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

The treatment of congestive heart failure has seen considerable changes: while treatment with diuretics, digitalis glycosides and vasodilators has remained the mainstay of therapy, recently neurohumeral inhibition has been developed as an important principle: ACE-inhibitors have been shown to significantly improve quality of life and exercise performance and to substantially reduce mortality. Beta-blockers have been employed with increasing success mainly in congestive heart failure due to dilated idiopathic cardiomyopathy, in which a significant improvement in symptoms and life expectancy has been demonstrated. However, the precise mechanisms by which beta-blockade improves congestive heart failure remain to be elucidated. In addition to direct sympathoadrenal inhibition, reduction of heart rate may also play a major role in the therapeutic efficacy of beta-blockade in congestive heart failure. In the normal human heart increase in heart rate is accompanied by an increase in myocardial contractile performance (Bowditch-Treppe phenomenon). In chronic heart failure the myocardium undergoes a phenotype change which includes alterations of the activity of enzymes regulating calcium homoeostasis. The sarcoplasmic reticulum calcium ATPase (SERCA) is depressed both in function, as well as in expression. At the same time the sarcolemmal sodium-calcium exchanger is increased both in function and in expression. The result is a characteristic change in calcium homoeostasis with decreased diastolic uptake of calcium into the sarcoplasmic reticulum with subsequently reduced calcium release during the next systole, resulting in reduced contractile performance. At the same time increased capacity of the sodium-calcium exchanger extrudes intracellular calcium ions to the extra-cellular space, thereby rendering these ions unavailable for the contractile cycle. A result of these, seemingly specific, phenotype changes is an alteration of the force/frequency relationship. Instead of increasing force of contraction with increasing heart rates, in the chronically failing myocardium the contractile performance declines with increasing heart rates and only improves with decreasing rates. Optimal performance can be seen at heart rates as low as 30 beats.min. Studies employing photoluminescence markers of free cytosolic calcium, such as aequorin, have shown that there is a direct correlation between free cytosolic calcium and contractile performance at different levels of heart rate. It is likely, therefore, that the heart rate reduction with beta-blockade may provide the major explanation for the therapeutic benefits of beta-blockade in chronic congestive heart failure.
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PMID:Pathophysiological targets for beta-blocker therapy in congestive heart failure. 873 64

The rationale for beta-blockade in heart failure is now well established. Heart failure mortality, which is predicted by neurohormonal activation, remains high despite modern treatment including ACE inhibition, and additional neurohormonal blockade has further therapeutic potential. Previous clinical trial experience in heart failure, most of which has been in patients with idiopathic cardiomyopathy, indicates consistent improvement in ventricular function although variable changes in symptoms and exercise performance. However, the major burden of heart failure occurs in patients with ischaemic heart disease and in this respect it is notable that beta-blockade following myocardial infarction confers significant mortality benefit in subgroups with heart failure. The Australia and New Zealand carvedilol heart failure study is the largest completed study of beta-blocker treatment in patients with heart failure of ischaemic aetiology, including 415 patients randomized to carvedilol or placebo and indicating excellent tolerability of a titrated dose regimen and improved ventricular function after 6 months of treatment. An overview of all currently available randomized clinical trials of beta-blockade in heart failure, which includes more than 1600 patients, indicates a mortality risk reduction of approximately 20% but with wide confidence intervals. A large scale trial with several thousand patients is required to detect reliably a plausible 15-20% mortality reduction with beta-blockade in heart failure. The dissociation of clinical and mortality effects demonstrated with other heart failure treatments indicates the necessity for an appropriately powered mortality study which could define a major improvement in heart failure therapy for the future.
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PMID:Beta-blockers in heart failure. Future directions. 873 70

Quality of life in heart failure patients is receiving increased attention as a reflection of a treatment's potential secondary benefit of general well-being and daily functioning. The Metoprolol in Dilated Cardiomyopathy (MDC) trial was conducted as a large, multicenter trial to establish the effects of metoprolol on mortality and need for heart transplantation in patients with symptomatic idiopathic cardiomyopathy. It was found that metoprolol was well tolerated, improved symptoms and cardiac function, and prevented clinical deterioration in patients with symptomatic idiopathic dilated cardiomyopathy. Quality of life was evaluated as a secondary endpoint in 345 out of 383 randomized patients using a disease-specific questionnaire, the Quality of Life in Heart Failure Questionnaire, depicting physical activity, somatic symptoms, emotions, and life satisfaction. In a comparison of patients treated with metoprolol or placebo, patients treated with metoprolol noted a significantly more favorable response than those treated with placebo in terms of the overall treatment evaluation (p < 0.05). Additionally, an analysis of the changes from baseline to 18 months, using 95% confidence intervals, revealed that patients treated with metoprolol showed a significant improvement from baseline to 18 months in life satisfaction, physical activity, and the total score, while patients treated with placebo did not change at all. The improvement in quality of life was supported by the correlations with improvement in traditional clinical parameters.
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PMID:Quality of life on treatment with metoprolol in dilated cardiomyopathy: results from the MDC trial. Metoprolol in Dilated Cardiomyopathy trial. 887 80

