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

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.
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PMID:Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats. 153 55

To elucidate mechanisms of adaptation and maladaptation in heart failure, abnormalities of left ventricular function and their relationships to myocardial contractile protein were studied in the Syrian hamster Bio 14.6. Left ventricular and heart weights were both increased in 20-week-old cardiomyopathic hamsters, indicating cardiac hypertrophy as a compensatory mechanism to the disease process of cardiomyopathy. However further increase in the left ventricular weight was not observed in older (40-week-old) cardiomyopathic hamsters. On the other hand left ventricular volume and volume/mass ratio were increased progressively. Correspondingly, V3 type myosin was increased and myosin sliding velocity was decreased. Left ventricular function of cardiomyopathic hamsters evaluated using an isovolumically beating perfused heart preparation was depressed, and this functional impairment was also progressive. Chronic administration of metoprolol, a beta-blocking agent, induced further increase in left ventricular volume and mass without changing left ventricular function and myosin isozyme pattern. Thus in cardiomyopathic hamsters, left ventricular function progressively deteriorates in spite of a variety of adaptive mechanisms, and remodeling occurs.
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PMID:Cardiac adaptation and its limitation in an experimental model of congestive heart failure. 153 56

Experimental myocardial infarction is a model of cardiac overload due to amputation of part of the cardiac muscle. The development of cardiac failure depends on the size of the infarct and the time factor. This model of overload is associated with changes of the phenotype of the remaining healthy muscle and with peripheral vascular modifications partially dependent of the activation of pressor and/or deactivation of dilator systems. These changes are proportional to the size of the infarction at a given time after induction of the model. The degree of right ventricular hypertrophy and the decrease in blood pressure reflect the severity of infarction and the deterioration of the remaining myocardial function, affecting the haemodynamics both before and after the left ventricle. The increases in the 1/3 forms of isomyosins, the amount of subendocardial collagen, the biosynthesis, stocking and secretion of ANF are related to the infarct size and degree of overload. Similarly, the concentration of cyclic GMP is proportional to the infarct size. These parameters reflect ventricular overload, the increase of stress and energy deprivation of the remaining healthy muscle. The activation of peripheral pressor systems is also dependent on the infarct size reflects the effect of cardiac pump dysfunction on the kidney, liver, brain and endothelium. Large infarcts are associated with increased circulating renin and renal concentrations, with a decrease in angiotensinogen levels related to its consumption by the renin and to reduced hepatic synthesis and also with increased secretion and biosynthesis of vasopressin by the hypothalamus. In this model, Perindopril is beneficial by decreasing the cardiac load. It reduces the blood pressure, causes regression of bi-auricular and right ventricular hypertrophy. Changes in myosin isoenzyme configuration regress and subendocardial fibrosis and ANF concentrations are normalised. The effects of ACE inhibitors in this context, though very beneficial, are limited by the impossibility of normalising cardiac load and stress when the initial amputation of cardiac contractile mass exceeds 40%.
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PMID:[Experimental myocardial infarction in the rat. Effect of perindopril]. 166 27

Attempts at treating idiopathic cardiomyopathy have been made both clinically and experimentally using the cardiomyopathic Syrian hamster. In recent years, the angiotensin converting enzyme (ACE) inhibitor has attracted considerable attention as an agent to treat heart failure. We administered the ACE inhibitor captopril to the cardiomyopathic hamster. In this study, 15 mg/kg body weight of captopril was administered to the cardiomyopathic hamster J2N at 5 weeks of age for 10 weeks; age matched J2N hamsters were used as non-treated control animals. At the end of captopril administration, blood was collected from the ventral aorta. Serum malondialdehyde (MDA), serum CPK, aldolase and LDH were determined, and myosin isoenzyme patterns of the extirpated myocardium were compared. Additionally, ECGs were compared and the fibrotic ratio of both ventricles determined. Serum MDA, CPK, and aldolase increased significantly in the cardiomyopathic hamster, whereas these indices were significantly inhibited in the hamster treated with captopril. The pathological ECG findings and the ventricular V3 predominant myosin isoenzyme patterns of the J2N were also much improved in the captopril group. However, the improvement in these parameters by enalapril administration was less than that seen with captopril. These results suggested that the effect of captopril is not only due to decrease of the angiotensin II level, but also due to increase in tissue kinin and vasodilatory prostaglandin which play an important role in the beneficial effect of captopril.
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PMID:Protective effect of ACE- and kininase-inhibitor on the onset of cardiomyopathy. 178 64

