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

The two major causes of death in congestive heart failure (CHF) are progressive heart failure (approximately 60% of cases) and sudden death (30%). Sudden death in CHF is caused primarily by malignant ventricular arrhythmias. The underlying mechanism has yet to be established, but myocardial metabolic factors are probably involved. Although there is a clear association between complex ventricular arrhythmias and left ventricular function, it has not been shown convincingly that antiarrhythmic agents can reduce sudden death in CHF. Progressive deterioration of myocardial function is associated with altered myocardial energy production. Notably, the physiological effects of neuroendocrine activation in chronic CHF may be deleterious to myocardial function. The CONSENSUS study was carried out to evaluate the association between neuroendocrine activation and deterioration of myocardial function using ACE inhibitors. A marked reduction in mortality rate occurred in the enalapril-treated group, where the one-year mortality was reduced by 31%. The reduction in mortality was solely among patients with progressive CHF (a reduction of 50%); there was no difference in the incidence of sudden death. Analysis of blood samples drawn at baseline in the placebo group showed a significant positive correlation between mortality and plasma angiotensin II (P less than 0.05), aldosterone (P = 0.003), noradrenaline (P less than 0.001), adrenal levels (P less than 0.001), and atrial natriuretic peptide (P = 0.003). This was not observed in enalapril-treated patients. The significant reduction in mortality in the enalapril group was found consistently among patients with baseline hormone levels above the median value. In CHF, the underlying disease may induce serious arrhythmias and/or progressive failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms for improved survival in heart failure. 255 Jun 46

Milrinone and enalapril, which inhibit PDE-III and ACE, respectively, are able to prolong survival of myocardially infarcted (MI) rats. This study sought to identify oral hemodynamic effects of these agents which could underlie such efficacy in this heart failure model. Four weeks after ligation of the left main coronary artery, basal left ventricular (LV) systolic pressure and dP/dtmax, heart rate and mean blood pressure of the MI rats were significantly less than that of sham-operated controls, and LV end-diastolic pressure (LVEDP) was markedly elevated. Milrinone, at 2.0 mg/kg, reduced LVEDP and renal blood flow of these 4-week MI rats by an average of 39 and 18%, respectively (P less than 0.05) within 1 h. At 4.0 mg/kg, it reduced LVEDP by 46% and raised heart rate by 16% (P less than 0.05). Enalapril (1.0 mg/kg) increased small intestine blood flow of these compromised rats by 16% (P less than 0.05), and tended to reduce LVEDP (-28%) within 1.5 h. Treatment with milrinone (2.0 mg/kg) plus enalapril (1.0 mg/kg) promoted LV dP/dtmax, coronary blood flow, and heart rate by 48, 40 and 13%, and reduced LVEDP by 40% (P less than 0.05 for all effects). Thus these agents can reduce LVEDP and redistribute cardiac output of MI rats. Furthermore, the combination of enalapril and milrinone can restore LVEDP and LV dP/dtmax of MI rats to near normal and promote coronary blood flow without compromising cardiac output or renal blood flow. Such effects, it timely or sustained, may prolong survival.
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PMID:Beneficial hemodynamic effects of milrinone and enalapril in conscious rats with healed myocardial infarction. 255 83

