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

In patients with Duchenne muscular dystrophy (DMD), heart failure appears in later stage of the disease due to myocardial degeneration and respiratory insufficiency, and sometimes causes death. However, there have been no adequate parameters which can be used easily to evaluate the grade of heart failure in DMD, except cardiac enlargement and pulmonary congestion observed by chest X-ray picture. Thus, we measured the plasma concentrations of atrial natriuretic peptide (ANP) in the patients with muscular dystrophy of various types, and studied a relationship between plasma ANP concentration and heart failure, expecting that it could be an index of heart failure in DMD patients. The plasma ANP concentrations in patients with DMD were 35.5 +/- 3.3pg/ml (mean +/- SE) and higher than in normal subjects (19.3 +/- 1.0pg/ml). In the patients with limb-girdle muscular dystrophy, facioscapulohumeral muscular dystrophy and neurogenic muscular atrophy, the plasma ANP concentration showed a tendency to elevate. However, no elevation of plasma ANP levels was observed in the patients with other types of muscular dystrophy. In DMD, number of the patients having a high plasma ANP concentration was increased with progress of disability grade, and decrease in serum creatine kinase activity and serum myoglobin concentration. There was a significant correlation (p less than 0.01) between plasma ANP concentration and cardiothoracic ratio or PEP/LVET, but no correlation between the concentration and respiratory failure. Immunohistochemistry of the atrial cardiac muscle of an autopsied DMD case revealed many ANP-positive atrial muscle cells, indicating the preservation of ANP-secreting function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Secretion and clinical significance of atrial natriuretic peptide in patients with muscular dystrophy]. 252 1

The interstitium of the myocardium is composed of predominantly type I collagen; type III collagen is present to a lesser extent. The fibrillar collagens serve as tethers between muscle cells, muscle fibers, and blood vessels while also providing a scaffolding that supports the muscular and vascular compartments. In pressure overload hypertrophy, a continuous structural remodeling of the fibrillar collagen matrix is seen. What is initially an adaptive process that enhances tensile strength can eventuate in pathologic hypertrophy with muscle fiber entrapment, cell loss, and abnormal diastolic and systolic stiffness of the myocardium. Morphologically distinct patterns of myocardial collagen accumulation, or fibrosis, have been identified based on the alignment of thick and thin collagen fibers to one another and to cardiac muscle. Each pattern, representing either a reactive (without necrosis) or reparative process, can alter stiffness in a unique manner. The manner in which the interstitium regulates the nature and proportion of fibrillar collagen formation is unknown and deserving of further study. Such information may lead to the development of antifibrotic agents that counteract, prevent or modify disproportionate collagen remodeling in pressure overload hypertrophy. These agents may thereby ultimately represent corrective forms of therapy for the management of heart failure.
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PMID:Patterns of myocardial fibrosis. 253 37

Angiotensin-converting enzyme (ACE) inhibitors are of benefit in the management of heart failure. In some studies in patients with heart failure, a decline in renal function occurred more frequently in patients treated with enalapril maleate, a longer-acting agent, than in those treated with captopril, a shorter-acting drug. Patients experiencing a decline in renal function had a number of predisposing hormonal and hemodynamic factors. In one report, these factors included an initial fall in blood pressure that was sustained, lower cardiac output, and a relatively high fixed dose of enalapril that contributed to renal impairment. In a second study, the decline in renal function was most severe in patients with a lower systemic arterial pressure in whom glomerular filtration may have been dependent on angiotensin II. In a third study, intravascular volume depletion and an activated renin-angiotensin system led to reduced renal function. Reduction of angiotensin II level in plasma and tissues by ACE inhibitors decreases systemic vascular resistance and efferent arteriolar tone, which tends to decrease glomerular filtration rate. If compensatory increases in cardiac output are inadequate or preexisting renal impairment or volume depletion is present, renal function will deteriorate. Long-acting ACE inhibitors prolong the decreased efferent arteriolar tone and may compromise cardiac muscle response to catecholamines. The use of shorter-acting agents in patients who exhibit deterioration in renal function may be preferable.
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PMID:Renal hemodynamic consequences of angiotensin-converting enzyme inhibition in congestive heart failure. 253 12

To understand physiopathology of contractibility in heart failure is needed the previous knowledge of normal muscle contractibility, calcium regulation, methods of assessment of isolated cardiac muscle and in situ heart contraction. Models of calcium movements during rest and contraction are presented and concepts of preload, afterload, Vmax and Po introduced. The importance of assessment of cardiac diastolic function is referred. Biochemical alterations in the failing myocardium are presented.
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PMID:[Heart insufficiency. Physiology and physiopathology of muscle contraction of the heart]. 256 Oct 71

