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The authors present a case report of self-terminating ventricular fibrillation during an episode of variant angina. The causes of ventricular fibrillation in this disorder and the possible mechanisms for its rare spontaneous interruption are discussed.
To elucidate the response of conductance and resistance vessels of the coronary artery after intracoronary isosorbide dinitrate (ISDN), we evaluated 11 patients with variant angina and 13 controls with a Doppler guidewire. Epicardial arterial diameter increased significantly after ISDN in patients with variant angina while it did not change significantly in the controls. Coronary diastolic flow velocity increased significantly in controls (p < 0.05), but was unchanged in patients with vasospastic angina. Coronary flow volume increased from 23.8 +/- 18.6 to 46.5 +/- 28.4 ml/min in patients with vasospastic angina as well as in the controls from 32.2 +/- 24.2 to 54.7 +/- 44.4 ml/min. Coronary resistance did not differ between the two groups before or after the injection of ISDN. Conductance vessels were dilated to a greater extent in the patients with variant angina. However, the response of resistance vessels did not differ significantly between the two groups.
The Food and Drug Administration has banned the sale of ephedrine-based weight-loss products because of their association with many cardiovascular adverse effects. Bitter orange is now being used as a stimulant in "ephedra-free" weight-loss supplements but was recently implicated in adverse cardiovascular sequelae. To our knowledge, this report describes the first case of variant angina associated with bitter orange in a dietary supplement.
The successive onset of spasms of distal arteries of the limbs and complicated migraine in a young migrainous woman raised the possibility of a common mechanism for both disorders. Three similar cases have been reported and two recent epidemiological studies have shown the frequent association of migraine attacks and Raynaud's phenomenon or variant angina in a individual patient. The possible role of vasospasm in triggering the migrainous aura is discussed.
BACKGROUND: ST elevation during ergometric stress test (EST) is relatively rare. Its prevalence depends upon the tested population but occurs more frequently in patients who have had myocardial infarction or variant angina. This phenomenon is very rare in patients with typical exertional angina and its pathogenesis is still unclear. MATERIAL AND METHODS: We studied a group of 75 consecutive patients with exertional angina who underwent EST and coronary angiography. A symptom limited EST was performed in the upright position on a cycloergometer with load increases of 25 watts every 3 minutes and 12 leads were monitored during all test. Coronary angiography was performed according to Judkins technique. From these patients, according to Froelicher's criteria, a group of 49 patients (age 32-68, mean 51.6 years), without myocardial infarction and/or left ventricular asynergy, was selected. RESULTS: All patients had a coronary artery disease (16 patients with 3 vessels, 11 patients with 2 vessels and 22 patients with 1 vessel disease). The EST was positive for ST depression in 31 patients (63.3%) and for ST elevation in 5 patients (10.1%), while 13 patients (26.6%) had a non diagnostic EST. The ST elevation occurs in V1-V2 and it was associated in all cases with a stenosis in the left anterior descending (LAD) artery. Therefore we divided the 19 patients with LAD stenosis into two subgroups: subgroups A (9 patients, mean age 49.6 years) with LAD stenosis > or = 90% and subgroups B with LAD stenosis between 70% and 90%. ST elevation occurs in 5 patients (55.5%) of subgroup A and in no patient of the subgroup B. Moreover, in the subgroup A ST elevation seems to be related to the anatomic localization of the stenosis: in fact it appears in 83.3% of patients with LAD stenosis located before the onset of the first diagonal branch. CONCLUSIONS: From these data it can be desumed that ST elevation in V1-V2 that occurs in patients with exertional angina and without myocardial infarction or variant angina is strongly predictive of a very important LAD stenosis.
Atherosclerotic CAD is the most common cause of cardiac chest pain in Western countries. Other cardiac syndromes may also cause anginalike pain and may be difficult to differentiate from atherosclerotic CAD. It is essential to make this distinction, because management and prognosis of these conditions are entirely different. A detailed history and, in some cases, special diagnostic methods can help make the diagnosis. When evaluating patients with anginalike chest pain and normal coronary arteries, physicians need to consider this group of diseases and tailor workup and diagnosis on an individual basis.