This review updates some recent advances of a new and exciting developments in basic and clinical cardiology: a) the role, in the congestive heart failure (CHF), of the neurohormonal systems (NHS) which act to maintain circulatory homeostatic equilibrium, and b) the therapeutic implications of such a role. Six NHS, acting in CHF, have presently been identified: three of them induce vasoconstriction and sodium retention (sympathetic nervous systems, renin-angiotensin-aldosterone system and arginine-vasopressine system); the remaining three offset or balance the former ones, acting, therefore as "counterregulators" (prostaglandins--PGE2 and PGI2--, dopaminergic system and atrial natriuretic factor). Each one of these NHS influences the "compensatory" mechanisms of heart failure, acting on the target-organs both by direct effects and by interaction with other NHS; consequently, in heart failure, all the NHS are stimulated with the respective increase in the plasma levels of their agents. In asymptomatic stages of ventricular dysfunction the stimulation of the vasodilator-and-natriuretic systems appears to be predominant and able to maintain circulatory equilibrium. However, as the heart dysfunction increases and becomes symptomatic, the vasoconstrictor and sodium-retaining forces appear to predominate; this phenomenon becomes increasingly apparent as the functional class becomes more advanced. The hyperstimulation of these last systems has an extremely important role in the pathophysiology and clinical manifestations of congestive heart failure, as well as in its prognosis. Therefore, the attempts to correct these neurohormonal imbalance in patients with heart failure has a sound rational basis, not only to improve the symptoms and the exercise capacity but also to increase the survival of these patients. At the present time, amongst the potential pharmacological interventions acting on NHS in CHF, the blockade of the SRA system with ACE-inhibitors is generally accepted as the most feasible, the safer and the most effective therapeutic tool. In fact, its application has broadened from an earlier use in severe CHF to other symptomatic stages of cardiac failure, including the milder forms. In addition, preliminary data strongly suggest its unique usefulness in asymptomatic phases of ventricular dysfunction. Looking back at the medical therapy of heart failure, it can be concluded that we are starting a new era. Throughout 200 years (since the introduction of digitalis) the therapeutic goal in CHF has been the improvement of symptoms. With the developments of the present decade, a new and exciting goal is being offered to these patients, called by Packer "the second frontier", that is, the prolongation of their lives.
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PMID:[Neuro-hormonal mechanisms in heart insufficiency--from physiopathology to treatment]. 257 35

Digitalis therapy is usually ineffective in heart failure complicating myocardial infarction but may be of benefit in some selected patients with chronic heart failure. However, digitalis therapy in the long-term should be considered in conjunction with vasodilators or ACE inhibitors. This article reviews the practical and clinical aspects of vasodilator and digitalis therapy.
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PMID:Digitalis and non-ACE inhibitor vasodilators in heart failure. 265 Aug 76

A number of theoretical and practical aspects of acute myocardial infarction suggest a potential role for ACE inhibition in enhancing coronary blood flow and limitation of infarct size. Indeed, the use of ACE inhibitors in acute myocardial infarction could be viewed as a logical intervention in the face of the neuroendocrine response which accompanies the acute phase. During the first 24 h post-infarction, very high plasma concentrations of arginine-vasopressin and catecholamines occur. This is followed by a sharp rise in the concentration of angiotensin II (ANG II) over the next few days. The neuroendocrine response is most marked in those patients with larger infarcts, who frequently develop left ventricular failure. The extent to which these factors influence coronary flow in acute myocardial infarction is unknown, although in chronic heart failure ACE inhibition does not reduce coronary blood flow despite a reduction in rate-pressure product, suggesting a coronary vasodilator effect. However, in the presence of fixed coronary stenoses, the fall in blood pressure and, therefore, of coronary perfusion pressure must be taken into account. Whether or not the use of ACE inhibitors can limit infarct size in man also remains to be determined, although it has been clearly demonstrated that concentrations of ANG II similar to those observed in the early phase of myocardial infarction can cause myocardial cell damage in experimental animals. Post-infarction ventricular enlargement can be reduced by ACE inhibitors. Additionally, ACE inhibitors, through their balanced vasodilator effect, maintain cardiac output whilst reducing filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of angiotensin-converting enzyme inhibition on coronary blood flow and infarct size limitation. 267 35

Arterial stiffness (the inverse of compliance) is the major determinant of left ventricular and central aortic peak systolic pressure. Recent prospective epidemiological studies (MRFIT, Framingham) have confirmed the importance of systolic (rather than diastolic) pressure in the development of cardiac failure and stroke, and in all-cause mortality. Arteries stiffen in hypertension and with increasing age. Arterial stiffening increases systolic pressure by two mechanisms. The first is by causing a higher pressure to be generated at the peak of ventricular ejection (through increase in aortic characteristic impedance), and the second is by causing a secondary rise attributable to early return of wave reflection from peripheral sites (through an increase in arterial pulse wave velocity). ACE inhibitors, and also nitrates, decrease arterial stiffness. They also dilate peripheral conduit arteries; this reduces wave reflection. These drugs thus reduce systolic pressure in central arteries not only by reducing arterial stiffness but also by reducing inappropriately early wave reflection. Quantitatively, the latter action seems to be more important than the former. Neither action is seen with beta-blocking agents. These beneficial actions on central systolic pressure are not always apparent when pressure is measured in a peripheral artery such as the brachial or radial. This is because the reflected wave constitutes the peak of the pressure wave in central arteries but is usually just an undulation on the downstroke of the wave in peripheral arteries. Hence sphygmomanometric recordings underestimate reduction in central systolic pressure and in left ventricular load brought about by ACE inhibitors and by nitrates.
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PMID:Systolic blood pressure: arterial compliance and early wave reflection, and their modification by antihypertensive therapy. 267 41