It was first reported by our group in 1975 that heart failure due to idiopathic dilated cardiomyopathy (IDC) could be improved by long term treatment with a beta-blocker, starting at a low dose and continuing with a stepwise up-titration. Since then, many studies have been performed in patients with heart failure of various aetiologies and the beneficial effects of long term beta-blockade have been confirmed. About 3000 patients have been included in randomised studies in which beta-blockade, given for more than 2 months, mostly elicited significant improvements in functional class, exercise capacity, cardiac function, quality of life and/or morbidity. When started at a very low dose (one-tenth to one-twentieth of the doses generally used in angina or hypertension), the treatment is well tolerated in most patients. In these studies, various types of beta-blockers were used, including beta1-selective blockers and nonselective blockers with additional properties (vasodilator and antioxidative) such as metoprolol, bisoprolol, bucindolol and carvedilol. Several large studies have also reported benefits on mortality and morbidity. In the Metoprolol in Dilated Cardiomyopathy (MDC) trial, metoprolol treatment in patients with IDC resulted in a 34% reduction of the primary combined endpoint, total number of deaths and need for cardiac transplantation. In the Cardiac Insufficiency Bisoprolol Study (CIBIS), in patients with idiopathic as well as ischaemic cardiomyopathy, there was a nonsignificant 20% reduction in mortality. In the US carvedilol studies (n = 1094), also in patients with ischaemic and idiopathic cardiomyopathy, carvedilol reduced mortality by 65%, which was highly significant. A nonsignificant reduction in mortality was observed in the Australia-New Zealand (ANZ) Heart Failure Study with carvedilol. In all these studies there was a reduction in hospitalisations, with all drugs being generally well tolerated. It can thus be concluded that the beneficial effects of beta-blockers on cardiac function and morbidity have been documented in a large number of studies in selected groups of patients. The treatment has been accepted in some countries by the regulatory authorities. Larger, placebo-controlled studies are needed to convincingly demonstrate a reduction in total mortality as observed in the pooling of the 4 US carvedilol studies. Such studies are in progress for various beta-blockers, which may lead to acceptance of their routine clinical use in patients with congestive heart failure.
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PMID:The role of beta-blockers in left ventricular dysfunction and heart failure. 933 58

Congestive heart failure is a major and growing public health problem. Its prevalence is 3-20 per 1,000, and increases steeply with age. Coronary heart disease is the underlying cause in 50% of the cases, idiopathic cardiomyopathy in 20%. Survival at 5 years after the onset of heart failure in the Framingham study was 25% in men and 38% in women; the mortality rate of heart failure patients was 6-7 times that of the general population. Three variables--functional class, natremia, left ventricular ejection fraction--are powerful prognostic factors. Quality of life of heart failure patients is severely impaired.
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PMID:[Epidemiology and natural history of cardiac failure]. 950 2

Nitric oxide (NO) plays a role in controlling vascular tone and regulates the contractile properties of cardiac myocytes. Patients with heart failure exhibit high plasma levels of nitrite/nitrate (NOx), a stable metabolite of NO, and of cytokines such as tumor necrosis factor-alpha, a potent inducer of NO synthase. An increase in inducible NO synthase activity has been found in cardiac tissue from patients with dilated cardiomyopathy. These findings raise the possibility that local or systemic overproduction of NO induced by cytokines exerts a chronic negative inotropic effect on the myocardium and may have detrimental effects on systemic hemodynamics in patients with heart failure. Plasma levels of NG,NG-dimethylarginine (asymmetric dimethylarginine; ADMA), a circulating endogenous NO synthase inhibitor, were measured in control subjects and patients with valvular, hypertensive, or ischemic heart diseases or idiopathic cardiomyopathy. The plasma levels of NOx and ADMA were assessed by high performance liquid chromatography. The plasma levels of NOx and ADMA were significantly elevated in patients with heart failure. Both NOx and ADMA were positively correlated with New York Heart Association functional class. There was a significant inverse correlation between plasma NOx and ejection fraction, as estimated by echocardiography. A significant relationship between plasma NOx and ADMA was found only in patients with moderate to severe heart failure (r=0.41, p=0.01). Findings suggest a compensatory role of a circulating endogenous NO synthase inhibitor against induced NO synthase activity in patients with heart failure.
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PMID:Increased endogenous nitric oxide synthase inhibitor in patients with congestive heart failure. 965 Nov 9

