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

Although calcium antagonists are drugs which have been introduced relatively recently, their use is already so widespread, at least in the treatment of cardiovascular diseases as to represent one of the main therapies for diseases such as ischaemic cardiopathy, arterial hypertension, and, to a lesser extent, arrhythmias. Together with the development of clinical applications, deeper insight has been gained into the clinical and experimental pharmacology of these drugs. The authors of this review concentrate their attention on some of the less frequently discussed aspects of calcium antagonists. On the one hand, they describe some "nonprimary" uses of these drugs, both in the cardiovascular and in other therapeutic fields, which already receive confirmation from relatively solid experimental data. On the other hand, they review the side effects and some pharmacological interactions of calcium antagonists, both of which should be held in due consideration, seeing that these drugs are widely employed in clinical practice and their use often requires prolonged, intensive treatment. The most common side effects are described, together with others relatively less well known ones, and outline is given of potential undesirable effects on the cardiovascular as well as on other systems.
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PMID:[Calcium antagonists: accounts on new perspectives of their use and an update on side effects]. 252 6

After successful resuscitation only few patients present without any findings indicative of the causes of their cardiac arrest. We report on a 39-year-old woman who had normal clinical, electrocardiographic, and angiographic findings after she was successfully resuscitated. In contrast to other patients without apparent organic heart disease she had three cardiac arrests within 10 months; each episode was preceded by an ascending epigastric pain. During an attack with epigastric pain a long-term ECG recording documented an increasing ST-segment elevation followed by rapid, non-sustained ventricular tachycardia. Intravenous ergonovine induced a spasm of the right coronary artery with a subtotal vessel occlusion and an ST-elevation in lead III. After medication with a calcium antagonist no coronary vasospasm was demonstrated. For 11 months the patient has been without any complaints.
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PMID:[Coronary artery spasm as a rare cause of sudden heart arrest]. 258 57

In clinical arrhythmias, the main therapeutic role of calcium channel entry blockers is related to their effect on the sinus and atrioventricular (AV) node. Consequently, in cardiac arrhythmias where the AV node is part of the reentry circuit, a beneficial effect of diltiazem and verapamil can be demonstrated. These include AV nodal reentry and orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome. In addition, the ventricular response by the AV node during atrial tachycardias can also be controlled with these agents. A specific type of ventricular tachycardia seen in the absence of structural heart disease has also been reported to respond to intravenous and oral verapamil. Calcium channel blockers have no proven depressant effect on accessory pathway conduction. Similarly, the value of these agents in the treatment of ventricular tachycardia in association with chronic coronary artery disease and idiopathic dilated cardiomyopathy is rather limited. The use of calcium entry blockers in patients with wide QRS tachycardia, therefore, is to be discouraged unless it can be proved that supraventricular tachycardia with aberrant conduction is the underlying basis.
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PMID:Use of calcium channel entry blockers in the treatment of cardiac arrhythmias. 268 83

The cardiomyopathies are defined and classified into hypertrophic, dilated and restrictive types. In hypertrophic cardiomyopathy the major abnormalities of structure (massive ventricular hypertrophy, myofibrillar disarray, and narrow intramural coronary arteries) and of function (excessive ventricular contraction, systolic pressure gradients, increased ventricular stiffness with impaired relaxation and a tendency for sudden death) are used as the basis for selective and rational treatment with beta-blocking, calcium blocking, or antiarrhythmic agents, or a combination. Treatment is aimed at relieving symptoms, improving prognosis and slowing the progress of disease. Additional methods of treatment involving pacemakers and defibrillators are covered, and the place of septal resection, mitral valve replacement and cardiac transplantation discussed. General management and advice to the patient, and the treatment of complications such as atrial fibrillation, congestive heart failure and infective endocarditis, are also covered. In dilated cardiomyopathy measures to improve ventricular function by vasodilator therapy and the place of antiarrhythmic and anticoagulant drugs are discussed. The controversial treatment with beta-adrenergic blocking agents is reviewed, and the place of immunosuppressive therapy assessed. The possible use of antiviral agents in the future is commented upon, and cardiac transplantation is emphasised as the most effective, although radical, means of improving prognosis in intractable cases. In restrictive cardiomyopathy due to endomyocardial fibrosis, treatment of the initial inflammatory stage with steroids or sulphonylurea, and of the later fibrotic and thrombotic stage with anticoagulants and endocardectomy, is surveyed. The possible place of cardiac transplantation both for endomyocardial fibrosis and amyloid heart disease is mentioned, caution being urged when either of these conditions involves organs other than the heart.
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PMID:Clinical decisions in the management of the cardiomyopathies. 269 49

