Variant angina is defined by chest pain occurring at rest associated with transitory ST segment elevation on ECG, and is caused by a spasm of a coronary artery. Frequently, variant angina is associated with atherosclerotic coronary obstruction and patients with normal coronary arteries are rare. Patients with variant angina and normal coronary arteries have good prognosis, and the development of ventricular arrhythmias or sudden death is rare. The authors present two cases of sudden cardiac death in patients with variant angina and normal coronary arteries. (+info)
Usefulness of massive oral nicorandil in a patient with variant angina refractory to conventional treatment.
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A 67-year-old man, who was previously diagnosed with vasospastic angina and treated with standard therapy, was admitted to our hospital because of recurrent chest pain refractory to sublingual nitroglycerin. Admission electrocardiography revealed ST segment elevation in II, III and aV(F), and his symptoms were relieved by intravenous bolus administration of nicorandil. He was diagnosed to have active variant angina, and remained symptomatic even after treatment with calcium antagonists and nitrates at optimal doses. Intravenous bolus administration of nicorandil was consistently effective to relieve his symptoms. Anginal attack was finally prevented by massive oral nicorandil in addition to conventional treatment. (+info)
Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms.
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OBJECTIVE: A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms. MATHEMATICAL MODEL: The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism. CLINICAL OBSERVATION: To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (> 1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability < 200 ms) over a wide range of RR intervals (> 700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39.3%) in whom coupling interval/RR diagrams were not definitive. CONCLUSION: These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms. (+info)
Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.
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Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 micrograms/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 micrograms/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction. (+info)
Postpartum acute myocardial infarction induced by ergonovine administration.
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We report a primigravida woman with acute myocardial infarction caused by coronary artery spasm induced by intravenous administration of methyl ergometrine maleate just after delivery. Despite the frequent usage of ergot derivatives to promote uterine contractions, cardiac complications related to this drug are rare. Myocardial infarction may be overlooked in young women in the early postpartum period. Careful monitoring and prompt evaluation should be performed when this drug is administered for obstetrical purposes. (+info)
Prinzmetal variant angina associated with multiple sclerosis.
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We report the case of a young woman with an acute coronary syndrome in the setting of a multiple sclerosis exacerbation. A connection between the 2, possibly caused by spinal cord pathology, is suggested. (+info)
A case of vasospastic angina resulting from coronary emboli in a patient with prosthetic valves.
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In addition to coronary atherosclerotic disease, coronary thromboembolism can also lead to acute coronary syndromes. However, coronary thromboembolism due to prosthetic heart valves is very rare and not very well-known. It have been reported only a few cases. In this paper, we present a rare case with vasospastic angina pectoris secondary to coronary thromboembolism in a patient with prosthetic heart valves. (+info)
Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis.
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BACKGROUND: It is not known whether multivessel coronary spasm occurs spontaneously in patients who have variant angina (VA) with demonstrated multivessel spasm induced by intracoronary injection of acetylcholine (ACh). Regional left ventricular (LV) diastolic dysfunction or wall motion abnormality may persist after an episode of coronary vasospasm. Color kinesis (CK) is a recent development that facilitates the echocardiographic evaluation of regional diastolic wall motion. METHODS AND RESULTS: Regional diastolic wall motion was evaluated using CK in 26 patients with VA within 1 week of the last episode of angina. The LV segmental filling fraction in the short-axis view during the first 30% of the diastolic filling time, expressed as a percentage, was used to objectively identify postischemic diastolic endocardial motion asynchrony. Diastolic asynchrony or regional LV delayed relaxation was noted in all 26 (100%) patients and in 14 (54%) it was detected in multiple vascular territories, suggesting multivessel spasm. Multivessel spasm was induced by ACh in 11 (79%) of the patients with suspected multivessel spasm by CK. In 11 (92%) of the 12 patients with multivessel spasm induced by ACh multiple regions of delayed relaxation had been noted by CK. The regions of delayed relaxation were largely consistent with the territories perfused by the arteries reacting to ACh (sensitivity: 96%, specificity: 91%). CONCLUSION: ACh induced spasm in the same coronary arteries as those perfusing the regions with delayed diastolic wall motion detected by CK in most of the patients with VA, suggesting that multivessel spasm does occur spontaneously in patients with susceptible arteries. (+info)