Prinzmetal's variant agina occurred in a 52-year-old man 10-11 h after the ingestion of alcohol, when blood levels of alcohol decreased almost to the zero level. Coronary arteriograms revealed significant narrowing in the left circumflex artery and the left anterior descending artery and minimal wall irregularity in the right coronary artery; however, both exercise and pharmacologic stress tests were negative. A withdrawal from an acute exposure to alcohol was discussed as a possible causative mechanism of the alcohol-induced Prinzmetal's variant angina in this case.
Acetylcholine (20 to 100 micrograms) was infused directly into coronary arteries in 10 patients with variant angina (group A), 13 subjects without coronary artery disease (group B) and 8 patients with significant organic coronary artery stenosis (greater than or equal to 50%) but without variant angina (group C) during coronary arteriography, to clarify the action of this agent on coronary arteries. Temporary pacing was performed at a demand heart rate of 40 beats/min while bradyarrhythmia developed. Coronary arteriography after administration of acetylcholine showed coronary vasoconstriction in all 10 patients (100%) of group A. Angina accompanied by electrocardiographic ischemic changes in 9 of 10 (90%, 7 ST-segment elevation and 2 depression) was provoked during this test. In the patients of group B, acetylcholine also induced vasoconstriction in 8 of 22 (36%) coronary arterial systems examined, chest pain in 3 (14%) and ST-segment deviation in none (0%). In the patients of group C, acetylcholine induced vasoconstriction in 3 of 9 (33%), chest pain in 2 (22%) and ST-segment depression in 1 (11%). No definite coronary artery dilation induced by acetylcholine was noted. Coronary vasoconstriction (p less than 0.05), electrocardiographic ischemic findings (p less than 0.01) and chest pain (p less than 0.01) were induced significantly more frequently in group A than in both groups B and group C. No significant difference was found between group B and group C. The coronary arteries in the patients with variant angina seem to be more susceptible to acetylcholine than those of patients without variant angina irrespective of the presence of significant atherosclerosis.
Myocardial thallium scintigraphy was performed in four subjects with variant angina and in one subject with isolated, fixed coronary obstruction. Three subjects with variant angina had short episodes of ischemic ST-segment elevation that lasted 20--100 seconds. Thallium scintigrams demonstrated excess uptake in regions judged to be ischemic by angiographic and electrocardiographic criteria. Two subjects, one with variant angina and the other with a fixed coronary lesion, had prolonged episodes of ischemia that lasted 390--900 seconds. Both had reduced thallium uptake in the ischemic regions. We conclude that myocardial reactive hyperemia is the cause of excess thallium uptake in patients with variant angina who have short episodes of myocardial ischemia.
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.
The effect of alcohol on variant angina was studied in six patients who had a history of chest pain occurring with alcohol ingestion. On alcohol testing, Holter ECG monitoring was performed and a 12-lead ECG was recorded at the time of chest pain. In five, chest pain with ST elevation occurred 5.5 to 17.5 h after the ingestion of alcohol (100 to 150 ml as ethanol). These showed recurrent ST elevation on Holter ECG, most episodes being asymptomatic. Results of provocation testing were reproducible in all four patients in whom tests were repeated and ST elevation occurred in the same leads. No complications were observed. The Holter ECG revealed a higher heart rate after alcohol ingestion. The plasma level of alcohol was zero when angina occurred and plasma epinephrine, norepinephrine and serotonin were unchanged following alcohol ingestion. Alcohol ingestion may be a useful method of provoking variant angina, particularly in those who have a history of angina related to alcohol ingestion.
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BACKGROUND: Oxidative modification of LDL has been suggested to increase coronary vasoreactivity to agonists. A deficiency of vitamin E, a major antioxidant, may be related to the occurrence of coronary artery spasm. METHODS AND RESULTS: Vitamin E levels were determined with the use of high-performance liquid chromatography in normolipidemic subjects, including 29 patients with active variant angina (group 1), 13 patients with inactive stage of variant angina without anginal attacks during the past 6 months (group 2), 32 patients with a significant (>75%) organic coronary stenosis and stable effort angina (group 3), and 30 patients without coronary artery disease (group 4). Total lipid levels in blood were calculated as total cholesterol plus triglyceride levels. The plasma alpha-tocopherol levels as well as alpha-tocopherol/lipids were significantly lower in group 1 than in groups 2 through 4. Also, the plasma gamma-tocopherol levels were significantly lower in group 1 than in groups 2 through 4. The vitamin E levels were not significantly different between group 1 patients with and those without a significant organic stenosis. In group 1, both alpha- and gamma-tocopherol levels were significantly elevated after a > or = 6-month angina-free period. The alpha-tocopherol levels in the LDL fraction were significantly lower in group 1 than in group 4. Plasma alpha-tocopherol levels were significantly correlated with those in the LDL fractions. In 6 patients of group 1 still having anginal attacks while receiving calcium channel blockers, the addition of vitamin E acetate (300 mg/d) significantly elevated plasma alpha-tocopherol levels and inhibited the occurrence of angina. CONCLUSIONS: Plasma vitamin E levels were significantly lower in patients with active variant angina than in subjects without coronary spasm, suggesting an association between vitamin E deficiency and coronary artery spasm.
