The left ventricular response to aortic stenosis is not simple. It consists of a combination of wall thickening and a change in cavity size with associated effects on systolic and diastolic function. It is determined by numerous factors in addition to the transaortic resistance. These include coexistent coronary disease and hypertension, but also sex, age, and genetic factors. This review will give evidence to suggest that aortic stenosis should be regarded as a clinical syndrome involving the left ventricle as well as the aortic valve. This carries the implication that the left ventricle should be given greater priority when assessing and treating aortic stenosis.

EFFECT OF PRESSURE LOAD ON THE LEFT VENTRICLE

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