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PubMed1981

Ergonovine testing to detect spontaneous remissions of variant angina during long-term treatment with calcium antagonist drugs.

A subgroup of 22 patients with variant angina who had responded well to calcium antagonist drugs were studied to determine if ergonovine testing could help assess the need for continued therapy. Before treatment all 22 patients exhibited angina with S-T elevation during ergonovine testing done in the coronary care unit according to a previously described protocol with sequential ergonovine doses of 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4 mg administered at 5 minute intervals. After 9.4 +/- 4.7 (range 1 to 24) months of treatment (nifedipine 7 patients, diltiazem 3, verapamil 8, perhexiline 3, nifedipine and diltiazem 1), all patients were free from anginal attacks. Medication was discontinued and ergonovine testing repeated 24 to 48 hours later (3 weeks for perhexiline). In 12 of the 22 patients, angina or S-T segment shifts did not occur during the second ergonovine test to a maximal dose of 0.4 mg. Treatment was not restarted in these patients and all 12 remain free of variant anginal attacks 4.2 +/- 2.9 (range 1 to 13) months later. In seven patients angina and S-T elevation occurred during the second ergonovine test, in the same electrocardiographic leads as during the test before treatment. In three patients the ergonovine test induced angina with S-T depression in the leads where S-T elevation had occurred during the previous test. Treatment was reinstituted in these 10 patients with a positive test. No complications resulted from ergonovine testing in any patient. We conclude that in many patients with variant angina, symptoms will disappear spontaneously and the ergonovine test will revert to negative. Treatment with calcium antagonist drugs can probably be safely discontinued in some patients with variant angina; ergonovine testing appears to be helpful in identifying such patients. Longer periods of follow-up are required to confirm that symptoms do not recur.

Adult↗
PubMed1988

Suppression of exercise-induced angina by magnesium sulfate in patients with variant angina.

The effects of intravenous magnesium on exercise-induced angina were examined in 15 patients with variant angina and in 13 patients with stable effort angina and were compared with those of placebo. Symptom-limited bicycle exercise and thallium-201 myocardial scintigraphy were performed after intravenous administration of 0.27 mmol/kg body weight of magnesium sulfate and after placebo on different days. In all patients, serum magnesium levels after administration of magnesium sulfate were about twofold higher than levels after placebo. Exercise-induced angina associated with transient ST segment elevation occurred in 11 patients with variant angina receiving placebo and in only 2 of these patients receiving magnesium (p less than 0.005). On the other hand, exercise-induced angina was not suppressed by magnesium in any patient with stable effort angina. In these patients there was no significant difference in exercise duration after administration of placebo versus after administration of magnesium. The size of the perfusion defect as measured by thallium-201 scintigraphy was significantly less in patients with variant angina receiving magnesium than that in those receiving placebo (p less than 0.001), whereas it was not significantly different in patients with stable effort angina receiving placebo versus magnesium. In conclusion, exercise-induced angina is suppressed by intravenous magnesium in patients with variant angina but not in patients with stable effort angina. This beneficial effect of magnesium in patients with variant angina is most likely due to improvement of regional myocardial blood flow by suppression of coronary artery spasm.

Adult↗
PubMed1981

Prinzmetal's variant angina.

A series of 12 consecutive patients with Prinzmetal's variant angina is presented. There was a preponderance of males (eight/12) and individuals less than 60 years of age (nine/12). Delay in diagnosis was frequent, primarily due to difficulty in achieving a proper 12 lead ECG recording of the attack which often occurred late at night or in the early morning, subsiding within minutes. In some cases, moreover, ST-depression was observed in the ECG monitoring lead as a reciprocal manifestation of subepicardial ischaemia or due to incorrect polarity in the monitoring lead. The incidence of serious arrhythmias, AV-block and ventricular tachycardia was high (eight/12); two patients had to be DC-converted. Coronary arteriography revealed a spectrum from normal or nearly normal coronary arteries to single vessel disease. Nitroglycerin was well suited for treatment of acute attacks. Long-term treatment with calcium antagonists was effective and without serious side-effects. The follow-up time was from 8 months to 5 years (mean 2 years). It is concluded that Prinzmetal's variant angina as such is a rare disease, but that coronary artery spasm is most likely an important contributory factor in the clinical manifestations of coronary artery disease: arrhythmias, sudden death and myocardial infarction.

