Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ACE-inhibitors improve symptoms and prognosis in patients with heart failure. The V-Heft II trial has demonstrated that the beneficial effect of these agents is superior to unspecific vasodilators. Besides sustained arterial and venous vasodilation the inhibition of the neurohumoral axis is thought to play an important role. Angiotensin II and catecholamines not only exert vasoconstrictor effects, but might also contribute to vascular and myocardial growth. Thus, it may not be surprising that the beneficial effects of ACE inhibitors in heart failure only emerge during long-term therapy rather than after short-term administration. It has been shown that these agents improve blood flow to skeletal muscle during exercise after chronic therapy (not acutely), and there is some preliminary evidence that improvement of endothelial function might be involved in this effect, i.e., by reducing the degradation of bradykinin, an endothelial vasodilator. ACE inhibitors reduce LV hypertrophy, an important risk factor for cardiovascular disease and prognosis. Moreover, there is experimental evidence that ACE inhibitors can prevent and even reverse interstitial fibrosis in the left ventricle. Although the plasma renin activity may be normal in patients with chronic heart failure, recent data using polymerase chain reaction indicate that the tissue cardiac renin angiotensin system is activated in the failing human heart as assessed by measurements of angiotensin converting enzyme mRNA and angiotensinogen mRNA which may be an important target for ACE-inhibition.
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PMID:[The value of ACE inhibitors in heart failure (mechanism of action)]. 129 Mar 8

The use of ACE-inhibitors in patients with severe congestive heart failure is established on the basis of the results of the CONSENSUS I-study, which has shown that ACE-inhibitors in patients in NYHA class IV not only have improved functional parameters, but also improved survival. Recently published controlled data from studies including patients with mild to moderate heart failure (SOLVD-study) show a significant improvement of mortality in this subgroup. Comparing placebo and ACE-inhibitors, the effect of ACE-inhibitors on mortality is due to a reduction of progression of pump failure. Comparing vasodilator-therapy (hydralazine/isosorbide dinitrate) and ACE-inhibition in the V-HeFT II-trial showed, despite a transient increase in ejection fraction and exercise capacity during the vasodilator-therapy, a significant improvement in survival in the patients treated with an ACE-inhibitor. This was achieved by a reduction of the incidence of sudden cardiac death. From these recent data it can be concluded that ACE-inhibition is the therapy of choice in patients with mild to severe heart failure.
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PMID:[Value of ACE inhibitors in heart failure (clinical aspects)]. 129 Mar 9

Treatment of chronic heart failure with ACE-inhibitors has greatly improved the prognosis. In addition to ACE-inhibitors, diuretics seem to be necessary to decrease mortality, whereas the importance of cardiac glycosides has not been demonstrated unequivocally. Nevertheless, modern treatment of chronic heart failure in all stages should be a combination of diuretics, digitalis, and ACE-inhibitors rather than a stepwise addition of drugs depending on the severity of the disease. An increased heart rate leads to increased myocardial O2-consumption, decreased O2-supply, ischemia, and reduced contractility. Betablocker-induced reduction of heart rate does, however, not necessarily improve symptoms or hemodynamic conditions. The optimal heart rate in large failing hearts is not known yet. Probably, it is dependent on the type and severity of myocardial disease or impairment. In this respect, the sarcoplasmatic release and uptake of Ca2+ plays the most important role in the disordered force-frequency-relation in chronic heart failure.
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PMID:[Clinical aspects of differential drug therapy of chronic heart failure]. 129 Mar 10

The main objectives of the treatment of Congestive Heart Failure are the improvement of quality of life and the reduction of mortality. Both are accomplished by the ACE inhibitors. The most important trials on the effect of ACE inhibitors on the improvement of the quality of life are reviewed. Trials about the reduction of mortality with ACE inhibitors are analysed. The sudden death problem was considered and so the relationship of this with ventricular arrhythmias. The recent evidence of a beneficial effect of captopril was reported. At last we analyse secondary effects of these drugs on the treatment of Heart Failure in old patients.
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PMID:[Treatment of heart insufficiency in the elderly with converting enzyme inhibitors]. 129 Jun 44

Left ventricular hypertrophy is a major risk factor associated with the appearance of adverse cardiovascular events. A distortion in myocardial structure, mediated by an abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighbouring interstitial spaces, alters the electrical and mechanical behaviour of the myocardium. The mechanisms responsible for the regulation of cardiac myocyte growth and collagen accumulation are therefore of considerable interest. Herein we review results of in vivo studies conducted in the authors' laboratory that addressed these issues in various experimental models. The findings indicate that in arterial hypertension myocardial hypertrophy is related to ventricular systolic pressure work. Myocardial fibrosis, on the other hand, is not related to haemodynamic workload, but rather the presence of mineralocorticoid excess relative to sodium intake and excretion. Accordingly, fibrosis can appear in both the hypertensive left and non-hypertensive right ventricles. Pharmacological probes, administered in variable doses, were used to further test and support this hypothesis. In both primary and secondary hyperaldosteronism, it was possible to prevent the pathological structural remodelling of the myocardium with an aldosterone receptor antagonist, while in unilateral renal ischaemia ACE inhibition was similarly cardioprotective. Other studies demonstrated that it was feasible to regress the fibrous tissue response and normalise diastolic stiffness. This concept of cardioreparation suggests that heart failure due to this type of structural remodelling may be reversible.
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PMID:Regulatory mechanisms of myocardial hypertrophy and fibrosis: results of in vivo studies. 130 Dec 54