In heart failure, many alterations occur in the ventricle as a whole, as well as in the myocardial cell. In the first part of this review we report on the macroscopic structure of the left ventricle by analysing the relation between left ventricular dilatation and left ventricular hypertrophy in terms of ventricular wall stress. Peak systolic stress in dilated ventricles of patients with compensated heart failure does not differ from values obtained in normal ventricles, whereas the systolic stress-time integral is increased by more than 40%. The stress-time integral is a major determinant of myocardial oxygen consumption, and its reduction by peripheral vasodilation leads to a proportional decrease in left ventricular oxygen consumption. In contrast, the phosphodiesterase inhibitor, enoximone, decreases the stress-time integral without a proportional decrease in myocardial oxygen consumption, due to the competition between positive inotropic effect with increased oxygen consumption and a vasodilating effect with decreased oxygen consumption. Beta-1 adrenoceptor agonists increase myocardial oxygen consumption. In the second part of this review we report on the functional alterations of the following subcellular and molecular structures in the failing myocardium: (1) adrenoceptors and G-proteins; (2) sarcoplasmic reticulum with an altered force-frequency relationship; (3) the acto-myosin system with decreased velocity of shortening and increased economy of force generation. On the basis of these alterations, a disadvantageous chain of events develops in the failing myocardial cell.
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PMID:The heart in heart failure. Ventricular and myocardial alterations. 183 95

Sodium has been identified as a causal factor in the development of hypertension in experimental animal models as well as in clinical human subjects. Sodium is also known to play a role in modulating myocardial mass and its pattern of myosin isozyme distribution. In the rodent model, the accumulation of V3 myosin isozyme (MI), due to the modulating influence of sodium, has been shown to be associated with persistent cardiac hypertrophy and heart failure. In this paper, we have examined the effect of the restriction of dietary sodium on blood pressure, ventricular weight and myosin isoforms in spontaneously hypertensive rats (SHR) and the relationship of these parameters with age. In 10- to 11-week-old SHR, dietary sodium restriction for 14 weeks resulted in a significant reduction in ventricular mass associated with systolic shifting of myosin isoform from V3 type to V1 type with no change in systolic blood pressure level; dietary sodium restriction also showed a significant reduction in body weight. When the effect of dietary sodium restriction (for 8 weeks) was studied in relation to age (in 11-, 16- and 24-week-old rats) a significant shift in myosin isoform from the V3 to the V1 type was noted in the 11-week-old rats; a slight but significant shift was noted in 16-week-old rats, and no change in myosin isoform distribution was noted in the 24-week-old SHR. The alteration in myosin isoform and myocardial mass in the 11- and 16-week-old rats was independent of changes in systolic blood pressure. This study demonstrates that sodium plays an important role not only in modulating myocardial mass but also in changing the biochemical composition of the heart. This study also suggests that in genetic hypertension, the restriction of sodium at a very young age may fully prevent the development of hypertension and hypertrophy. However, the mechanism by which the sodium ion modulates myocardial mass and the expression of either V1 or V3 myosin genes is unknown; the question of how sodium affects the cardiac function also remains. Some evidence suggests that sympathetic outflow may play an important role, but further studies are needed to validate this.
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PMID:Effect of sodium deprivation on cardiac hypertrophy in spontaneously hypertensive rats: influence of aging. 183 55

