Effects of Hypoxia on Relaxation of the Hypertrophied Ventricle

Abstract

Cardiac hypertrophy is a compensatory response to chronic pressure-overload of the heart. However, studies in both animal models and in patients provide evidence that adaptive pressure-overload cardiac hypertrophy may be associated with an increased susceptibility to the development of diastolic dysfunction during ischemia or hypoxia. In this regard, Bache and coworkers have shown that left ventricular end-diastolic pressure rises in response to ischemia induced by pacing tachycardia in dogs with chronic left ventricular hypertrophy [1]. Similarly, Fifer and coworkers have recently shown that patients with normal coronary arteries and pressure-overload hypertrophy due to aortic stenosis demonstrate a striking rise in left ventricular diastolic pressure and an impairment of left ventricular relaxation during transient angina induced by pacing tachycardia [2]. It is likely that these transient changes in diastolic function in hearts with pressure-overload hypertrophy are related in part to the development of global left ventricular subendocardial ischemia. Coronary vascular reserve appears to be impaired in dogs with chronic aortic stenosis and in patients with pressure-overload hypertrophy [3–5]. Furthermore, relative hypoperfusion of the subendocardium has been shown in dogs with aortic stenosis in whom metabolic evidence of ischemia was induced by pacing tachycardia [1].