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)

The most common cardiotoxic effects of 5-fluorouracil (5-FU) are chest pain and ischemic ECG abnormalities. Coronary vasospasm may be the underlying mechanism. If so, prophylactic treatment with calcium channel blockers might have a beneficial effect. In the present study, prophylaxis with verapamil (120 mg three times daily) was given to 58 patients with esophageal or advanced head and neck carcinoma during induction chemotherapy with cisplatin and continuous infusion with 5-FU. Signs of ischemia appeared in 12% of the patients as compared to 13% in a previously studied compatible group of patients not receiving prophylaxis. The study does not support the hypothesis that prophylactic treatment with verapamil reduces the incidence of ischemia in patients undergoing 5-FU treatment. Verapamil might, however, modify the adverse cardiac effects of 5-FU by preventing supraventricular tachyarrhythmia.
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PMID:Failure of preventing 5-fluorouracil cardiotoxicity by prophylactic treatment with verapamil. 227 19

The effects of single-vessel coronary occlusion on simultaneously evaluated right (RV) and left ventricular (LV) performance were assessed and compared with LV perfusion patterns in 25 patients with variant angina. Coronary spasm involved the right coronary artery in 15 patients (group 1) and the left anterior descending coronary artery in 10 patients (group 2). Biventricular function was assessed by radionuclide angiography under basal conditions, during spontaneous or ergonovine-induced ischemia, and after resolution of the ischemic attack. Myocardial perfusion was assessed by thallium 201 scintigraphy in 21 patients of this series during superimposable ischemic episodes. In group 1, ischemia caused RV (14 of 15 patients) and LV (13 of 15 patients) regional dysfunction with significant reduction in RV and LV ejection fractions. The interventricular spetum was involved in six of 15 patients, causing a more pronounced LV impairment. In group 2, all patients showed septal dyssynergies associated with a reduction of LV ejection fraction; absent or trivial RV involvement was observed. In both groups, LV perfusion defects were present in all patients with LV wall motion abnormalities during ischemia, matching the site of regional dyssynergies. Thus, in a group of patients with variant angina and single-vessel disease, transient occlusion of the right coronary artery directly caused RV and LV impairment; in these patients, the extent of LV but not RV dysfunction appeared related to the presence of septal ischemia. Vasospasm of the left anterior descending coronary artery consistently caused LV dysfunction not associated with secondary effects on RV systolic function.
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PMID:Behavior of right and left ventricles during episodes of variant angina in relation to the site of coronary vasospasm. 229 62

Anesthesia-induced coronary vasospasm has been reported only rarely. We report a case, without previous cardiac history, in which immediately after anesthesia induction a marked ST elevation was noted on the EKG monitor. Premature ventricular contractions as well as non-sustained ventricular tachycardia were noted. These changes resolved immediately after nitroglycerin infusion and 75 mg of lidocaine were given. A coronary angiogram revealed normal coronary arteries and left ventriculogram. Ergonovine stimulation was not performed. The patient was discharged home on calcium entry blockers and nitrates. Exercise stress test two weeks after discharge was negative for ischemia. Induction of anesthesia triggering coronary spasm has been reported rarely, and to our knowledge never in the presence of angiographically normal coronary anatomy. Coronary vasospasm with typical EKG changes--namely, ST elevation and ventricular arrhythmias--has to be included as a possible complication of general anesthesia. Recognition of this syndrome allows prompt treatment and prevention of future episodes.
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PMID:Coronary artery spasm induced by anesthesia: a case report and review of the literature. 229 59

To analyze the usefulness of a single exercise test to predict the presence of fixed obstructive coronary artery disease in patients with active coronary spasm, 91 consecutive patients with angiographically proven symptomatic coronary artery spasm who had performed a symptom-limited exercise test within the week before diagnostic coronary angiography were studied. Coronary angiography revealed significant coronary obstructions in 61 patients (67%). According to the type of angina, the prevalence of significant coronary stenosis was 53% for patients with angina at rest, 68% for those with effort angina, and 92% for those with mixed angina. Exercise-induced ST segment elevation was present in eight patients (9%), ST segment depression was seen in 37 patients (41%), and no ST abnormalities in 46 (50%). There was not a significant relationship between the ST segment response to exercise and the clinical variables assessed except for coronary anatomy. Abnormal exercise test results were significantly more frequent in patients with significant coronary obstructions than in those without significant coronary occlusions (62% versus 23%; p less than 0.01). ST elevation was not useful to predict the presence of fixed coronary lesions. However, ST depression strongly suggested the presence of underlying coronary lesions with a sensitivity of 54%, a specificity of 87%, and a positive predictive value of 89%. Using this criterion, 65% of the patients were correctly classified. The results indicate that despite the functional component of ischemia in patients with coronary spasm, ST segment depression with exercise is still a highly specific sign with a high positive predictive value for the presence of significant coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The value of exercise testing in patients with coronary artery spasm. 203 10

