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)

Six patients who survived episodes of coronary arterial spasm occurring immediately after coronary bypass grafting were followed up for 15 to 30 (mean 20) months after operation. In all patients coronary spasm occurred in an unobstructed dominant right coronary artery and caused inferior transmural ischemia. Sudden circulatory collapse occurred in five of the six patients as a consequence of acute coronary spasm. All patients were treated with nitroglycerin followed by nifedipine. No patient has had recurrent angina or other evidence of spontaneous coronary spasm since surgery. Cardiac catheterization studies, including ergonovine maleate testing, were repeated 3 to 12 months after surgery in five of the six patients. The right coronary artery and all bypass grafts were patent in all five. Four patients had new inferior wall motion abnormalities. Ergonovine provoked focal right coronary arterial spasm in one patient. It is concluded that manifestations of coronary spasm after myocardial revascularization range from asymptomatic S-T segment elevation to severe hypotension. These episodes of perioperative spasm may cause myocardial necrosis. Coronary spasm has not recurred in patients who survived perioperative spasm, but some patients may have a continued predisposition to development of coronary spasm late after surgery.
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PMID:Perioperative coronary arterial spasm: long-term follow-up. 681 Jun 84

Recent concepts on the role of coronary artery spasm and other forms of vasoconstriction in coronary artery disease are studied with particular reference to episodes of transient ischemia and their therapeutic implications. The possible contribution of spasm and other obstructive mechanisms such as platelet agregation, to the different forms of angina, myocardial infarction and sudden death, is analysed in the light of clinical observations, some of which have not previously been reported. Based on these concepts and clinical considerations, new orientations for future research and treatment are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives and calcium antagonists has led to a reduction in mortality and in the incidence of myocardial infarction over periods ranging from 2 to 4 years.
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PMID:[The role of spasm in angina pectoris, myocardial infarction and sudden death. Indications for future research and treatment]. 681 Jul 99

Ischaemic ST-segment changes may occur in patients with coronary artery disease when myocardial oxygen consumption is increased as a result of hypertension, tachycardia or increased contractility. Ischaemia can also occur as the result of decreased coronary perfusion pressure caused by hypotension or coronary artery spasm. We report ST-segment depression in the absence of hypertension, tachycardia or hypotension. The response to bolus intravenous nitroglycerin suggested coronary artery spasm as the cause.
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PMID:Bolus intravenous nitroglycerin for ST-segment depression not associated with increased myocardial oxygen demand. 681 34

To examine the possible existence of collateral circulation during coronary artery spasm, we attempted to visualize the transient appearance of collateral vessels that could serve to salvage otherwise jeopardized ischemic areas. In three patients with vasospastic angina, total spastic obstruction of a major coronary artery was associated with transient collateral augmentation, which was supplied by the nonspastic artery during anginal period associated with ST-segment depression. These collateral vessels disappeared when the angina and ST changes resolved after nitroglycerin administration. These findings suggest that the collateral blood supply could transiently occur through preexisting vessels to perfuse the ischemic area during coronary artery spasm and that such collateral flow could have a role in preventing transmural myocardial ischemia, resulting in a lesser degree of ischemia associated with ST-segment depression.
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PMID:Transient collateral augmentation during coronary arterial spasm associated with ST-segment depression. 682 15

We studied plasma catecholamine levels in 10 patients with frequent spontaneous episodes of coronary artery spasm to evaluate the role of the sympathetic nervous system. Peripheral venous norepinephrine in supine and upright postures, urinary excretion of catecholamines, and functional testing of the sympathetic nervous system did not differ from the same measurements in control subjects. Arterial and coronary sinus levels of norepinephrine and epinephrine drawn early in ischemia were not elevated over baseline; coronary sinus norepinephrine levels were higher than those in arterial samples and rose from 315 +/- 32 (pg/ml +/- SE) at the onset of ST elevation to 490 +/- 49 pg/ml late in ischemia (p less than 0.05). Plasma epinephrine levels, higher in arterial than coronary sinus samples, also rose significantly only late in ischemia, from 44 +/- 14 pg/ml to 148 +/- 35 pg/ml (p less than 0.05) in arterial blood and from 33 +/- 10 pg/ml to 108 +/- 29 pg/ml in coronary sinus samples (p less than 0.05). Generalized sympathetic nervous system activation is not likely to be the sole cause of coronary artery spasm.
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PMID:Arterial and coronary sinus catecholamines in the course of spontaneous coronary artery spasm. 685 35

