Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Though the efficacies of procainamide and disopyramide in treating arrhythmias are well established, their precise mechanisms of antiarrhythmic action remain unclear. Arrhythmias which occur during acute myocardial ischemia can be explained partly on a metabolic basis. The accumulation of intermediates subsequent to impaired beta-oxidation of free fatty acids has been suggested as a cause of serious arrhythmias. The purpose of this study was to investigate changes in free carnitine, long chain acyl carnitine and long chain acyl CoA concentrations in the ischemic canine heart following the administration of procainamide and disopyramide. The coronary artery was occluded for 40 min and myocardial samples were prepared from both nonischemic and ischemic areas. Procainamide and disopyramide prevented the accumulation of long chain acyl carnitine and long chain acyl CoA in the ischemic myocardium. The results showed that procainamide and disopyramide had beneficial effects on fatty acid metabolism. It was suggested that one of the antiarrhythmic mechanisms of these drugs might be the prevention of the accumulation of fatty acyl derivatives in the ischemic myocardium.
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PMID:Effects of procainamide and disopyramide on long chain acyl carnitine and long chain acyl CoA concentrations in the ischemic heart. 324 36

This report represents the first application of immunohistochemical methods for localizing an exogenously administered drug. Intravenously administered procainamide was localized in normal, ischemic, and necrotic myocardium in 23 dogs. Rabbit antiprocainamide antibodies were used in an avidin-biotin-peroxidase complex staining method. Normal myocardium demonstrated diffusely positive immunostaining for procainamide, as did the cardiac conduction system and vascular endothelial cells. Necrotic myocardium demonstrated markedly reduced to absent immunostaining. By contrast, in regions of myocardial ischemia without necrosis, immunostaining for procainamide was similar to that in the normal myocardium. Procainamide myocardial tissue levels were reduced in necrotic and ischemic zones compared to normal (p less than 0.05) only in those animals in which procainamide was administered after rather than before the onset of coronary occlusion. The demonstration of the absence of drug binding in the necrotic cells suggests that myocardial tissue levels or radiolabelled assessment of drug distribution can be misleading when nonhomogeneous tissue is sampled. The immunohistochemical technique provides additional information about the regional and cellular distribution of procainamide that is complementary to the information obtainable by radiolabelling microspheres and from biochemical assays.
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PMID:Immunohistochemical localization of procainamide in normal, ischemic, and necrotic canine myocardium during acute experimental myocardial infarction. 359 7

In an open, randomized, crossover study, the efficacy of sotalol and procainamide was compared in 33 patients with frequent, chronic premature ventricular contractions (PVCs). A 75% reduction in PVCs/24 hours (two 24-hour recordings) was arbitrarily considered to constitute an adequate therapeutic effect. Sotalol was started at a dose of 160 mg once daily for 1 week, followed by a 24-hour recording. In the absence of any therapeutic effect, the same procedure was repeated with 320 mg, 480 mg, and 640 mg daily. Procainamide, 1 gm three times/day, was given or, if plasma concentrations were insufficient, 1.5 gm three times/day for 1 week. PVC control was obtained in 22 (67%) patients on sotalol, including all 12 with ischemic heart disease. Procainamide was successful in 13 (39%) patients. Effects on the number of attacks of ventricular tachycardia were achieved by both drugs in those patients where PVCs were reduced by at least 75%. Sotalol caused side effects in five patients, who therefore could not accept planned increases in dosage. Side effects were noted by 12 patients with procainamide. Nine patients responded to both drugs, seven to neither. Thirteen responded to sotalol only and four to procainamide only. We conclude that sotalol is a useful alternative to procainamide in controlling chronic PVCs, especially in patients with ischemic heart disease.
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PMID:Comparative efficacy of oral sotalol and procainamide in patients with chronic ventricular arrhythmias: a multicenter study. 388 77

This report describes a case of syncope with an initial ECG that showed ST-segment elevation in the right precordial leads suggestive of Brugada syndrome. Procainamide infusion induced a significant increase in the ST-segment abnormalities, further increasing the suspicion for this syndrome. Cardiac catheterization showed lesions in the proximal left anterior descending artery and distal right coronary artery. Following percutaneous coronary intervention at these sites, the ST-segment abnormalities resolved and a repeat procainamide challenge was negative. Electrophysiological study did not provoke any ventricular arrhythmias. Silent myocardial ischemia may result in ECG changes that resemble those seen in patients with Brugada syndrome.
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PMID:Syncope with ST-segment abnormalities resembling Brugada syndrome due to reversible myocardial ischemia. 1235 80