To identify a cardiac protein that could cause a serious autoimmune myocarditis, membranous proteins and myosin as antigens were investigated. In mice immunized with membranous proteins, the lesions induced were limited on the histological level. On the other hand, in Lewis rats immunized with cardiac myosin, serious myocarditis was induced. Every rat showed evidence of heart failure which was fatal in a few. Histology disclosed extensive cell infiltrates and myocardial necrosis. Among those lesions, giant cells were present. This myocarditis could be also transferred adoptively by lectin-activated spleen cells, T-lymphocytes, but not by IgG fraction. Thus, cardiac myosin can induce autoimmune giant cell myocarditis in Lewis rats.
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PMID:Experimental giant cell myocarditis induced by cardiac myosin immunization. 191 48

In this study we tested the hypothesis that reduced myofibrillar ATPase activities in end-stage heart failure are associated with a redistribution of myosin isozymes. Cardiac myofibrils were isolated from left ventricular free wall from normal human hearts and hearts at end-stage heart failure caused by coronary artery diseases, cardiomyopathy or immunological rejection. The hearts had been excised in preparation for a heart transplant. Myofibrillar Ca2(+)-dependent Mg-ATPase and myosin Ca2(+)- and K+EDTA-ATPase activities were compared. Possible changes in myosin isozyme distribution in the diseased heart were investigated using polyacrylamide gel electrophoresis of native myosin in the presence of pyrophosphate. Significant reduction in myofibrillar Ca2(+)-dependent Mg-ATPase with no changes in the sensitivity of the myofibrils to Ca2+ was observed in heart with coronary artery diseases (25.2 to 27.1% at pCa 5.83 to pCa 5.05), cardiomyopathy (21.1 to 25.5% at pCa 5.41 to pCa 5.05), and in the immunologically rejected heart (18.4 to 22.8% at pCa 5.41 to pCa 5.05). Significantly lower myosin Ca2(+)-ATPase was observed with coronary artery diseases only and myosin K-EDTA activities did not differ in diseased and normal hearts. Polyacrylamide gel electrophoresis of native myosin from the normal and three models of end-stage heart failure revealed two distinct bands in the human left ventricle and one diffuse band in the human right atria. No apparent differences in myosin isoenzyme pattern were observed between the normal and diseased hearts. Further evaluation is needed to clarify the ATPase nature of the two bands.
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PMID:Reduced cardiac myofibrillar Mg-ATPase activity without changes in myosin isozymes in patients with end-stage heart failure. 214 90

Alterations of cardiac contractility caused by thiamine deficiency were studied on three groups of 2 month old male Wistar rats: B1, fed a thiamine deficient diet, PF pair fed, which received an amount of thiamine free diet determined on the daily consumption of B1 animals, supplemented with appropriate thiamine supply, C ad libitum fed controls. The animals were studied after 35 days of dietary treatment. Force-velocity curves were determined in right ventricle papillary muscles. Shortening velocity was significantly lower in B1 and PF than in C muscles and in B1 than in PF muscles. The ability to develop tension was not altered. Myosin ATPase activity was assayed in preparations of myofibrils and in preparations of purified myosin. Both Ca-Mg activated myofibrillar ATPase activity and Ca-activated myosin ATPase activity were significantly reduced in B1 and PF compared to C myocardium. Furthermore Ca-activated ATPase activity was lower in B1 than in PF myocardium. Myosin isoenzyme distribution was determined by pyrophosphate gel electrophoresis of purified myosin preparations. When compared to C animals both B1 and PF animals showed a myosin electrophoretic pattern shifted towards the slow isoform V3; such a shift was more pronounced in B1 animals. Information concerning excitation-contraction coupling was obtained by determining the steady state and transient force-interval relation and by recording transmembrane action potential. B1 and PF myocardium exhibited, when compared to C, a less sensitivity to a reduction of the interval of stimulation, a faster mechanical restitution, a prolonged action potential duration. Such alterations were generally more pronounced in B1 than in PF myocardium. The results support the view that in the rat cardiac contractility is deeply affected by thiamine deficiency. The alterations of cardiac contractility seem to be caused by adaptive mechanisms rather than by cardiac failure and seem to be attributable for a big part to the reduction of food supply.
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PMID:Altered contractile properties of rat cardiac muscle during experimental thiamine deficiency and food deprivation. 215 36

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37


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