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In aortic stenosis (AS), narrowing of the valve results in an increased pressure gradient between the left ventricle and aorta.1 The related chronic elevation in the afterload leads to a rise in the systolic wall stress of the left ventricle, causing concentric hypertrophy, which is considered a mechanism to maintain cardiac output despite the increased narrowing of the aortic valve. In the long term, however, left ventricular hypertrophy is a two-edged sword that is connected with unfavourable changes in myocardial function. The myocardium in AS is characterised by an increased myocardial cell mass and myocardial fibrosis. This remodelling results in elevated myocardial stiffness, impaired relaxation and increased left ventricular filling pressures, with the development of diastolic heart failure. In addition, patients with AS often have concomitant arterial hypertension—particularly among elderly patients with calcific AS. This means a double loading of the left ventricle with additive unfavourable changes in the myocardial function. The question arises whether there is a drug therapy that can favourably affect this double burden on the left ventricle.
In patients with arterial hypertension, the pathophysiological changes of the increased afterload can be partly reversed by effective drug therapy. The extent of left ventricular hypertrophy and its regression under therapy has a prognostic significance.2 Previous studies suggest, in particular, the use of a renin-angiotensin system (RAS) blockade, which may have direct cardiac positive effects besides the effect …
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