Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The elderly segment of our society may triple by the year 2050. Specific cardiovascular data on the normal aging heart will be needed to provide proper medical and surgical therapy for this patient group. This report reviews normal aging changes of the very elderly heart. Expected or normal aging changes include brown atrophy of the myocardium, increased subepicardial fat, focal amyloid deposits, sigmoid-shaped ventricular septum, and calcific deposits in the aortic valve, mitral annulus and epicardial coronary arteries. Certain normal aging changes may produce clinical heart disease: aortic valve calcium (aortic stenosis), mitral valve annular calcium (mitral stenosis), amyloid deposits (amyloid heart disease). Certain normal aging changes may mimic heart disease: sigmoid-shaped ventricular septum (hypertrophic cardiomyopathy), mitral leaflet "buckling" (floppy mitral valve).
 ...
PMID:The old-age heart: normal aging changes which can produce or mimic cardiac disease. 304 29

The cardiomyopathic Syrian hamster has a genetically transmitted form of dilated cardiomyopathy and is an important paradigm of myocardial disease, particularly for studies addressing the earliest stages of myocardial dysfunction. This model exhibits an increase in cardiac sympathetic tone in the presence of an altered expression of sarcolemmal calcium channels or of alpha 1 receptors, and a defective handling of calcium by both cardiomyocytes and vascular smooth muscle cells. Increased expression of the oncogene c-myc is evident in cardiomyocytes before any overt evidence of heart disease. Alterations in a nuclear phosphoprotein, which appears to be important in the regulation of gene expression, have also been identified. The disease becomes phenotypically manifest by the development of microvascular spasm, reperfusion injury and myocyte loss. Myocyte loss, in turn, burdens the remaining cells with an increasing load, increasing sympathetic stimulation, myocyte hypertrophy and further cell loss--a continuing vicious spiral that culminates in the development of myocardial failure. All of the features of hamster cardiomyopathy may be prevented by the administration of verapamil or prazosin to juvenile hamsters before the phenotypic onset of their heart disease. This understanding has led to the study of new imaging agents that promise the detection of such forms of cardiomyopathy in their earliest stages and a means by which the effects of therapy can be assessed. If such mechanisms are applicable to human cardiomyopathy, early treatment of patients with adrenergic antagonists or calcium antagonists should be beneficial.
 ...
PMID:Catecholamines, calcium and cardiomyopathy. 305 92

In previous studies ribose has been recognized as a substrate that has beneficial effects on myocardial metabolism. It leads to an elevation of the available 5-phosphoribosyl-1-pyrophosphate pool and stimulates adenine nucleotide de novo synthesis in the rat heart under control and various pathophysiological conditions (Zimmer and Gerlach, 1978; Zimmer and Ibel, 1983, 1984). When the clinical application of ribose in patients with heart disease is envisaged, it is understood that conventional cardiac therapy must be continued. It is therefore necessary to demonstrate in animal experiments that ribose retains its stimulating metabolic effect when administered in conjunction with therapeutically used drugs. In this study we have selected representatives of two pharmacological principles, the calcium antagonist verapamil and the beta 1-specific adrenoceptor blocker metoprolol. Measurements of functional parameters in closed-chest rats revealed that i.v. administration of ribose alone for 24 h (200 mg/kg/h) had no hemodynamic or vasoactive influence, whereas verapamil and metoprolol (i.v. infusion of 2 mg/kg/h each for 24 h) induced negative chronotropic and negative inotropic effects. Cardiac output was reduced by metoprolol, but not by verapamil. Ribose did not affect these drug-induced hemodynamic alterations, and verapamil as well as metoprolol did not interfere with the characteristic metabolic effect of ribose, the stimulation of cardiac adenine nucleotide de novo synthesis. Administration of ribose in combination with these pharmacological agents is therefore compatible.
 ...
PMID:Combination of ribose with calcium antagonist and beta-blocker treatment in closed-chest rats. 311 64

From a retrospective study of 18 cases of obstructive cardiomyopathy in elderly people collected over a 5-year period, it appears that the incidence of the disease is probably underestimated. It seems to vary in severity, but only one-third of the patients present suggestive clinical symptoms associated with an obvious obstructive syndrome. The best diagnostic method is phonomechanography, which is easy to perform, systematically completed by a pharmaco-dynamic test. Hyperkinesia and disorders of cardiac compliance add useful specific data to the clinical picture. Echocardiography provides information on cardiac anatomy and on the obstructive mechanism. Left ventricular function tests are of particular interest in these old-age patients with cardiopathy. In our opinion, the two non-invasive methods are sufficient for a firm diagnosis, even when some criteria, notably ultrasonic, are lacking. Once the condition is diagnosed, the patient should be put on beta-blockers or calcium inhibitors, such as verapamil, which constitute an effective treatment.
 ...
PMID:[Obstructive myocardiopathy in the elderly. A retrospective study of 18 cases]. 315 75

