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)

Primary prevention of death from ischemic heart disease requires further understanding of the pathogenesis of this disorder. Cellular defects of cholesterol metabolism may be more significant markers that serum lipid levels for the identification and treatment of atherosclerotic risk. Coronary spasm has been shown to be an important cause of ischemia in the presence and absence of atherosclerotic lesions. Careful manipulation of physiologic variables with vasodilator agents during cardiopulmonary bypass can substantially alter the myocardial oxygen supply-demand relation, thereby minimizing ischemic injury. The cellular basis for loss of mechanical function during ischemia and the factors that determine irreversible injury are yet unknown.
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PMID:Pathophysiology of myocardial infarction. 19 8

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.
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PMID:Alternans of the ST segment in Prinzmetal's angina. 83 98

Prinzmetal's variant angina is commonly referred to as a syndrome apart from the usual spectrum of atherosclerotic disease. 2 well-studied patients with this form of angina gave past histories compatible with classical angina. They were found to have, in addition to severe atheromatous lesions, coronary artery spasm resulting in complete obstruction of the vessel during Prinzmetal attacks. The concomitant electrocardiographic ST segment elevations are probably the reflection of transmural ischemia injury resulting from the transient complete occlusion of the corresponding coronary artery. Electrocardiograms taken during milder resting anginal attacks showed minimal nonspecific changes of the electrocardiogram or T wave inversions which may possibly reflect less severe ischemia, secondary to milder coronary spasm. These observations support the possibility that at least in some cases, Prinzmetal's angina may just be a phase in the life history of patients with atherosclerotic disease, during which recurrent severe coronary spasms may occur.
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PMID:Another look at Prinzmetal's variant angina. 91 86

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
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PMID:Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases. 99 29

Six patients (2 males and 4 females, mean age of 46 years) with X syndrome were reported in this paper. All patients presented with typical exertional angina pectoris. In 4 patients the angina had a variable threshold of onset, it often occurred at rest and occasionally nocturnally. The electrocardiogram during chest pain showed ST segment depression of more than 0.05-0.1 mV in all 6 patients. The treadmill or bicycle ergometer exercise test was positive in 4 cases (ST segment depression > 0.1 mV), equivocal in 1 (ST segment < 0.1 mV) in whom the 201Tl exercise myocardial perfusion scan showed sign of ischemia, and negative in 1 in whom atrial pacing at heart rate of 135 beats/min induced angina and ST segment depression of 0.1-0.15 mV. Echocardiograms and X ray chest films revealed no sign of ventricular hypertrophy or enlargement. The 201Tl exercise myocardial perfusion scan was performed in 5 patients, which showed signs of ischemia in 4 patients and suspected to have ischemia in 1. Left ventriculograms and coronary angiograms were normal in all 6 patients. Ergonovine provoking test (total dose of 0.4 mg) was negative in 5 patients, it was not performed in 1 in whom there was no evidence of coronary artery spasm by angiogram during appearance of electrocardiographic ischemic changes and chest pain. Left ventricular endomyocardial biopsy was performed in 1 patient, which showed significant smooth muscle cell proliferation in the medial layer of a small artery with diameter of 62.5 mu which produced narrowing of the lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[X syndrome--report of six cases]. 130 21

A number of studies have addressed the response to calcium antagonists, used alone or combined with other therapy, in patients with silent myocardial ischemia (SMI). Nifedipine, the first calcium antagonist to be studied, was shown to be superior to pindolol in patients with effort angina. Although both nifedipine and diltiazem significantly reduced episodes of ST depression, compared with placebo, in patients with stable effort angina, the addition of nifedipine to diltiazem removed the beneficial effect of diltiazem in another study. Studies have shown a reduced incidence of ischemic episodes during nicardipine treatment in patients with ambulatory ischemia, predominantly SMI, and rest angina due to coronary artery spasm. Other workers similarly reported that verapamil was superior to both placebo and propranolol in reducing painful and painless ischemia in patients with angina at rest. It has been demonstrated that, compared with placebo, nifedipine reduced ischemic episodes by 50% and also markedly reduced total ischemic time in totally asymptomatic men with coronary artery disease and SMI. It was suggested that the well-documented increase in SMI occurring between 0600 and 1200 h was reduced, but not eliminated, by nifedipine. Diltiazem may also attenuate the circadian variation in SMI. Nifedipine has been shown to be particularly effective in SMI when combined with a beta-blocker. This has been substantiated in a large group of patients; both drugs reduced the number of episodes of SMI when used as monotherapy, and the combination decreased the incidence by 95%. These findings collectively indicate that calcium antagonists are effective in reducing or preventing SMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effects of calcium antagonists in silent ischemia. 136 8

The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the "high") in all patients. However there was no significant change in coronary artery diameter (assessed by computer-assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two-dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p less than 0.007). Despite a significant elevation in heart rate (average 56%, p less than 0.007), mean systemic arterial pressure (average 12%, p less than 0.05) and rate-pressure product (average 69%, p less than 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does cocaine cause coronary vasospasm in chronic cocaine abusers? A study of coronary and systemic hemodynamics. 156 28

Electrocardiographic signs of diffuse three-vessel coronary artery spasm may show various findings including no ST segment changes, according to whether or not a difference of an electrical gradient develops between the anterior and inferior regions because of global ischemia. This study suggests that diffuse three-vessel coronary artery spasm must be considered when the 12-lead electrocardiogram (ECG) shows no important ST segment changes with episodes of angina and diffuse coronary artery spasm during an ergonovine provocation test in patients with strongly suspected variant angina.
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PMID:Various 12-lead electrocardiographic findings of diffuse three-vessel coronary artery spasm. 157 31

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

An anaphylactic reaction in the isolated perfused heart is characterized by a drastic coronary constriction, arrhythmias, and an impairment of contractility. In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to ascertain the electrocardiographic and cardiovascular changes during systemic hypersensitivity reactions. In addition, an attempt was made to differentiate cardiac from respiratory events. In guinea pigs, sensitization was produced by s.c. administration of ovalbumin together with Freund's adjuvant solution. Fourteen days after sensitization, the effects of an i.v. infusion of ovalbumin were tested in the anesthetized guinea pigs, which were ventilated with room air or 100% oxygen. A second administration of the antigen induced the development of cardiovascular collapse, leading to death within 12 min. Within 3 min, cardiac output decreased by 90% and end-diastolic left ventricular pressure increased significantly, indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in the form of atrioventricular block. Left ventricular contractility declined continuously within the first 4 min. Finally, after 4 min, blood pressure steadily decreased. During ventilation with room air, severe hypoxia developed, with arterial PO2 decreasing from 94 mmHg to 14 mmHg after 3 min. However, under ventilation with 100% oxygen, a dissociation between cardiac damage and respiratory distress occurred. Myocardial ischemia and signs of cardiac failure preceded the development of hypoxia by a significant time interval. It is to be concluded that cardiac damage is a primary event in anaphylactic shock. Furthermore, the electrocardiographic signs of ischemia are interpreted as a result of coronary artery spasm.
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PMID:Systemic anaphylaxis--separation of cardiac reactions from respiratory and peripheral vascular events. 221 74


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