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

The relationship between energy metabolism and the extent of irreversible ischemic damage was examined in an isolated perfused working rat heart. The amount of cardiac work recovered after reperfusion of hearts exposed to severe global ischemia was dependent upon both the duration of ischemia and the type of substrate provided (either 5 mM glucose or 5 mM glucose + acetate). There appear to be two distinct phases in the ability to recover mechanical function in the reperfused ischemic heart. The second phase corresponds to the onset of severe irreversible tissue damage. Irreversible mitochondrial damage was not found to correspond with the onset of heart failure since the ATP/ADP ratio remained constant in the reperfused myocardium. Furthermore, there does not appear to be a direct correlation between the total ATP content and the extent of irreversible damage, either during ischemia or following reperfusion. However, the total adenine nucleotide content during ischemia showed dramatic changes which correspond temporally with the initiation of the second phase of damage. The observation that the adenine nucleotide pool becomes further depleted during reperfusion suggests that alterations in the salvage pathway for adenine nucleotide synthesis have occurred. Loss of adenine nucleotides appears to be an excellent marker for irreversible heart failure. Acetate provides some protection the the ischemic myocardium. The mechanism by which acetate mediates this protective effect is discussed.
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PMID:Relationship between adenine nucleotide metabolism and irreversible ischemic tissue damage in isolated perfused rat heart. 44 6

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

Electron spin resonance spin trapping technique was used to measure the generation of active oxygen free radicals during the respiratory burst of phorbol myristate acetate-stimulated leukocytes, and the superoxide dismutase activity in healthy subjects and in patients with congestive heart failure. The authors also measured the concentration of peroxidation products (primarily malondialdehyde) by the thiobarbituric acid method. Experimental results showed that the electron spin resonance spectra obtained during the respiratory burst of polymorphonuclear leukocytes stimulated with phorbol myristate acetate primarily were those of the spin adduct of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) with the superoxide anion and to a lesser extent those of DMPO with hydroxyl radical. Compared with healthy subjects, the release of oxygen free radicals in the respiratory burst of polymorphonuclear leukocytes stimulated with phorbol myristate acetate and the concentration of thiobarbituric acid reactive product in plasma were significantly increased in patients with congestive heart failure while the activity of superoxide dismutase was markedly lower. The increased production of oxygen free radicals by polymorphonuclear leukocytes and the decreased capability of antioxidative defences might play an important role in the generation and development of cardiac failure.
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PMID:Electron spin resonance determination and superoxide dismutase activity in polymorphonuclear leukocytes in congestive heart failure. 133 Feb 41

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


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