We report a rare case, the second in the literature, of Prinzmetal's Variant Angina (VA) caused by cis-diamminodichloroplatinum (CDDP) infusion. We also discuss the possible underlying mechanism of ischemia.
Continuous electrocardiographic recordings during anginal attacks in patients with variant angina were reviewed. Twenty-seven attacks in 15 patients were associated with transient T-wave inversion during recovery periods of angina (type A), while in another 69 attacks in 28 patients there was no T-wave inversion (type B). In none of the patients was there an ischemic T-wave inversion during angina-free periods. Both the maximum elevation (0.79 +/- 0.57 mV) and duration (5.3 +/- 1.2 min) of ST-segment deviation of type A attacks were significantly higher and longer than those of type B (0.44 +/- 0.27 mV, 2.8 +/- 1.4 min). Ten patients who had both type A and type B attacks one time or the other were selected for further evaluation. In these 10, the duration of ST-segment elevation was significantly longer during type A attacks (5.2 +/- 1.2 min, n = 18) than during type B attacks (2.7 +/- 1.2 min, n = 20) but there was no significant difference in the maximum ST-segment elevation. Giant U-wave inversion appeared in 15% of the type A attacks, but never in type B. Therefore, the T-wave abnormality related to ischemic episodes in patients with variant angina seems to be associated with more severe ischemia of longer duration than milder episodes of transient ischemia.
Variant angina was diagnosed after coronary artery bypass surgery in six patients over a 22-month period. Although all six patients had at least occasional angina at rest preoperatively, all but one had predominantly exertional angina. After surgery, rest angina with transient ST-segment elevation appeared in all six after an asymptomatic interval of 1 week to 4 years. In two patients the involved artery had not been bypassed, in two patients it was perfused by a patent graft and in two patients the graft to the involved vessel was occluded. Treatment with calcium antagonist drugs (four cases) or isosorbide dinitrate (one case) eliminated symptoms; one patient spontaneously became asymptomatic. The diagnosis of variant angina should be considered when rest angina occurs after bypass surgery, particularly if exertional angina is absent and grafts are patent.
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Functional factors are known to precipitate ischemic episodes at rest in variant angina, but the role of fixed coronary lesions is still debated. The prevalence, extent, severity and prognostic implications of organic coronary stenoses in variant angina were evaluated in 162 patients with transient ST segment elevation documented during hospitalization. Seventy-eight patients had normal coronary arteries or single-vessel coronary lesions (group 1) and 84 patients had multivessel coronary stenoses (group 2). Both groups were followed up for 82 +/- 41 months. Angiographically normal coronary arteries were observed in only 11 patients (7%). In 59 patients with single-vessel coronary stenoses, the internal luminal diameter was reduced by 51 +/- 12%. There were 20 deaths (16 from cardiac causes) during the 5-year follow-up. Kaplan-Meier survival analysis revealed a significantly lower 5-year survival rate in group 2 (80.1%) compared to group 1 (94.6%, p = 0.006 by Mantel-Haenszel test). If only cardiac causes of death were considered, the 5-year survival rate was still lower in group 2 (84.0%) than in group 1 (97.1%, p = 0.004). Considering both revascularized patients and those treated medically for the entire duration of the follow-up, the survival rate was significantly lower in group 2 than in group 1. Finally, the extent of coronary lesions was an independent predictor of survival by Cox multivariate regression analysis. Organic coronary stenoses are frequent in patients with variant angina and are important for the long-term prognosis.