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

The human heart can exceed the critical heart weight of 500 g in the course of pathological structural adaptation. This abnormal growth is performed not only by an increase in size (hypertrophy) but also in number (hyperplasia) of cardiac muscle cells. Coronary insufficiency, dilatation and chronic heart failure are noted frequently in hearts above this critical heart weight. Chronic heart failure is not a direct consequence of local destruction and scar formation following coronary insufficiency. Unlike acute cardiac dilatation with failure, chronic dilatation is not associated with stretching or overstretching of cardiac muscle cells. Starling's law is not applicable for explaining heart failure in these chronic cases. Chronic dilatation is a structural dilatation (Gefugedilatation) produced by sliding displacements (slippage) of heart muscle cells leading to a decrease in the number of muscle layers in the ventricular wall. Chronic heart failure in man therefore is rather a physical consequence of structural dilatation which severely impairs the working conditions, the efficiency and the effectiveness of the heart muscle cells than an immediate result of coronary insufficiency of inflammation with local metabolic alterations, which, of course, additionally impair the quality of the myocardium and the conducting system.
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PMID:Hypertrophy, hyperplasia and structural dilatation of the human heart. 13 71

Chronic heart failure is a common clinical condition with a high mortality and morbidity. Patients with the condition suffer from shortness of breath and fatigue on exercise. This article reviews the recent advances made in the understanding of the pathophysiology of chronic heart failure and explores further possible research options.
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PMID:The mechanisms underlying the increased ventilatory response to exercise in chronic stable heart failure. 128 2

Chronic heart failure has been called the final common pathway of all heart diseases. It is a long-term illness, often associated with disability and characterized by life-threatening exacerbations, that results in multiple problems for patients and their families. This paper will provide a framework for nursing action designed to maximize the quality of life of chronic heart failure patients and their families. The approaches suggested by Strauss et al. (1984) and the principles of self-care as outlined by Levin, Katz and Holst (1979) provide the theoretical basis for the suggested nursing actions. A brief overview of the pathophysiology and current treatment of heart failure is also included.
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PMID:Chronic heart failure and quality of life: the impact of nursing. 129 May 81

1. Chronic heart failure was induced in rats by ligation of the left coronary artery to produce a left ventricular myocardial infarct. 2. Cardiac angiotensin-converting enzyme (ACE) was estimated by radioligand binding in myocardial homogenates and by autoradiography studies of radioligand binding to ACE in heart sections. 3. Radioligand binding studies demonstrated an increase in binding sites in animals with myocardial infarction, compared with sham operated animals. Mean increases were 457% in right atrium, 295% in left atrium, 326% in right ventricle, 187% in left ventricle and 530% in the region of the left ventricular infarct, compared with the sham left ventricle. 4. Autoradiography studies confirmed tissue homogenate binding studies, demonstrating (i) a marked increase in ligand binding in the infarct area and (ii) an increase in binding density in the hypertrophied myocardium of right and left atrium, and right and left ventricle. 5. The induction of cardiac ACE in the myocardium of rats with chronic heart failure may participate in the pathophysiology of cardiac hypertrophy.
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PMID:Increased cardiac angiotensin-converting enzyme in rats with chronic heart failure. 216 5

Chronic heart failure is characterized by the inability of the heart to pump the blood at a rate commensurate with the requirements of the peripheral organs at rest and under exercise conditions. The most common cause of heart failure is coronary artery disease, followed by hypertensive, valvular and myocardial heart disease. Different forms of chronic heart failure have been described (acute and chronic heart failure, forward and backward failure, right and left heart failure, systolic pump and diastolic compliance failure, etc.). The compensatory mechanisms in heart failure are related to hemodynamic and structural as well as metabolic and neurohumoral changes. Prognosis of chronic heart failure is usually poor and the annual mortality rate ranges between 20 and 50% depending on the degree of functional impairment.
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PMID:[Pathophysiology of heart insufficiency]. 226 22

Chronic heart failure is associated with a high risk of ventricular arrhythmias and sudden death, although the mechanisms leading to these arrhythmias are not fully understood. To determine if the adaptation of ventricular refractoriness to an abrupt increase in heart rate is impaired in heart failure, electrophysiologic findings in 11 patients with structurally normal hearts (group I) were compared to findings in 28 patients with chronic heart failure (mean left ventricular ejection fraction 0.23 +/- 0.05). Heart failure was due to coronary artery disease in 14 patients (group II) and to idiopathic dilated cardiomyopathy in 14 patients (group III). The effective refractory period at the right ventricular apex was measured during unipolar cathodal pacing at twice diastolic threshold following a 12-beat ventricular drive at a cycle length of 600 msec. The pacing cycle length was then decreased to 400 msec for one, two, and three beats and the refractory period was determined for each beat at the faster rate. For each beat the mean refractory periods of group II and III patients were similar and were significantly longer than those of group I patients (p less than 0.01). The refractory period progressively shortened at the 400 msec cycle length and the percent decrease for each beat was similar among all three groups (p greater than 0.10). In the group II and III patients there was no correlation of the refractory period or change in refractory period with the pulmonary artery, right atrial, and pulmonary capillary wedge pressures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is the adaptation of right ventricular refractoriness to an abrupt increase in heart rate impaired in chronic heart failure? 246 81