The concentrations of magnesium and total calcium human vitreous humors obtained postmortem was tested. In the groups of heart disease and asphyxia a correlation between the postmortem interval and calcium or magnesium concentrations was found. There was no correlation between postmortem interval and calcium respectively magnesium in the other causes of death. It seems possible that the analysis of vitreous humor may be useful in both diagnosis and determination of postmortem interval in the cases of heart death and asphyxia.
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PMID:Determination of calcium and magnesium in postmortem human vitreous humor as a test to ascertain the cause and time of death. 271 68

The effects of enalapril maleate were studied in a group of 6 patients with arterial hypertension, hypertensive cardiopathy, multiple metabolic disorders and habitual snoring. Earlier treatment with antihypertensive drugs (diuretics, antiadrenergics, calcium antagonists) had been suspended when a marked deterioration was noted in metabolic parameters and plasmatic electrolytes as well as extremely disturbed sleep. The latter is probably attributable to increased respiratory obstruction during the night as a result of the increased hypertonia of the muscles of the upper air ways due to low blood potassium as well as the central and peripheral effects of the antiadrenergic drugs. After the wash-out period there was a marked improvement in laboratory parameters that continued after treatment with enalapril maleate. In particular, apart from a further slight fall in blood cholesterol and uricaemia there was a statistically significant drop in triglyceride levels. The improvement in the laboratory parameters made it possible to reduce the doses of the drugs being taken for the metabolic disorders. A distinct improvement was also noted in the sleep disturbances especially the excessive drowsiness during the day. There was also a statistically significant drop in arterial, systolic, diastolic and mean blood pressure without any significant change in heart beat. The results indicate that enalapril maleate should be the treatment of choice for those patients in whom high blood pressure is accompanied by alterations to the main metabolic parameters and habitual snoring.
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PMID:[Treatment with enalapril maleate in patients with arterial hypertension, pluri-metabolic syndrome and habitual snoring]. 282 86

In the clinical management of heart disease, calcium channel blockers are generally prescribed in combination with one or more anti-angina, antiarrhythmic, or antihypertensive agents. Two different mechanisms are involved in drug interactions: pharmacokinetic and pharmacodynamic. In the former, the disposition of one drug is altered by the action of another, causing an increase or decrease in its absorption or its modified distribution, metabolism, or excretion. In pharmacodynamic interactions, the physiologic effects of one drug interfere either directly or indirectly with those of another, for instance, by alterations in fluid or electrolyte balance. This effect may be antagonistic or additive. The present work outlines the possible adverse interactions between the three main calcium antagonists and other therapeutic agents, including digoxin, beta blockers and antiarrhythmic, anesthetic, antihypertensive, antiasthmatic, and antidiabetic drugs and contrast media. Knowledge of these effects is of major clinical importance in the treatment of cardiac patients.
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PMID:Calcium antagonists--adverse drug interactions. 290 14

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

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

Diabetes mellitus is frequently associated with a primary cardiomyopathy. The mechanisms responsible for this heart disease are not clear, but an alteration in myocardial Ca2+ transport is believed to be involved in its development. Even though sarcolemma plays a crucial role in cellular Ca2+ transport, little appears to be known about its Ca2+ transporting capability in the diabetic myocardium. In this regard, we have examined the status of the cardiac sarcolemmal Ca2+ pump during diabetes mellitus. Purified sarcolemmal membranes were isolated from male Wistar diabetic rat hearts 8 wk after streptozotocin injection (55 mg/kg iv). Ca2+ pump activity assessed by measuring its Ca2+-stimulated adenosine triphosphatase and Ca2+-uptake ability in the absence and presence of calmodulin was significantly depressed in the diabetic myocardium relative to controls. These results did not appear to have been influenced by the minimal sarcoplasmic reticular and mitochondrial contamination of this membrane preparation. Hence, it appears that the sarcolemmal Ca2+ pump is defective in the diabetic myocardium and may be involved in the altered Ca2+ transport of the heart during diabetes mellitus.
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PMID:Alterations in cardiac sarcolemmal Ca2+ pump activity during diabetes mellitus. 303 Jan 40


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