Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.
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PMID:Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes. 9 18

Biopsy specimens of the myocardium for electron microscopical study were taken from patients who were having surgical operations for correction of aortic and mitral valve lesions. Ultranstructural changes characteristic of hypertrophy and ischemia were found in the left ventricles of groups with aortic and mitral lesions. The severity of the cardiomyopathy was greater in hearts that had aortic lesions than in those that had mitral lesions. Both groups, however, displayed degenerative changes to an extent not readily appreciated or expected when their clinical histories and catheterization data were obtained.
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PMID:Human left ventricular ultrastructure. Clinical and laboratory catheterization correlation. 13 36

A total of 25 cases (12 men, 13 women) of complete left bundle branch block (LBBB) were found among 1,400 consecutive autopsy in the aged. Their ages ranged from 70 to 86 years (average 78.9). ECG was analyzed as for the occurrence of LBBB and myocardial infarction (MI). Pathological examinations included observations of the conduction system by serial sections. They were divided into group A with MI and group B without MI. Duration of LBBB was 1 to 3 days in 4 cases, more than 1 month in 7, and more than 1 year in 14. From the temporal sequence of LBBB and MI in group A, cases were classified into (1) MI preceding LBBB in 5, (2) both coexistent in 5, and (3) LBBB preceding MI in 1. There were 8 cases of normal electrical axis, 17 left axis deviation, 7 first degree A-V block, and 2 atrial fibrillation. Various heart diseases were underlying in 21 cases, including hypertension, MI, mitral and aortic regurgitation, and primary myocardial disease, and there were 4 cases with no cardiac diseases. Cause of death was cardiac in 12; MI, congestive heart failure, and sudden death. Heart weight was 410 Gm on the average (240 to 550 Gm). MI was found in 11, with stenotic index of 12/15, while it was 9/15 in group B. Lesions of the conduction system were slight to moderate (1.5 to 2.4) except left bundle branch, which showed marked changes in posterior (4.9) and anterior (4.8) fascicles. Site of interruption of the left bundle branch was the junction between the branching portion of the A-V bundle and the left bundle branch (Junctional type) in 17, and peripheral portion of the left bundle branch about 10 mm or more below the junction in 8 (Peripheral type). In conclusion, 2/3 of cases of LBBB belonged to the junctional type and most of them were not related to MI, but to the lesions caused by mechanical injuries at the septal summit. One third of the cases were as peripheral type, which was mainly related to the various types of lesions including septal ischemia (necrosis and fibrosis).
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PMID:A clinicopathological study on 25 cases of complete left bundle branch block. 44 51

Examples of toxic cardiomyopathies of various characteristics are presented. Daunomycin and doxorubicin, antineoplastic drugs, cause multifocal cardiomyopathies and intractable heart failure by cardiotoxic mechanisms; these effects are delayed and related to the cumulative dose. Cobalt caused diffuse vacuolar cardiomyopathy in chronic beer drinkers. The development of fulminant heart failure was the function of factors that increased the adsorption of cobalt or sensitized the myocardium to its cytotoxic effect. Beta-adrenergic receptor stimulant bronchodilators like isoproterenol or vasodilating antihypersensitive drugs like hydralazine are able to produce focal subendocardial necroses. This lesion is due to ischemia brought about by the acute exxagerated pharmacological effects of these compounds.
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PMID:Toxic cardiomyopathies. 79 2

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
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PMID:Amaurosis fugax: a clinical comparison. 117 55

Treatment of chronic heart failure with ACE-inhibitors has greatly improved the prognosis. In addition to ACE-inhibitors, diuretics seem to be necessary to decrease mortality, whereas the importance of cardiac glycosides has not been demonstrated unequivocally. Nevertheless, modern treatment of chronic heart failure in all stages should be a combination of diuretics, digitalis, and ACE-inhibitors rather than a stepwise addition of drugs depending on the severity of the disease. An increased heart rate leads to increased myocardial O2-consumption, decreased O2-supply, ischemia, and reduced contractility. Betablocker-induced reduction of heart rate does, however, not necessarily improve symptoms or hemodynamic conditions. The optimal heart rate in large failing hearts is not known yet. Probably, it is dependent on the type and severity of myocardial disease or impairment. In this respect, the sarcoplasmatic release and uptake of Ca2+ plays the most important role in the disordered force-frequency-relation in chronic heart failure.
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PMID:[Clinical aspects of differential drug therapy of chronic heart failure]. 129 Mar 10

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Sudden death accounts for about 15-20% of all natural fatalities in the industrially developed world. Most of the victims have a substrate of extensive myocardial injury caused by coronary heart disease, cardiomyopathy and hypertensive heart disease. In most cases, the immediate cause of death is triggered by ventricular tachycardia which degenerates into ventricular fibrillation. Changes in myocardial electrical properties may be critically modified by ischemia, imbalance in the autonomic nervous system, electrolytic disorders, and haemodynamic factors. We review the causes of sudden cardiac death, giving special attention to the effect of beta-adrenoceptor blockade as a preventive measure.
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PMID:[Sudden cardiac death. Significance of beta blockaders]. 135 74

Our purpose in this article is to examine the hypothesis that both myocardial disease and ischemia can alter the electrophysiologic function of the ion channels responsible for the cellular electrical activity of the heart. Changes in the intracellular and extracellular milieus occur during ischemia and can alter the electrophysiology of several species of ionic channels and the cellular electrophysiologic activity of cardiac myocytes. Included are 1) changes in extracellular [K+] and pH and in intracellular [Na+], [Ca2+], and pH; 2) accumulation of noxious metabolic products such as lysophosphatidylcholine; and 3) depletion of intracellular ATP. Finally, ischemia or disease (e.g., hypertrophy) can alter the electrophysiology of at least two types of K+ channels, the A-like channels underlying the transient outward current and the inward rectifier, by mechanisms that apparently do not involve alteration of either the intra- or extracellular milieus. Findings suggest that the expression of cardiac A-like channel function can be altered by hypertrophy and that at least one intrinsic conductance property of the inward rectifier can be altered by ischemia. We speculate that the control of expression, function, and regulation of cardiac ion channels can be affected at the molecular level by heart disease and myocardial ischemia.
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PMID:Connections: heart disease, cellular electrophysiology, and ion channels. 137 69


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