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

Oxygen free radicals have been linked to a wide variety of cellular damage in biological systems. Polymorphonuclear (PMN) leukocytes stimulation is one of the known sources for oxygen free radicals. It has been suggested that oxygen free radicals depress the excitation-contraction coupling in cardiac muscle. It is possible that a decrease in the myocardial contractility in heart failure might be due to an increased oxygen-free-radical-producing activity of PMN leukocytes. The authors studied, therefore, the release of oxygen free radicals, as measured by luminol-dependent chemiluminescence activity, from the PMN leukocytes in dogs with heart failure due to aortic stenosis. Hemodynamics and phagocytic activity of PMN leukocytes were studied in 6 control dogs and 6 dogs with aortic stenosis of six to nine months' duration. There was a significant decrease in the index of myocardial contractility and an increase in the left ventricular end-diastolic pressure in dogs with aortic stenosis, suggesting left ventricular failure in these dogs. Although there was a tendency for a decrease in the cardiac index in dogs with aortic stenosis, the decrease was not significant. Phagocytic activity of PMN leukocytes in blood was studied in control dogs and dogs with aortic stenosis. Phagocytosis was initiated by addition of opsonized zymosan and chemiluminescence was monitored by use of a luminometer. The peak chemiluminescence activity of the PMN leukocytes in blood of dogs with heart failure was about threefold greater than that in the blood from control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased production of oxygen free radicals by polymorphonuclear leukocytes in heart failure due to aortic stenosis. 270 49

A misconception regarding the ultrastructural basis of myocardial failure has been observed in laboratory studies involving medical students and practicing physicians, in medical textbooks, and in clinical instruction of students. This misconception attributes heart failure to overextension of individual cardiac muscle fibres and their sarcomeres, resulting in a mechanically based decline in contractile force production. The basis of the misconception is a set of component misconceptions which interact in reciprocally supportive ways. The interlocking nature of the component misunderstandings strengthens the overall misconception, making it difficult to undermine. A contributor to many aspects of the faulty account of heart failure is a tendency toward oversimplification of complex phenomena in learning, instruction, and scientific research. Implications for medical education are considered.
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PMID:Foundations of a misunderstanding of the ultrastructural basis of myocardial failure: a reciprocation network of oversimplifications. 276 11

Cardiac tamponade is a frequent cause of death in acute myocardial infarction--in as many 23%. It is encountered in particular in the 7th and 8th decade, in patients with a first infarction which is frequently situated in the anterior wall of the left ventricle. 93% of the patients have obvious ECG manifestations of Q infarction. The diagnosis of cardiac tamponade is easy when during an acute terminal attack slow activity on the ECG tracing is found without a haemodynamic response and the pulse on the great arteries is not palpable even after external cardiac massage. In 80% the onset of cardiac tamponade is very sudden. The presence of shock or cardiac failure makes the diagnosis of cardiac tamponade more difficult. As to investigated indicators, in the development of cardiac tamponade the systemic pressure--systolic as well as diastolic--on admission or during hospitalization, may play a part. The patients have a less marked coronary sclerosis, fibrosis of the cardiac muscle is less frequently present. Previous necroses of the heart muscle may have probably a certain protective effect on the development of cardiac tamponade. Anticoagulants obviously do not influence the development of cardiac tamponade.
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PMID:[Cardiac tamponade as a complication of acute myocardial infarct. (Clinical and pathologico-anatomic analysis of patients with acute myocardial infarct and cardiac tamponade)]. 280 Mar 57

The acute and prolonged effects of alcohol and smoking on the oxidative and energy processes of cardiac muscle in experimental animals were studied at the subcellular level. The acute effect of alcohol manifested itself by decreasing mitochondrial respiration, compensated by increased glycolytic activity of the myocardium so that myocardial energy phosphate concentration remained unchanged. The prolonged effect of alcohol (for a period of 14 days) resulted in a decrease in oxidative processes as well as in glycolytic activity with a subsequent decline in myocardial ATP and CP levels. Smoking led to a significant decrease in oxidative and total bioenergetic processes of cardiac muscle mitochondria both after acute and prolonged smoking. This metabolic disorder is localized in the terminal segment of the respiratory chain of the mitochondria at the level of cytochrome oxidase. The authors conclude that the above-mentioned disorders may play a role in the development of heart failure on the basis of alcoholic or smoke cardiomyopathy.
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PMID:Metabolic disorders of cardiac muscle in alcoholic and smoke cardiomyopathy. 280 6

Chronic cardiac insufficiency can be produced by a variety of causes which may be partly determined by means of macroscopic, histological and electron microscopic investigations. By using quantitative histochemical methods, changes of substances in the myocardium can be observed indicating myocardial insufficiency and giving an explanation of its cause. Hypertrophied hearts without insufficiency show cardiac muscle fibres having increased in width, volume and dry weight up to a maximum value which will not be exceeded even in further progressing cardiac hypertrophy. The biochemically determined amount of collagen increases significantly with the growing weight of the myocardium. Both the myocardial amount of DNA and the amount of myoglobin, correlated with the width of the fibres, have also increased. The heart muscle nuclei showed a polyploidization which is also correlated with the weight of the myocardium. In insufficient hearts suffering from myocardial hypertrophy, the increase of the total DNA content is significantly decreased as compared to non-insufficient hearts. The mean ploidy level is increased in case of lower weights of the myocardium and decreased in higher weights in comparison to non-insufficient hearts of the same weight. In insufficient hearts a more significantly increased amount of the connective tissue cells is observed than in the case of cardiac hypertrophy alone. In contrast to this, the increase of the heart muscle cells is significantly reduced. A lack of contractile proteins, decreased DNA synthesis, increased fibrozation and, in particular, the reduced number of cardiac muscle cells must be considered as essential factors for cardiac insufficiency.
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PMID:Histochemically determinable changes in cardiac insufficiency and their functional significance. 294 64


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