Most patients presenting with heart failure have severe coronary artery disease. The identification of viable hibernating myocardium is of paramount clinical importance for a correct indication of revascularization. Contractile reserve may be identified when regional asynergy improves during low or moderate doses of dobutamine. Dipyridamole, given at infra-low dose, alone or preferably in association with a low dose of dobutamine, is another possible pharmacologic stress protocol. Dobutamine echocardiography has been found to be more specific than thallium scintigraphy for predicting functional recovery after revascularization. However, the absence of contractile reserve does not exclude the presence of myocardial viability: perfusion reserve may be too low because of a critical coronary artery stenosis, or profound ultrastructural changes of myocardial cells may be present, including significant loss of contractile material. Inotropic reserve can also be assessed by dobutamine stress echocardiography in patients with idiopathic cardiomyopathy. The evolution of hemodynamic variables can be measured during the stress test. Stress echocardiography, especially during exercise, could probably provide important information about heart failure associated with valvular heart disease.
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PMID:Role of stress echocardiography in heart failure. 966 40

The main indications for left ventricular assist system (LVAS) support are postcardiotomy ventricular failure as temporary circulatory support and end-stage cardiomyopathy as chronic circulatory support. To clarify the efficacy of LVAS support, we assessed the clinical outcome of a pneumatic LVAS and an electromagnetic LVAS for patients with severe ventricular failure. As of March 1998, 5 patients with postcardiotomy ventricular failure had received the pneumatic LVAS support, and 2 other patients with end-stage idiopathic cardiomyopathy had undergone implantation of the electromagnetic LVAS. The drive control of the LVAS was mainly counterpulsation in the diastole of the native heart. In the 5 postcardiotomy patients, the duration of pneumatic LVAS support ranged from 30 to 312 h (mean, 109.2). All 3 patients with more than 72 h support were successfully weaned, and 2 of them survived. The other 2 patients with cardiogenic shock and less than 36 h support could not be weaned from the LVAS. In the 2 cardiomyopathy patients, 1 patient was well maintained by the electromagnetic LVAS support and underwent successful heart transplantation 7 months later. The other patient has been chronically supported by the LVAS for 2 months and is doing well so far. These results suggest that selective application of the pneumatic LVAS as a temporary support and the electromagnetic LVAS as a chronic support might be appropriate for maximizing the effectiveness of LVAS treatment for profound cardiac failure.
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PMID:Clinical experience of left ventricular assist systems at the Heart Institute of Japan. 1019 22

The prevalence of nonischemic heart failure including idiopathic dilative cardiomyopathy is not well known. It may vary considerably in different population sub-groups and geographic areas. In ambulatory and hospitalized patients with clinically manifest heart failure primary cardiomyopathy is diagnosed in 2-15%, while in recent large scale therapeutic trials the proportion of patients with nonischemic heart failure ranged from 18% to 53%. There is a relation between sex, age and etiology of chronic heart failure, nonischemic cardiomyopathy being more frequent in women and in younger individuals. In contrast to ischemic heart failure, where the severity usually correlates with the extent of coronary artery lesions, the pathophysiology of cardiomyopathy is less clear. Genetic factors, myocarditis from infectious agents, auto-immune mechanisms, cytokine activation, hormonal and metabolic influences can play a role. The functional consequences of myocardial damage in nonischemic heart failure is a global instead of localized abnormality of ventricular contractility. There is epidemiological evidence that in general the prognosis of nonischemic heart failure is better than in ischemic heart failure. The mortality of patients with ischemic heart failure was usually higher in the placebo groups of recent heart failure trials than in patients with nonischemic etiology. Furthermore, therapeutic responses to angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, amlodipine and amiodarone were also different in some studies. The outcome of nonischemic heart failure is better even in transplant candidates with the most advanced stages of heart failure, they survive longer and respond better to intensified drug regimens than patients with similar clinical severity of ischemic heart failure. Thus, an early and precise diagnosis of the etiology of heart failure should be encouraged not only in clinical trials but also in every day patient management. As more therapeutic options are developed, individualized drug selection for patients with various etiologies of heart failure may become possible.
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PMID:Nonischemic heart failure: epidemiology, pathophysiology, and progression of disease. 1044 82

Peripartum cardiomyopathy (PPCM) is a rare form of heart failure affecting women in the last month of pregnancy or the first six months post-partum. The etiology of PPCM remains poorly understood although some risk factors were described. Diagnosis is often difficult and is always necessary to exclude other prior heart disease and other cause of left ventricular dysfunction in pregnancy. Medical therapy for PPCM is similar to that for other forms of congestive heart failure; prognosis is better than in idiopathic cardiomyopathy but many authors observed that women who have had one episode of PPCM are likely to have recurrences in subsequent pregnancies. The present report describes the case of a woman presenting with severe cardiac failure immediately after cesarean section for twin pregnancy. The patient is a 35-year-old nulliparous white woman, with history of anorexia, subsequent amenorrhea, sterility and pregnancy induced with Gn-Rh. The diagnosis of PPCM was difficult for the presence of preeclampsia and acute pulmonary edema occurred four hours after delivery. The successful outcome was possible with an intensive treatment (mechanical ventilation, Swan-Ganz catheter). The whole resolution of the heart failure, six months post-partum, was demonstrated by ultrasonography.
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PMID:[Peripartum dilatative cardiomyopathy. Case report with literature review]. 1052 39


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