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.
 ...
PMID:Control of cardiac arrhythmias by calcium antagonism. 328 60

Globally, among mortality and morbidity indices for man, ischemic heart disease (IHD) ranks at the top of the list. In the industrialized world, IHD is the leading killer and accounts for approximately 35% of all deaths each year. This most common cause of death results from insufficient coronary blood flow. IHD is a general term used to describe a pathophysiologic state in which cardiac output is inadequate as a consequence of coronary blood flow deficits brought about when the latter cannot deliver enough O2 to meet the needs of the myocardium. This review is concerned with the etiology of IHD, special forms of IHD such as angina pectoris and variant angina, as well as sudden death ischemia heart disease. The diverse conditions that cause IHD are discussed. Important etiologic factors such as the pathogenesis of atherosclerotic obstruction as well as localized coronary vasospasm are reviewed. Implications of dietary and metabolic alterations in electrolytes are a special focus of this view. Evidence implicating Mg2+-K+ and Mg2+-Ca2+ alterations in the pathogenesis of IHD is reviewed. Special attention is devoted to the role of Mg in vascular tone, coronary blood flow and in clinical management of IHD. It is concluded that judicious use of Mg salts in IHD could be expected to reduce myocardial oxygen demand and influence the myocardial oxygen supply/demand ratio in a favorable manner.
 ...
PMID:Ischemic heart disease and magnesium. 329 17

The ability to induce alcoholic cardiomyopathy has been tested in a variety of animal species. Myocardial alterations consistent with subclinical heart disease have been produced in many of these studies through a direct effect of ethanol or its metabolites upon the heart or a neurohumoral mechanism. In the rat most studies have, however, failed to finding diminished contractility in the basal state. In long-term animals the acute left ventricular responses to isoproterenol and calcium as well as pacing were reduced. Long-term studies in mongrel dogs fed 36 per cent of calories as ethanol produced an early decrease in left ventricular diastolic compliance related to interstitial collagen accumulation. Diminished contractility developed by four years. In addition to the morphologic evidence of distorted sarcoplasmic reticulum, in vitro experiments suggest important acute effects. Each mole of ethanol is bound tightly to each mole of protein comprising the Ca-ATPase pump, which is inhibited. Impaired uptake and binding of calcium by the sarcoplasmic reticulum has been observed in chronic alcohol models at one to two day intervals following the last exposure to ethanol. In addition, the flux of calcium ion does not appear normal in terms of access to contractile protein, where the calcium regulated inhibition of the troponin interaction with myosin is impaired. Experimental studies in a canine model of alcoholism revealed that the ventricular fibrillation threshold was moderately reduced in the basal state after 18 months and was diminished further after acute exposure.
 ...
PMID:Experimental models for studying the effects of ethanol on the myocardium. 331 64

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.
 ...
PMID:Neurogenic heart disease: a unifying hypothesis. 332 64

Evidence for an abnormal myocardial cell function in diabetes mellitus, influenced by acute metabolic changes, has appeared within recent years. Few but interesting clinical studies focus on this aspect of diabetic cardiopathy, and experimental studies have delivered possible explanations at the cellular level. These are concerned with the intracellular calcium homeostasis and transsarcolemmal receptor signaling. Because these changes are reversible by short-term insulin treatment, a new aspect for the study of diabetic heart disease has appeared.
 ...
PMID:Myocardial cell dysfunction in diabetes mellitus. A review of clinical and experimental studies. 353 Aug 45

In this paper, the authors present the case of hypocalcemic cardiopathy observed in a female patient who underwent thyroidectomy which was complicated post-operatively by the development of hypoparathyroidism. Two attacks of heart failure experienced by this patient were improved by the administration of calcium in combination with digitalis treatment. A study of cases published in the medical literature reveals that this condition is a rare cause of heart failure which develops only in the course of chronic hypocalcemia, with few neuromuscular clinical manifestations. The dual negative inotropic and hypovolemic effects caused by hypocalcemia explain the efficacy observed with the administration of calcium therapy, while the usual symptomatic treatment of this condition is inadequate.
 ...
PMID:[A rare cause of heart failure: hypocalcemic cardiopathy]. 366 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>