Aged↗
PubMed1979

Nifedipine in the treatment of life threatening Prinzmetal angina.

Nifedipine is a non-nitrate vasodilator which has proved effective, in oral form, in Europe, Japan, and the USA for treatment of Prinzmetal Angina. The drug has not been used before in Australia. We report a patient with Prinzmetal's variant angina, complicated by recurrent syncopal episodes due to ventricular arrhythmias. The attacks were resistant to standard therapy except sublingual nitroglycerin but ceased completely during treatment with nifedipine.

Adult↗
PubMed1982

Percutaneous transluminal coronary angioplasty in patients with variant angina.

Among the first 83 patients treated with percutaneous transluminal coronary angioplasty (PTCA) at our institution, typical variant angina was recognized beforehand in five cases and was discovered within 4 months of PTCA in six others. All patients had a 65-95% proximal left anterior descending coronary artery stenosis and only one had a coronary lesion greater than 50% in other coronary arteries. Before PTCA, all patients were premedicated with calcium-antagonist drugs. Thirteen of 15 PTCAs, including three of four repeat PTCAs, were technically successful. However, variant angina recurred after successful PTCA in three of the five patients in whom it was documented beforehand and in an additional two of two patients with variant angina before a successful repeat PTCA. Overall, among the nine patients with variant angina after successful PTCA, five had restenosis at the site of PTCA and two others developed severe lesions adjacent to the site of PTCA within 4 months of the procedure. The three patients without restenosis have been treated with calcium-antagonist drugs from soon after PTCA and have remained angina-free. These results suggest that PTCA is technically feasible in patients with variant angina who have organic lesions, but symptoms due to coronary spasm usually persist or recur, often with restenosis.

Adult↗
PubMed1999

Consumption of vitamin E in coronary circulation in patients with variant angina.

OBJECTIVES: The plasma status of vitamin E has been suggested to be linked to the activity of coronary artery spasm. This study was designed to determine whether vitamin E is actually consumed in the coronary circulation in patients with active variant angina having repetitive spasm-induced transient myocardial ischemia and reperfusion. METHODS: Blood samples were obtained simultaneously from the aortic root, coronary sinus and right atrium in 12 patients with variant angina due to spasm of the left coronary artery, nine patients with stable effort angina and nine control subjects. Plasma vitamin E (alpha- and gamma-tocopherol) concentrations were determined by use of high-performance liquid chromatography and plasma lipid peroxides were measured as thiobarbituric acid-reactive substances (TBARS). RESULTS: At baseline, both plasma alpha- (p < 0.01) and gamma- (p < 0.05) tocopherol levels were significantly lower in the coronary sinus (5.50 +/- 0.50 and 0.55 +/- 0.07 mg/l, mean +/- SEM) than in the aortic root (6.63 +/- 0.57 and 0.63 +/- 0.08 mg/l) and also in the right atrium (6.44 +/- 0.61 and 0.63 +/- 0.09 mg/l) in the variant angina group. The TBARS level was significantly (p < 0.05) higher in the coronary sinus than in the aortic in this group. In contrast, these levels were not significantly different between the samples from the coronary sinus and the aortic root or the right atrium in the control group and also in the stable effort angina group. The coronary sinus-aortic difference in plasma vitamin E levels in the variant angina group was not significantly altered after left coronary artery spasm induced by intracoronary injection of acetylcholine. Also, the plasma vitamin E levels in the aortic root, coronary sinus and right atrium all remained unchanged in the stable effort angina group after pacing-induced angina and in the control group after intracoronary administration of acetylcholine. CONCLUSIONS: Transcardiac reduction in plasma vitamin E concentrations concomitant with lipid peroxide formation was demonstrated in patients with active variant angina, suggesting actual consumption of this major endogenous antioxidant. Oxidative stress and vitamin E exhaustion may be involved in the pathogenesis of coronary artery spasm.

