic stenosis is superimposed on arterial hypertension or vice-versa might produce different changes in LV geometry, depending on the initial LV geometric pattern and the loading conditions on which the second condition takes place. Despite the limitations in the evaluation of severity of aortic stenosis, the SEAS study provides strong evidence that in the absence of symptoms attributable to valve disease – but in the presence of arterial hypertension – only hypertension influences LV adaptation, whereas severity of aortic stenosis, assessed with established Doppler-echocardiographic evaluation of pressure gradients, does not significantly contribute to explain the variance of LV mass, whatsoever criterion is used (orifice area or energy loss coefficient). This finding is further reinforced by the evidence that the predominant LV geometry in the SEAS study was the eccentric-type, thus likely more influenced by hypertension than by aortic stenosis. The distribution of the four LV geometric patterns reported in the SEAS participants with aortic stenosis is in fact similar to the distribution of LV geometry reported in the hypertensive subpopulation without aortic stenosis, as well as in other hypertensive unselected populations with or without aortic stenosis [16,25]. The distinctive characteristics of the patients with the highest tertile of PGmax was the more severe LV concentric hypertrophy or remodeling with consequent lower wall stress and depressed myocardial contractility (stress-corrected midwall-shortening), a cardiovascular phenotype that might well be considered as a marker of severity of the hemodynamic burden [26] and often associated with low-flow output [27], suggesting that these characteristics might provide useful information on the severity of aortic stenosis in the presence of arterial hypertension. Recently, Dumesnil et al. [17] suggested that Doppler-echocardiographic severity of aortic stenosis should always be evaluated by including recording of cuff blood pressure and evaluation of both systemic arterial compliance and valve-arterial impedance. They also highlight that this additional estimation adds little time to the Doppler-echocardiography examination, because these parameters can be easily computerized adding only measurement of cuff blood pressure that will be merged with the evaluation of LV stroke volume and transaortic gradient. This might be particularly important in the presence of arterial hypertension. Implications The results of the SEAS study suggests that the management of arterial hypertension in the presence of asymptomatic aortic stenosis should not be different from, or at least not less aggressive than the management suggested in the absence of aortic stenosis. Rather, in the hypothesis that aortic stenosis is often an atherosclerotic complication of hypertension, even greater attention should be devoted to the other coexisting cardiovascular risk factors. If hypertension contributes to aortic valve disease, potentially better blood pressure control might prevent the progression of stenosis. The harmful characteristic of SEAS participants with asymptomatic aortic stenosis is not arterial hypertension, which can be treated and controlled, but rather aortic calcifications [28], which are actually present also in the normotensive participants." @default.
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• W1978178527 title "The difficult clinical management of the combination of hypertension with aortic stenosis" @default.
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