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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitors are being increasingly prescribed for the treatment of hypertension and heart failure. Not only are they efficacious but the incidence of serious adverse events with ACE inhibitors is similar to that with placebo. 'First-dose hypotension' mainly affects the renin-dependent patient. Neutropenia and agranulocytosis have been reported rarely for the nonsulfhydryl compounds. Comparative safety data are provided for captopril, enalapril, and quinapril, a new nonsulfhydryl ACE inhibitor that has been investigated extensively in over 2,000 patients. Results show that the proportion of patients reporting associated adverse events was lower with quinapril (11%) than with captopril (17%) or enalapril (15%). Similarly, there was a lower proportion of patients withdrawn due to adverse events with quinapril.
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PMID:The safety of ACE inhibitors for the treatment of hypertension and congestive heart failure. 267 Feb 22

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

Angiotensin-converting enzyme (ACE) inhibitors have been found effective in the treatment of congestive heart failure (CHF) and have been recommended as the first choice of vasodilator therapy by some observers. Favorable hemodynamic responses, apparent both at rest and during exercise, result from a considerable reduction in both systemic and pulmonary vascular resistance, apparently due to both the arterial and venodilating effects of these agents. In addition, the recently reported results of the Cooperative North Scandinavian Enalapril Survival Study demonstrate that ACE inhibitors reduce mortality rates in patients with CHF. The etiology of heart failure does not seem to predict clinical response to ACE inhibitors, nor do acute resting and exercise hemodynamic responses. A weak relation has been found between plasma renin activity and short-term hemodynamic and clinical responses, but this association is not evident over the long term. Therefore, a trial of therapy with ACE inhibitors is necessary to judge efficacy in an individual patient with advanced CHF symptoms. Two such agents--captopril and enalapril--are available. The former has a more rapid onset and shorter duration of action, whereas the latter may be given on a twice-daily basis, simplifying chronic therapy.
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PMID:When and how to use angiotensin-converting enzyme inhibition in congestive heart failure. 283 22

The fall in cardiac output observed in cardiac failure induces stimulation of the renin-angiotensin-aldosterone system. This results in strong constriction of the arterioles which in turn increases the fall in cardiac output and aggravates myocardial alteration. Angiotensin-converting enzyme inhibitors therefore act on a major physiological mechanism of cardiac failure. In this double-blind study 36 cardiac failure patients treated with digitalis derivatives and diuretics were divided into two groups: one group received enalapril in addition to the other drugs, the other group received a placebo. The functional symptoms, exercise tests, left ventricular function and haemodynamic values were improved in two-thirds of the patients treated with enalapril, whereas no improvement was observed in those who received the placebo. Enalapril maleate was given by injection to 10 patients with acute left ventricular failure following myocardial infarction; a useful fall in pulmonary capillary pressure and systemic arterial resistance occurred within one hour. Enalapril represents an effective physiopathological treatment of severe cardiac failure.
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PMID:[Treatment of cardiac failure with enalapril]. 300 28

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

Benefits from vasodilator therapy in patients with chronic heart failure are partly related to the severity of functional derangements. Agents with an arteriolar-dilating effect are more likely to be effective in patients with higher left ventricular outflow resistance. Vasodilators with primary venodilating properties are more likely to be effective in the presence of an increased ventricular preload. The mechanisms by which preload and left ventricular outflow resistance increase in patients with cardiac insufficiency are not well understood and may not be similar in all patients. Vasodilators also have the capacity to ameliorate myocardial metabolic functional abnormalities by influencing myocardial energetics, but the effects of different agents on coronary hemodynamics may not be uniform. Effects on renal hemodynamics may also vary, as may neurohumoral changes after therapy. Angiotensin-converting enzyme inhibitors have been shown to exert beneficial effects on both coronary and renal hemodynamics in patients with chronic heart failure, while producing favorable neurohumoral changes. These agents provide some advantages over direct-acting vasodilators in that myocardial oxygen consumption is decreased, myocardial metabolic function is improved, and norepinephrine and aldosterone levels are reduced. Further controlled studies are needed to assess the efficacy of angiotensin-converting enzyme inhibitors in relation to other vasodilators for the long-term management of these patients.
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PMID:Vasodilator therapy in chronic congestive heart failure. 329 94