Chronic heart failure is attended by a number of abnormalities of peripheral circulation. To a great extent, these abnormalities determine the patients' functional symptoms, their tolerance to exercise and their response to treatment, at least in the short term. The response to exercise of heart failure patients depends on their maximal oxygen consumption which is determined by their maximal cardiac output and by various peripheral adjustments, such as distribution of regional blood flow and peripheral oxygen extraction. Abnormalities of peripheral arteriolar and capillary dilatation are determined by hyperstimulation of neurohormonal systems. An increase in maximal muscular blood flow, which determines the patients' capacity of exercise, can be obtained with drugs which increase the muscular perfusion pressure (inotropic drugs) or which decrease muscular resistances without lowering the perfusion pressure (venous or balanced vasodilators, diuretics). Physical rehabilitation may improve maximal oxygen consumption by improving the peripheral use of oxygen. Thus, a better understanding of the physiopathology of heart failure will in the future improve the functional symptoms of these patients and prolong their survival, which has not always been the case with conventional therapies.
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PMID:[Abnormalities of the peripheral circulation and tolerance to exertion of patients with heart failure]. 250 Sep 14

Chronic heart failure results from two processes, i.e., myocardial and congestive failure. Myocardial failure is clinically silent, most often progresses slowly, and is documented by a depressed left ventricular ejection fraction. Multiple etiologic factors include systolic and diastolic overloads, myocardial necrosis and/or ischemia, and, perhaps, microvascular spasm. Myocardial failure ultimately leads to exaggerated neurohumoral compensatory mechanisms and derangements of the peripheral circulation, which are the hallmarks of congestive heart failure. At that stage of the syndrome, patients have symptoms, initially, with exercise and, later, at rest. Objective assessment of severity is afforded by determination of maximal oxygen uptake during maximal exercise testing. When congestive heart failure supervenes, the prognosis is poor. Current medical therapy is aimed at improving the derangements of the peripheral circulation, which relieves the symptoms but leaves the primary myocardial process unaffected. The goal of future therapy is to intervene at an earlier stage of the syndrome to halt or even partially reverse the myocardial failure.
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PMID:Central and peripheral components of cardiac failure. 293 38

The evaluation of the long-term treatment of heart failure is complicated by many biological, clinical and technical problems. Chronic heart failure results from a variety of causes, each resulting in fundamentally different histopathological profiles. Once established chronic heart failure is unremitting, but the speed of progression of the haemodynamic derangement varies widely between different individuals. Moreover, the extent of the haemodynamic disorder correlates poorly with the severity of symptoms. The metabolism of drugs and the response of the damaged myocardium to these drugs is often quite different in the patient with heart failure than in the normal subject. Finally chronic heart failure is a terminal condition of relatively short duration so that clinical trials designed to test the efficacy of a drug treatment will fail if they are continued for more than a brief period, as all patients will die. It is against this complex biological background that the long-term clinical efficacy of diuretics and digitalis in the treatment of chronic heart failure must be evaluated.
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PMID:Diuretics and digitalis in the treatment of chronic heart failure. 634 Oct 64

Chronic heart failure is associated with neurohumoral activation and alterations of the peripheral circulation and skeletal muscle. Several mechanisms are involved in the impaired peripheral perfusion, including increased sympathetic tone and increased vascular stiffness. Recently, data suggest an important role of the endothelium for perfusion of skeletal muscle in heart failure. Endothelium-dependent dilation of resistance vessels is blunted in patients with severe chronic heart failure and may be involved in the impaired reactive hyperemia in these patients. In conductance vessels, flow-dependent dilation and the nitroglycerin-induced dilator response is attenuated in congestive heart failure as compared to normal subjects, indicating both endothelial dysfunction and a defect of smooth muscle relaxation. Recent data suggest that angiotensin-converting enzyme (ACE) inhibitors can improve endothelial function of resistance vessels, reduce serum level of the soluble endothelial (vascular cell) adhesion molecule (VCAM-1) and, in addition, improve peripheral vascular function by reducing or limiting the influence of cyclo-oxygenase-dependent vasoconstricting factor(s). It is conceivable that these beneficial effects of chronic ACE inhibition are due, in part, to blockade of bradykinin degradation by the ACE and the increased endothelial synthesis of prostaglandins and/or the release of nitric oxide by enhanced tissue levels of bradykinin.
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PMID:Effect of chronic angiotensin-converting enzyme inhibition on endothelial function in patients with chronic heart failure. 748 81


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