Angiotensin converting enzyme inhibitors are now widely used in the treatment of hypertension and heart failure. They are clearly as effective as other conventional antihypertensive agents in reducing blood pressure and combined with diuretics seem likely to transform current management of chronic heart failure. Myocardial infarction remains the major cause of death in patients with raised blood pressure and current studies should establish whether the attractive features of ACE inhibitors translate into reduction in the rate of infarction or its consequences. Similarly, whilst symptomatic benefit undoubtedly accrues from their use in heart failure it is less clear that they can prolong life particularly when used in the immediate setting of a myocardial infarction. Again a number of ongoing major trials are set to establish whether these drugs reduce death in patients with chronic heart failure (V-HeFT II, SOLVD) and in patients immediately after myocardial infarction (CONSENSUS II, SAVE,. AIRE, GISSI III and ISIS IV). The physician has a wide choice of ACE inhibitors with different pharmacological profiles for clinical use.
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PMID:Cardioprotection and ACE inhibitors. 130 64

Cardiac failure remains a serious complication of myocardial infarction. In addition to therapeutic interventions to limit the infarct size, it would seem possible to influence the progressive changes in geometry and size of the left ventricle, known as remodeling. Experimental and clinical studies have shown beneficial effects of angiotensin converting enzyme inhibitors and the SAVE trial evaluated the prognostic consequences of this therapy, reporting a significant reduction in mortality after 10 months' treatment. Many questions remain which require further research in this field, mainly concerning the optimal time of introduction the treatment, the importance of the chemical molecule used, the most appropriate dosage and the influence of associated drug therapy. ACE inhibitors are now part of the therapeutic arsenal of myocardial infarction but their prescription should be strictly reserved for the population concerned by these trials, that is to say patients with a recent, extensive infarct with left ventricular dysfunction but without clinical signs of cardiac failure.
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PMID:[Prevention of postinfarction cardiac insufficiency: role of angiotensin converting enzyme inhibitors]. 130 44

In chronic heart failure, dysregulation of sympathetic nerve system activity and of release of several neurohormones is present. Increased plasma levels of circulating hormones together with other factors have a negative influence on myocardial beta adrenergic receptors and induce cardiac hypertrophy with myocardial fibrosis. ACE inhibitors possess an ability to reverse these phenomena. An endogenous factor with an ACE inhibitory ability was isolated from the bovine left ventricular myocardium.
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PMID:Humoral factors in chronic heart failure. A review. 133 31

Results of 16 international published studies (with a total of 397 patients in NYHA-classes II-III) concerning chronic therapy with beta-adrenoceptor blockade in idiopathic dilated cardiomyopathy were analyzed. 8 studies were placebo controlled. Under beta-blockade cardiac output increased significantly by about 15% and ejection fraction by approximately 30%, apparently due to an improvement in contractility and relaxation of LV myocardium. Therapy was tolerated without complications in 93% of patients when the loading dose was 5 to 15 mg metoprolol/d (or equivalent) and a long-term dose of 100-200 mg/d metropolol (or equivalent) was reached within 4 weeks. Patients with severe heart failure (NYHA IV) had a higher risk of complications. A positive effect of beta-blockade in IDC was achieved in most cases but not earlier than after 2-3 months after initiating therapy. Despite these positive results beta-blockade in patients with IDC may not yet be recommended generally. Sufficient results of controlled trials are still lacking. Important questions with regard to the prognosis under beta-blockade, to the effects of cardioselectivity and intrinsic activity, and to the efficacy of this kind of therapy in the presence of ACE inhibitors have not been answered. Thus, major trials with controlled design are needed.
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PMID:[Beta receptor blockers in dilated cardiomyopathy (clinical aspects)]. 136 61

We examined the influence of angiotensin converting enzyme inhibitors (ACE inhibitors) on mortality in patients with heart failure of both ischaemic or non-ischaemic origin. Eleven, randomized, placebo-controlled trials of ACE inhibitors involving 1266 patients were selected. The follow-up period varied from 3 to 6 months. Four different ACE inhibitors were used in the 11 clinical trials. A total of 679 patients presented with an ischaemic heart failure and 587 with a non-ischaemic heart failure. Meta-analysis, performed for both subgroups, showed that mortality was significantly decreased in the ischaemic subgroup only (ischaemic group: odds ratio 0.45; 95% confidence interval 0.28 to 0.71; non-ischaemic subgroup: odds ratio 0.7; 95% confidence interval 0.4 to 1.5). Although the two odds ratio are not significantly different, further randomized, placebo-controlled trials with ACE inhibitors are required in order to determine more precisely the benefit/risk ratio in patients with non-ischaemic heart failure.
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PMID:Relative efficacy of angiotensin converting enzyme inhibitors on mortality of patients with congestive heart failure: implications of randomized trials and role of the aetiology (ischaemic or non-ischaemic) of heart failure. 138 85


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