We investigated the factors able to stimulate (hormones, drugs, fluid volume changes and prostaglandin precursors) or inhibit (NSAIDs) renal prostaglandin synthesis. We then assessed the effects of NSAIDs on: A) the efficacy of certain drugs (furosemide, ACE-inhibitors), whose action is mediated by a stimulation of prostaglandin synthesis; B) the physiopathology of cardiovascular diseases such as myocardial infarction and heart failure, in which renal and circulatory output is reduced; C) arterial hypertension.
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PMID:Changes in prostaglandin renal synthesis in cardiovascular disease. 267 7

Recent evidence suggests that the most common form of idiopathic cardiomyopathy in our altitudes, the dilated cardiomyopathy (DCM), is a post-infectious autoimmune disease which is triggered by virus infections. In animal experiments, the development of the coxsackie virus B3 myocarditis to a congestive cardiac insufficiency resembling the clinical picture of DCM was demonstrated. In mice, species-dependent varying disease courses could be observed, which point to a genetically different behaviour of the animals' immunological reactions, either humoral or T-cell mediated immune reactions being responsible. In comparison with non-DCM patients, patients with DCM and chronic myocarditis exhibit significantly higher coxsackie virus antibody titres. Obviously, also a differently long viral persistency in the cardiac muscle plays a role, as enterovirus-specific RNA was detected in myocardial biopsies from patients with DCM. Along with myocardial fibroses, endomyocardial biopsies in DCM frequently reveal mononuclear cellular infiltrates, which, however, only in 20-25% of the cases may be regarded as chronic persisting myocarditis. The clinical and paraclinical findings in DCM and in the so-called latent cardiomyopathy are presented. In congestive heart failure, the best therapeutic results are achieved by the ACE inhibitors, along with vasodilator agents, digitalis glycosides and diuretics. Ultima ratio is the orthotopic heart transplantation, as it is only this intervention that will be able to improve the primarily bad prognosis decisively. Whether the treatment with immunosuppressive drugs exerts an influence upon the prognosis, has thus far remained an open question.
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PMID:[Dilated cardiomyopathy--heart muscle disease of unknown origin or an autoimmune disease? New aspects of etiology, pathogenesis and clinical practice]. 268 30

CHF afflicts 15 million persons worldwide despite advances made in its diagnosis and treatment. A thorough physical examination and basic, noninvasive evaluation are essential for establishing the diagnosis of heart failure and for designing an optimal, individualized treatment regimen. Although digitalis and diuretics continue to be used commonly for the treatment of CHF of all severities, the use of vasodilators and ACE inhibitors has increased dramatically, as they are used more widely and earlier in the course of the illness. Because the RAA system contributes significantly to the altered cardiovascular hemodynamics and symptomatology characteristic of heart failure, the ACE inhibitors provide a rational approach to therapy for many patients. Results of controlled clinical trials have shown that selected vasodilators and ACE inhibitors can improve survival in patients with CHF and that patients receiving ACE inhibitors show sustained improvement in clinical class, exercise tolerance, and hemodynamics. Thus the therapeutic spectrum available to the clinician dealing with patients with CHF has broadened substantively over the past decade.
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PMID:Mild heart failure: diagnosis and treatment. 268 81

In the case of heart failure of any etiology, so common in the elderly, symptomatic treatment predominates; causal therapy is hardly ever possible. The aim of treatment is to improve myocardial contractility and influence secondary compensation mechanisms which, although associated with a favorable effect in the early stage, in the late stage lead to an unacceptable elevation of afterload and an overall uneconomical cardiac performance, thus producing a negative effect on cardiac failure and its prognosis. In contrast, suitable treatment improves the quality of the patient's life and prolongs life expectancy. In the aged, suitable therapy includes, where indicated, in particular digitalis (there is no alternative!), ACE-inhibitors and diuretics. The incidence and extent of adverse reactions and interactions in the elderly are greater than in the young and middle-aged patient.
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PMID:[Drug therapy of heart failure in the elderly]. 268 40


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