The left ventricle in aortic stenosis: evidence for the use of ACE inhibitors

Abstract

Pressure overload causes left ventricular (LV) remodelling and ultimately hypertrophy.^{w1 w2} This is often seen as a means of limiting wall stress in order to maintain systolic function.^w2 Wall stress, by the law of Laplace, is related directly to intracavitary pressure and cavity size, but inversely to wall thickness. Concentric remodelling is defined by a normal LV mass associated with an increased relative wall thickness (fig 1). This is usually calculated as 2 × posterior wall thickness/LV diastolic diameter, and a value > 0.45 is abnormal.^{w3 w4} The reduction in cavity size and increase in wall thickness tend to offset the raised intracavitary pressure associated with aortic stenosis. Concentric hypertrophy is defined by a combination of left ventricular hypertrophy and increased relative wall thickness. Patients with aortic stenosis and no hypertrophy almost invariably have concentric remodelling.^w4–6