The action of endothelin-1 (ET-1) in canine and porcine coronary artery ring preparations and perfused canine and porcine myocardium was examined in vitro to determine the site of action of ET-1 in the coronary vasculature. ET-1 had a vasoconstrictor effect that was more potent in smaller diameter ring preparations. The EC50s for both canine and porcine ring preparations decreased with a decrease in vessel diameter and the EC50 of ET-1 in the perfused myocardium was three to four times lower than in the smallest ring preparation. The results suggest that ET-1 may cause cardiac ischemia by constriction of resistive vessels rather than by epicardial coronary artery spasm.
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PMID:Endothelin-1 is a potent constrictor in conductive and resistive coronary arteries. 247 1

Nitrates are old drugs, introduced into medical treatment more than 100 years ago, initially as a homeopathic remedy against headache (1850), and only later against angina pectoris (1867). Their typical hemodynamic, antiischemic effects were described in man in the 1950s and 1960s. They include: a reduction in venous return, lowering of the abnormally increased left ventricular enddiastolic pressure during ischemia, a decrease in left ventricular systolic wall stress, and changes in left ventricular geometry resulting in a decrease of myocardial oxygen consumption. The vasodilatory effect on large epicardial coronary arteries, especially on eccentric stenoses through relaxation of vascular smooth muscle tone was described even more recently (1980). This effect proved to be of considerable clinical importance both in angina at rest, that is during a primary increase in vasomotor tone (coronary artery spasm) as well as in angina provoked by exercise, where the increase in vasomotor tone and in the degree of stenosis is often due to a rise in alpha-sympathetic tone. The relaxing effect on the large coronary arteries is regarded as additive to the one on venous tone. The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. The tendency for coronary arteries to constrict in presence of atherosclerosis is explained by the lack of EDRF, especially in the region of atherosclerotic plaques where the endothelium is often absent or has lost its endocrine function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The mechanism of action of nitrates, 1988 status]. 251 90

The calcium entry-blocking drugs produce effects on the coronary vasculature that might be expected to exert anti-ischemia activity. Although these agents cause little vasodilation of the epicardial coronary arteries during basal conditions, they block vasoconstriction that can increase stenosis severity during isometric exercise and interrupt coronary artery spasm in patients with variant angina. Administration of the calcium blockers causes transient vasodilation of the coronary resistance vessels, followed by decreased responsiveness to a brief ischemic stimulus. This results in decreased coronary reactive hyperemia after transient coronary occlusion. By preventing excessive ischemic vasodilation of the resistance vessels, these agents can enhance perfusion of the subendocardium distal to a flow-limiting coronary stenosis. The calcium entry blockers have relatively little effect on the immature coronary collateral vessels that exist at the time of acute coronary occlusion. Diltiazem, however, has been demonstrated to increase collateral blood flow in animals in which chronic coronary occlusion has resulted in growth of moderately well-developed collateral vessels.
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PMID:Effects of calcium entry blockade on myocardial blood flow. 255 78

The incidence of perioperative myocardial ischemia and associated cardiac complications in patients with coronary artery disease (CAD) varies widely, as reported in the literature. Much of the confusion and contradictions surrounding this issue can be attributed to differences in populations studied, study protocols, and techniques employed to diagnose myocardial ischemia and infarction. Data obtained in recent years have indicated that a large proportion of intraoperative myocardial ischemic events are unrelated to hemodynamic aberrations. Coronary vasospasm and blood flow redistribution have both been suggested as important mechanisms for ischemia during anesthesia and surgery in patients with CAD. These findings challenge our concepts of how ischemia might be prevented by maintaining systemic hemodynamics within "normal limits". They also emphasize the importance of establishing new and more sensitive methods to detect myocardial ischemia in the operating room and recovery area. This paper focuses on myocardial ischemia related to coronary vasomotion during anesthesia and surgery.
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PMID:Coronary vasomotion during anesthesia. 265 73

A 27-year-old man was accidentally given 2 mg intravenous epinephrine instead of 2 mg naloxone. He immediately developed chest pain, nausea, and diaphoresis. An ECG taken shortly after the epinephrine administration showed widespread ischemia. Forty-five minutes later the tracing still showed an early repolarization pattern, but ST elevation was less marked and the patient was asymptomatic. Serum potassium was 3.2 mEq/L and serum catecholamines, drawn approximately 20 minutes after the epinephrine administration, were 10 times normal (dopamine, 173 ng/L; epinephrine, 1,628 ng/L; norepinephrine, 1,972 ng/L). There are seven other reports of intravenous epinephrine overdose in the English literature. Two of the previously reported cases had 12-lead ECGs within the first hour. In both there was evidence of transient ischemia similar to that observed in this case. Most of the patients had symptoms consistent with angina, and several developed pulmonary edema. These findings suggest that, in humans, large intravenous doses of epinephrine are likely to produce coronary artery spasm and may decrease coronary artery perfusion.
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PMID:Coronary artery spasm induced by intravenous epinephrine overdose. 275 14

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.
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PMID:Myocardial infarction and sudden death after sport: acute coronary angiographic findings. 276 51


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