We administered ergonovine and used both electrocardiographic monitoring and thallium-201 [201Tl] imaging to detect reversible ischemia in 100 patients. Patients already established as having coronary artery spasm and those with nonbypassed, proximal, high-grade coronary artery stenosis were excluded. No complication occurred in any patient. The use of thallium imaging in addition to electrocardiographic monitoring resulted in a higher degree of sensitivity than did ECG monitoring alone. Fourteen patients demonstrated evidence of coronary artery spasm as documented by 201Tl imaging but of the 14, significant ECG changes occurred in only 50%, and classic ST segment elevation in 21%. Thus, in carefully selected patients the noninvasive provocation of coronary spasm can be accomplished safely, but ECG monitoring must be combined with thallium-201 imaging to achieve an acceptable degree of sensitivity.
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PMID:Noninvasive ergonovine maleate provocative testing for coronary artery spasm: the need for routine thallium-201 imaging. 688 99

We describe a 50-year-old man with rest angina and ECG anterior wall subendocardial ischemia. During coronary angiography, a high-grade proximal left anterior descending stenosis was present. Spontaneous total spasm distal to the lesion occurred without chest pain or ST segment shifts. The patient underwent aortocoronary bypass surgery and continued to have the same pain as preoperatively. Repeated catheterization demonstrated total occlusion of the bypass graft with unchanged native coronary vessels. This suggests prolonged coronary artery spasm as the mechanism for graft occlusion.
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PMID:Coronary artery pain. A possible cause of graft occlusion in a patient with fixed obstructive coronary artery disease. 696 14

In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was perforned during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III). Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST-segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST-segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery. We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST-segment shift.
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PMID:Coronary arterial spasm in angina at rest associated with transient ST-segment changes. 737 78

Coronary artery spasm is not rare in patients with coronary artery disease, but the influence of regional anesthesia on spasm-induced myocardial ischemia is not known. We investigated the effects of spinal anesthesia on myocardial ischemia during coronary artery spasm in rats, and compared these with the effects of an alpha- and beta-adrenergic antagonist, and an alpha-adrenergic agonist. An intraaortic catheter was inserted via the right internal carotid artery so that the tip of the catheter was placed near the coronary ostium. An intrathecal catheter was placed at lumbar level. Coronary spasm was induced by the intraaortic injection of methacholine, and we identified the thresholds of myocardial ischemia, defined as the dose of methacholine that induced ST-segment elevation. Subsequently, the thresholds were determined after spinal anesthesia, and after the intraaortic injection of phentolamine and propranolol. The thresholds of myocardial ischemia increased significantly after intrathecal bupivacaine. In contrast, the threshold did not change after the injection of phentolamine. The thresholds increased significantly after the injection of propranolol. Methoxamine significantly decreased the threshold of ischemia. These results demonstrated that spinal anesthesia attenuated myocardial ischemia during methacholine-induced coronary spasm. This effect was equivalent to that of propranolol.
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PMID:Spinal anesthesia attenuates myocardial ischemia during coronary artery spasm induced by intraaortic methacholine in rats. 748 38

A 54 years-old man with a history of migraine, suffered from chest pain together with ST-segment elevation related to the intake of drugs against migraine attacks. The coronary arteriography showed normal coronary arteries. We suggest coronary artery spasm as the most probable cause of ischemia. We conclude that vasoactive drugs against migraine must be utilized with caution, or even avoided in patients with chest pain suggestive of myocardial ischemia.
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PMID:[Variant angina pectoris related to the treatment of migraine]. 756 65


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