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 (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

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

A frequent clinical problem is to document the elusive entity of electrocardiographically silent myocardial ischemia. Since echocardiography offers a practical tool to detect reversible mechanical changes due to ischemia, 32 patients with angina on effort, and coronary artery disease, and 15 patients with angina at rest were studied. In all 47 patients electrocardiographic changes during effort or rest pain were inconclusive. Combined 12 lead electrocardiographic and 2-Dimensional echocardiographic monitoring were performed: during ergonovine testing in the 15 patients with angina at rest; during dipyridamole testing in the 32 patients with effort angina and a non diagnostic stress test. Interpretable echocardiograms were obtained in all the patients studied. Positivity of both the Ergonovine-Echocardiographic test and the Dipyridamole-Echocardiographic test was based upon the detection of regional transient asynergy. Of the 15 patients who had chest pain at rest in the absence of diagnostic electrocardiographic changes, Ergonovine-Echocardiographic test was positive in 6 (40%). Of the 32 patients who had chest pain in absence of diagnostic electrocardiographic changes during exercise stress testing, the Dipyridamole-Echocardiographic test was positive in 18 (56%). Echocardiographic monitoring in combination with provocative testing (ergonovine and dipyridamole) may be a practical, non invasive, inexpensive tool which is feasible in all patients with good basal echocardiograms and is able to unmask electrocardiographically silent myocardial ischemia by providing objective mechanical evidence of the ischemic event.
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PMID:Echocardiographic documentation of myocardial ischemia in presence of angina pectoris without ST-T changes. 375 1

During Ergonovine-test a patient with Prinzmetal angina presented (in I, aVL, V3-V6) ST downsloping which, after a temporary phase of alternative normalization (AST) beat to beat in V5, progressed to ST upsloping with typical angina. The M-mode echo-study first discovered, before than ecg, septal impairment (hypokinesia which increased to akinesia in the AST phase) and also asynergy of posterior wall of left ventricle. After intravenous nitrate echo-alterations reversed more rapidly than ecg one (transitional phase of ST decrease). The authors relate the AST to temporary alternative pseudonormalization caused by a phase of electrical instability during progressive vasospastic ischemia involving first the endocardial layers and after the epicardium of a single myocardiocoronary district. Probably also other partially opposite ischaemic districts, as suggested from echo data of posterior wall asynergy took a part in these events. This rare ST-alternans type as new pseudonormalization phenomenon and the usefulness of echo-study during ischaemic attacks are stressed.
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PMID:[Clinical, electrocardiographic and echocardiographic findings in a case of vasospastic angina with alternating pseudonormalization of the ST segment]. 383 2

In 14 consecutive patients with variant angina we investigated the possible role of coronary alpha-adrenergic receptors in the genesis of coronary spasm. In eight patients, computerized, beat-by-beat analysis of the electrocardiogram recorded during continuous Holter monitoring failed to reveal any increase of heart rate and corrected QT interval (both indexes of cardiac sympathetic activation) in the period preceding the onset of ST segment changes in 197 episodes of ischemia caused by coronary spasm. In the same patients, analysis of the circadian distribution of ischemic episodes revealed a significantly higher incidence in the early morning hours, when sympathetic activity is at the lowest level. Twelve patients underwent serial provocative testing with cold pressor, phenylephrine, or norepinephrine infusion and administration of ergonovine maleate. Ergonovine consistently reproduced coronary spasm in all 12 patients, while results of cold pressor testing were positive in only one. Infusion of phenylephrine (eight patients) or norepinephrine after beta-blockade (four patients) failed to precipitate myocardial ischemia. In five patients infusion of phentolamine at the highest tolerated dose did not reduce significantly the number of ischemic attacks when compared with placebo. In contrast to results of previous reports, our data seem to rule out the hypothesis that an increase of sympathetic outflow to the heart plays an important role in the genesis of coronary spasm. We cannot, however, exclude the possibility of localized alpha-stimulation of epicardial arteries.
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PMID:alpha-Adrenergic receptors and coronary spasm: an elusive link. 631 61

Ergonovine administration during coronary angiography is frequently used to rule out coronary spasm as a cause of chest pain. We performed this study to determine which electrocardiographic variables (other than ST segment elevation with pain) and which chest pain characteristics might be predictive of ergonovine test outcome in patients without obstructive coronary disease. Thirty-one patients had an electrocardiogram recorded during chest pain. Three of four patients (75%) who had an ischemic electrocardiogram with pain had a positive ergonovine test while only 1 of 27 (4%) patients who had a nonischemic electrocardiogram during chest pain had a positive ergonovine test (p less than 0.001) Pain that occurred predominantly at rest was present in five of five patients with positive ergonovine tests but pain occurring predominantly at rest was also present in 76% of patients with negative ergonovine tests (85%). Prompt relief of pain with nitroglycerine was also present in all patients with a positive ergonovine test but was also seen in 58% of patients with a negative test (NS). Association of chest pain with nausea, vomiting, diaphoresis, or radiation to left arm, jaw or neck were similarly poor predictors of ergonovine test outcome. We conclude that ergonovine testing in patients without obstructive coronary disease is of low yield if an electrocardiogram recorded during pain does not show evidence of ischemia. Historical features of the chest pain are not good predictors of test outcome.
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PMID:Provocative ergonovine testing in patients without obstructive coronary disease. 641 49

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.
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PMID:Ventricular arrhythmias during ergonovine-induced episodes of variant angina. 641 72

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.
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PMID:Ergonovine-induced myocardial ischemia: no role for serotonergic receptors? 673 73

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

The authors present the role of the Ergonovine test in establishing the diagnosis of the angina produced by coronary spasm. ECG alterations induced by Ergonovine, like transparietal ischemia (monophasic wave) or subendocardic ischemia, not only make possible a correct diagnosis, but they also underline the mechanism of angina and the therapeutical measures. Severe arrhythmias and the danger of sudden death are the two elements illustrating the importance of this coronary spastic mechanism. Nitroglycerine, isosorbidinitrate and calcium antagonists are the drugs of election for the prevention and also for the treatment of coronary spasm.
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PMID:Ergonovine test in coronary disease. 712 9


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