Acetylcholine↗
PubMed1977

Prinzmetal's angina.

A 23-year-old man had Prinzmetal's variant angina. After strenuous exercise and isoprenaline infusion the electrocardiogram remained normal and the patient asymptomatic. Coronary angiography gave normal results which remained normal after administration of ergometrine. An injection of methacholine induced an attack.

Adult↗
PubMed1980

Ergonovine testing in a coronary care unit.

This study describes the results of ergonovine testing in 100 consecutive patients who underwent this procedure in a coronary care unit. All patients had recently undergone coronary arteriography. A bolus injection of ergonovine was administered at 5 minute intervals in the following doses (mg): 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4. The criterion for a positive test was the appearance of S-T elevation greater than 1 mm. The test was positive in all 17 patients known to have variant angina and in 18 (40 percent) of 45 patients who had a history of chest pain judged strongly suggestive of variant angina but who had no electrocardiogram recorded during pain. Of 38 patients with a history of chest pain classified as not entirely typical of variant angina, only 1 (2.6 percent) had a positive test. Of the 64 patients with a negative ergonovine test, 47 had chest pain and 25 had nausea but none had more serious complications. Ventricular arrhythmia accompanied S-T elevation in 18 of the 36 patients with a positive test but occurred in only 4 of the 64 with a negative test (p < 0.0005). No patient needed treatment with antiarrhythmic drugs. Four of the 36 patients with a positive test had serious complications: severe transient hypotension (2 patients), recurrent episodes of angina with S-T elevation (1 patient) and a subendocardial infarction (1 patient). Thus, ergonovine testing is useful in patients with a typical clinical history of variant angina but without an electrocardiogram recorded during pain. In this study, a small but definite incidence of serious complications occurred during a positive test.

Adult↗
PubMed1983

Natural history and prognosis of ischemic heart disease.

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.

Aged↗
PubMed2002

Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1.

The inwardly rectifying K(+) channel Kir6.1 forms K(+) channels by coupling with a sulfonylurea receptor in reconstituted systems, but the physiological roles of Kir6.1-containing K(+) channels have not been determined. We report here that mice lacking the gene encoding Kir6.1 (known as Kcnj8) have a high rate of sudden death associated with spontaneous ST elevation followed by atrioventricular block as seen on an electrocardiogram. The K(+) channel opener pinacidil did not induce K(+) currents in vascular smooth-muscle cells of Kir6.1-null mice, and there was no vasodilation response to pinacidil. The administration of methylergometrine, a vasoconstrictive agent, elicited ST elevation followed by cardiac death in Kir6.1-null mice but not in wild-type mice, indicating a phenotype characterized by hypercontractility of coronary arteries and resembling Prinzmetal (or variant) angina in humans. The Kir6.1-containing K(+) channel is critical in the regulation of vascular tonus, especially in the coronary arteries, and its disruption may cause Prinzmetal angina.

Angina Pectoris, Variant↗
PubMed1986

Calcitonin gene-related peptide: a potent dilator of human epicardial coronary arteries.

To investigate the action of calcitonin gene-related peptide (CGRP) on human epicardial coronary arteries, six patients received intracoronary CGRP at doses of 50,100, and 200 ng/min. The effect of CGRP was measured angiographically with a computerized analysis system. A dose-dependent increase in coronary arterial diameter was observed. At the highest dose there were 34%, 7%, 38%, and 40% mean increases in the diameters of the circumflex, proximal, mid, and distal left anterior descending arteries, respectively. No further increase in diameter was found after a subsequent dose of 1 mg intracoronary isosorbide dinitrate. Prior infusion of CGRP did not prevent coronary arterial spasm induced by ergonovine in two patients with variant angina, but a subsequent bolus of CGRP partially relieved the spasm. We propose that CGRP has a role in the regulation of coronary vascular smooth muscle tone.