Congestive heart failure is a complex clinical syndrome characterized by a number of neuroendocrine responses. These responses are probably an evolutionary vestige of mechanisms designed to defend volume and maintain circulatory homeostasis. Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and the release of vasopressin have been clearly documented in patients with heart failure. Unlike the normal ventricle, the failing ventricle responds to peripheral vasoconstriction and sodium retention with further hemodynamic embarrassment and circulatory congestion. Certain vasorelaxant natriuretic substances are also released during heart failure, perhaps in an attempt to offset excessive peripheral constriction and sodium retention. Prostaglandin E2, atrial natriuretic peptide (or atrial natriuretic factor) and plasma dopamine are found to be increased in some patients with heart failure. However, peripheral constriction and sodium retention appear to be dominant, particularly in the advanced stages of heart failure. An understanding of these neuroendocrine responses has led to new developments in therapy. Angiotensin-converting enzyme inhibitors have emerged as distinctly useful drugs in the treatment of heart failure. Agents designed to block excessive sympathetic drive and inhibit vasopressin are under investigation. Infusion of atrial natriuretic factors and the use of selective dopamine agonists are also undergoing clinical trials in patients with heart failure. Increased knowledge of the neuroendocrine responses will likely result in even newer and more imaginative therapy.
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PMID:Neuroendocrine manifestations of congestive heart failure. 329 96

Interaction between kininase II and anaesthesia is not well described. Twenty two patients treated by kininase II for congestive heart failure are studied during anaesthesia for cardiovascular surgery. A first group of seventeen homogeneous hemodynamic data are reported. High cardiac index contrasts with severe clinical cardiac failure. A second group of inhomogeneous patients are separately described. Vasoconstrictor can be codified in the situation of low systemic resistance with high cardiac index. Preoperative treatment can be continued, under requirement of hemodynamic monitoring.
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PMID:[Is it necessary to discontinue captopril before heart surgery?]. 355 42

The systemic and regional circulatory effects of angiotensin-converting enzyme inhibition were investigated in 30 normal subjects and in 36 patients with severe congestive heart failure. Regional blood flow was measured in individual patient groups. Cardiac index rose and systemic vascular resistance fell in normal subjects after angiotensin-converting enzyme inhibition. In the patients with heart failure, a similar rise in cardiac index and fall in systemic resistance occurred. In addition, right and left ventricular filling pressures decreased. The fall in systemic vascular resistance correlated with plasma renin activity (r = 0.57, p less than or equal to 0.001). Of the regional circulations investigated in normal subjects, only forearm blood flow increased after angiotensin-converting enzyme inhibition. Although over-all there was no change in renal or coronary blood flow, coronary flow dramatically increased in some patients and the increase in flow correlated with plasma renin activity (r = 0.939, p less than or equal to 0.001). In patients with heart failure, forearm, splanchnic, and coronary flow were unaffected by angiotensin-converting enzyme inhibition, whereas renal blood flow estimated from para-aminohippurate clearance increased 60 percent and accounted for 50 percent of the increase in cardiac output seen in these patients. Thus, redistribution of flow occurs in congestive heart failure with a significant reduction in the fraction flow to the kidneys when compared with normal flow. The contribution of the renin-angiotensin system to the regulation of regional blood flow is different in normal subjects and in patients with heart failure. Angiotensin-converting enzyme inhibition augments skeletal flow in normal subjects whereas it increases renal blood flow in patients with heart failure.
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PMID:Redistribution of regional blood flow following angiotensin-converting enzyme inhibition. Comparison of normal subjects and patients with heart failure. 620 5

Captopril is a specific inhibitor of kininase II which is responsible for the conversion of angiotensin I into the active angiotensin II and also for the inactivation of bradykinin. In different types of experimental and clinical hypertension, Captopril has a pronounced blood pressure-reducing action particularly when it is given together with a diuretic. Serious side-effects have hitherto restricted the use of Captopril to patients who do not respond or do not respond satisfactorily to routine antihypertensives. Since it has been shown that a considerable improvement in disturbed hemodynamics in hypertension and in certain forms of heart failure can be achieved with quite low doses of the preparation (2 x 2 mg daily) the use of Captopril may be indicated in greater amounts in moderate and severe hypertension.
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PMID:[Captopril - profile of a new antihypertensive (author's transl)]. 679 55


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