Influence of angiotensin converting enzyme inhibition on pump function and cardiac contractility in patients with chronic congestive heart failure.

Abstract

Eleven patients with coronary artery disease and chronic heart failure were studied before and three months after the angiotensin converting enzyme inhibitor enalapril was added to their frusemide medication. The following were measured: left ventricular pressure and volume with transient occlusion of the inferior vena cava, radionuclide angiography, and hormone concentrations in plasma. As in other reported studies, the clinical condition of the patients improved and their exercise tolerance increased moderately. Addition of enalapril reduced end diastolic and systolic pressure, reduced ventricular volume, and concomitantly increased the ejection fraction. The end systolic pressure-volume relation shifted to the left as it did in a similar animal study. In the animal study unloading by a vasodilator did not induce a leftward shift, so it can be inferred that in the present study unloading combined with a decrease in the angiotensin concentration was instrumental in remodelling the heart. Though unloading was expected to have a beneficial effect on the oxygen supply/demand ratio of the heart, the patients still showed the same drop in the ejection fraction during exercise as they did before treatment with enalapril, and early diastolic filling did not improve. Normally, regression of cardiac dilatation is only found if pump function improves; the present study showed that unloading in combination with angiotensin converting enzyme inhibition reshapes the ventricle without improving intrinsic pump function.

Contrasting effects of steroids and angiotensin‐converting‐enzyme inhibitors in a mouse model of dystrophin‐deficient cardiomyopathy

“…Our haemodynamic data suggest significant beneficial vasodilatory and direct myocardial effects, and absence of deterioration in histopathology and sarcolemmal injury. There have been several studies showing no direct effect of ACE‐I on myocardial contractility ,. However, a study in the cardiomyopathic hamster model, an animal model for limb girdle muscular dystrophy (LGMD2F) which has an autosomal recessive cardiomyopathy caused by a mutation in the delta‐sarcoglycan gene, showed significant beneficial effects of enalapril on contractility when started at a late stage in the development of the cardiomyopathy .…”

“…There have been several studies showing no direct effect of ACE-I on myocardial contractility. 27,28 However, a study in the cardiomyopathic hamster model, an animal model for limb girdle muscular dystrophy (LGMD2F) which has an autosomal recessive cardiomyopathy caused by a mutation in the delta-sarcoglycan gene, showed significant beneficial effects of enalapril on contractility when started at a late stage in the development of the cardiomyopathy. 29 This is similar There was no abnormal histopathology or Evans blue dye uptake in wild-type mice (A þ B).…”

Reversal of Chronic Ventricular Dilation in Patients With End-Stage Cardiomyopathy by Prolonged Mechanical Unloading

“…Recently, there has been some evidence from both experimental and clinical heart failure that angiotensinconverting enzyme inhibitors can limit or reverse remodeling to a small degree [3,[12][13][14]. However, such pharmacological therapies have been less effective than the mechanical assist device in normalizing ventricular size as reported in this study, perhaps because such agents produce only modest reductions in ventricular filling pressure and volume [13,15].…”

Reverse left ventricular remodeling by intermittent dobutamine infusions and amiodarone in end-stage heart failure due to idiopathic dilated cardiomyopathy

“…Physical stress [24] and neurohormonal activation [25 -27], together with the underlying disease create an environment that promotes the structural rearrangement and dilation of the failing heart [28]. In experimental and clinical studies, LV remodeling was eliminated or reversed by angiotensin converting-enzyme inhibitors [26,29], beta-adrenergic blockade [3], and spironolactone [30,31].…”