Origin and evaluation of depressed inotropism in hypertensive cardiomyopathy.

Abstract

Left ventricular pressure overload results in the development of left ventricular hypertrophy (LVH) which is considered an adaptive mechanism of the heart to normalize systolic wall-stress. Impairment of both contractility and relaxation occurs, implying that the hypertrophied myocardium is very sensitive to ischaemia, alterations in coronary haemodynamics and to mechanisms incompletely understood. Experimental data from papillary muscles and isolated coronary perfused hearts (renovascular hypertensive rats) demonstrated respectively: a decrease in velocity of shortening, an increase in isometric timing parameters, and an increase in developed pressure. In contrast, the first derivative of left ventricular pressure, normalized to developed pressure, was decreased for large balloon volumes, suggesting an impairment of systolic function at major loading in LVH. In humans, left ventricular systolic dysfunction occurs later (congestive heart failure) when ejection fraction is impaired. Increases in total minimal vascular coronary resistances observed both in humans and in animals could be related to structural and functional alterations in coronary microvessels. Studies of LVH regression under treatment with angiotensin-converting enzyme inhibitors, calcium-channel blockers and beta-receptor blockers have confirmed that only drugs that block the renin-angiotensin system or the sympathetic nervous system are effective in maximizing the reversal of LVH.