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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracardiac central hemodynamic parameters were studied and myocardial functional states were assessed in 46 patients with congenital heart disease, 20 of them had stenosed pulmonary artery; 26, presented with secondary atrial septal defect complicated with bacterial endocarditis. The mechanisms responsible for myocardial adaptation after defect correction are discussed. Attention is given to inadequacy of the performance of the heterometric mechanism of regulation due to altered elasticoviscous properties of the cardiac muscle. Plotting the functional curves enables one to gain an insight into the functional states of the myocardium.
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PMID:[Changes in the contractility of the myocardium in its various conditions in patients with congenital heart defects after surgery]. 253 Dec 50

Metabolic differences of the cardiac muscle in children with normoxaemic and hypoxaemic congenital heart disease were analyzed by means of representative enzymes of the energy metabolism in 95 specimens in 80 children with congenital heart disease. Tissue specimens from the right atria and ventricles were obtained during surgical operations. It was revealed that the myocardial metabolism of patients with congenital heart disease was markedly influenced by hypoxaemia: the aerobic capacity was significantly reduced in the atria as well as in the ventricles. Changes in the atrial musculature were, however, more marked: in addition to citrate synthase - similarly as in the ventricles - in the atria also activities of enzymes associated with lactate metabolism (LDH) and with glycolysis (TPDH, GPDH) were reduced. Patients with an atrial septal defect had a significantly lower activity of the enzyme involved in the fatty acid breakdown (HOADH) than patients with a ventricular septal defect. The described new adaptive mechanism is of practical importance for the treatment of congenital heart disease and other conditions associated with prolonged hypoxaemia.
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PMID:[Adaptation of cardiac energy metabolism in children with congenital heart defects]. 280 25

The size of cardiac muscle fibers was determined for 15 patients with Down syndrome who did not have congenital heart disease and for 15 age- and sex-matched control patients by counting the number of cardiac muscle cells in specified areas of microscopic sections (method of Black-Schaffer and Turner). Mean ratio of muscle cells per unit area for the Down patients versus controls was 84.9%, with mean cross-sectional area of Down fibers 117.8% of control value and calculated mean volume of Down cells 127.7% of control value. Mean weights of Down hearts related to normal for age, versus control hearts, was 79.8% of control values. Calculated ratio of total cardiac muscle cell number in Down hearts was 62.5% of the value for controls. This value corresponds closely to the 62.4%, which can be calculated from Naeye's data on cardiac muscle fiber size in Down syndrome based on a point-count method, and is also close to published values for liver cell size and number and skeletal muscle nuclear number in Down syndrome. This study demonstrates that the Black-Schaffer and Turner method gives results equivalent to those of the point-count method for studies of cardiac muscle fiber size, and further supports the suggestion that chromosome 21 controls the size and number of at least certain cell types.
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PMID:Increased cardiac muscle fiber size and reduced cell number in Down syndrome: heart muscle cell number in Down syndrome. 295 Mar 84

We experienced three cases of unusual cardiac hypertrophy of the right ventricle or interventricular septum with severe congestive heart failure in the neonatal period. One patient had congenital heart disease consisting of membranous tricuspid atresia, absent pulmonary valve, patent ductus arteriosus, left single coronary artery and a hypoplastic pouch-like right ventricle. Very marked cardiac hypertrophy was observed in the right ventricle and interventricular septum. Histologically, there was no appreciable disorganization of the cardiac muscle. The etiology of the unusual hypertrophy of cardiac muscle in this patient is uncertain. The other two patients had asymmetrical septal hypertrophy of the left ventricle evidenced by two-dimensional echocardiography. Cardiac catheterization was performed for these two patients. There was no evidence of congenital heart disease; however, one patient had a significant pressure gradient in the outflow tracts of the left and right ventricles. These two patients' faces appeared unusual and they had minor anomalies of their fingers and ears. This unusual cardiac hypertrophy associated with cardiac anomalies and minor anomalies of the face and extremities comprise a specific type of cardiomyopathy in neonates. This should be distinguished from hypertropic cardiomyopathy of older children and adults.
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PMID:[Unusual cardiac hypertrophy in neonates with congestive heart failure: report of three cases]. 295 60

Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.
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PMID:Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency. 296 7

Multiple manifestations of disordered or arrested cardiac muscle development are reported in a 14-year-old boy with clinical evidence of heart disease. These include persistent noncommunicating intramyocardial sinusoids, anomalous right ventricular muscle bands, muscular deficiency of ventricular septum, and papillary muscle underdevelopment. To our knowledge, this complex of findings has not been previously described.
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PMID:Dysplastic cardiac development presenting as cardiomyopathy. 319 Apr 11

In recent years calcium channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil, and bepridil; the dihydropyridines are devoid of significant electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the chronic control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias due to coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young subjects developing tachycardia with a right bundle branch block with left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity. The role of calcium antagonists in reducing the incidence of sudden death in the survivors of acute myocardial infarction remains uncertain.
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PMID:Control of cardiac arrhythmias by calcium antagonism. 328 60

Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.
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PMID:Neurogenic heart disease: a unifying hypothesis. 332 64

Reports of electrocardiographic abnormalities in association with myoglobinuria have been sparse and have included conduction disturbances, ST segment shifts, and T-wave changes. In many instances, these changes were noted in patients with underlying heart disease. We report a case of a 34-year-old woman with ST segment depression and T-wave inversion in the inferolateral leads during the acute episode of myoglobinuria. There was no demonstrable underlying heart disease, and there was parallel resolution of these ECG changes with myoglobinuria. We conclude that these ECG changes were produced by cardiac muscle involvement in a manner similar to that observed in skeletal muscle in myoglobinuria.
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PMID:ECG abnormalities in myoglobinuria: review of the literature. 381 48

In this article we have briefly reviewed the role of Ca2+ in the excitation contraction coupling in the myocardium and have indicated that cardiac contraction and relaxation are initiated upon raising and lowering the intracellular concentration of free Ca2+, respectively. Different mechanisms for the entry of Ca2+ through sarcolemma as well as release of Ca2+ from sarcoplasmic reticulum and possibly mitochondria have been outlined for initiating cardiac contraction. Relaxation of the cardiac muscle appears to be intimately dependent upon efflux of Ca2+ through sarcolemma as well as sequestration of Ca2+ by the intracellular storage sites, particularly sarcoplasmic reticulum and possibly mitochondria. The actions of some pharmacological and pathophysiological interventions have been explained on the basis of changes in subcellular Ca2+ movements in myocardium. Quinidine, which produced an initial positive inotropic action on rat heart was also found to increase sarcolemmal Ca2+-ATPase activity without any changes in the Na+-K+ ATPase. Other antiarrhythmic agents, procainamide and lidocaine, also increased sarcolemmal Ca2+-ATPase activity without affecting the Na+-K+ ATPase. On the other hand, both Ca2+-ATPase and Na+-K+ ATPase activities were increased in heart sarcolemma obtained from cardiomyopathic hamsters. In this model the increased Ca2+-ATPase activity may promote the occurrence of intracellular Ca2+ overload in the cardiac cell whereas the increased Na+-K+ ATPase activity may increase Ca2+ efflux through Na+-Ca2+ exchange systems as an adaptive mechanism. It has been suggested that some caution should be exercised while interpreting the data from in vitro experiments in terms of functional changes in the myocardium. Furthermore, it has been proposed that the pathophysiology and pharmacology of Ca2+ movements at different membrane sites be understood fully in normal and diseased myocardium in order to improve the therapy of heart disease.
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PMID:Progress and problems in understanding the involvement of calcium in heart function. 623 64


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