Angina Pectoris↗
PubMed1982

Clinical characteristics of patients with variant angina complicated by myocardial infarction or death within 1 month.

Of 132 consecutive patients hospitalized during a 5 year period because of active variant angina, 18 died or had a myocardial infarction within 1 month. In 4 patients an episode of pain and S-T elevation unrelieved by calcium antagonist drugs and intravenous nitroglycerin persisted for more than 1 hour, inducing cardiogenic shock and death before the appearance of Q waves and elevated serum enzyme levels. In the other 14 patients myocardial infarction developed in the electrocardiographic leads in which S-T elevation had occurred during attacks of variant angina. Clinical features were not helpful in distinguishing the 18 patients with complications from the other 114. Angina at rest had been present for less than 1 month in 7 of the 18 patients with infarction compared with 31 of 114 in the other group (probability [p] not significant [NS]). Before infarction the artery presumed to be perfusing the involved territory contained a fixed stenosis of 70 percent or more of luminal diameter in 8 of the 14 patients with complications who had coronary arteriograms compared with 50 of 112 in the other group (p = NS). In 13 of the 18 patients, complications occurred in spite of large doses of calcium antagonist drugs. In 11 of these 13, attacks of variant angina were monitored for 3 to 17 days both before and during treatment. All 11 had fewer attacks with treatment and 5 had no attacks. Daily attacks per patient decreased from 4.6 +/- 4.3 to 0.5 +/- 0.7 (mean +/- standard deviation) (p less than 0.01). It is concluded that in variant angina of recent onset myocardial infarction occurs frequently and unpredictably. Myocardial infarction may occur in the absence of severe fixed lesions and in spite of apparent clinical improvement with administration of calcium antagonist drugs.

Adult↗
PubMed1982

Exercise testing in patients with variant angina: results, correlation with clinical and angiographic features and prognostic significance.

Eighty-two patients with variant angina underwent a treadmill exercise test using 14 ECG leads, and 67 also underwent exercise thallium-201 scans. The test induced ST elevation in 25 patients (30%), ST depression in 21 (26%) and no ST-segment abnormality in 36 (44%). ST elevation during exercise occurred in the same ECG leads as during spontaneous attacks at rest, and was always associated with a large perfusion defect on the exercise thallium scan. In contrast, exercise-induced ST depression often did not occur in the leads that exhibited ST elevation during episodes at rest. The ST-segment response to exercise did not accurately predict coronary anatomy: Coronary stenoses greater than or equal to 70% were present in 14 of 25 patients (56%) with ST elevation, in 13 of 21 (62%) with ST depression and in 14 of 36 (39%) with no ST-segment abnormality (NS). However, the degree of disease activity did correlate with the result of the exercise test: ST elevation occurred during exercise in 11 of 14 patients who had an average of more than two spontaneous attacks per day, in 12 of 24 who had between two attacks per day and two per week, and in only two of 31 who had fewer than two attacks per week (p less than 0.005). St elevation during exercise was reproducible in five of five patients retested during an active phase of their disease, but not in three of three patients who had been angina-free for at least 1 month before the repeat test. Twelve patients wih exercise-induced ST elevation were retested during treatment with calcium antagonist drugs; in 10 of 12, ST elevation did not occur with the second test. During a mean follow-up of 20.3 +/- 14.5 months, death or myocardial infarction occurred in three of the 25 patients with ST elevation during exercise, none of 21 with ST depression and two of 36 with no ST abnormality. We conclude that in variant angina patients, the results of an exercise test correlate well with the degree of disease activity but not with coronary anatomy, and do not define a high-risk subgroup.

Adult↗
PubMed1986

Local coronary supersensitivity to diverse vasoconstrictive stimuli in patients with variant angina.

It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers and pharmacologic agents. It is not known, however, to what extent different stimuli can induce spasm in the same patient. To investigate whether coronary arterial spasm results from specific abnormal agonist-receptor interactions or from a local nonspecific coronary supersensitivity to different stimuli, 28 patients with vasospastic angina were submitted to a series of diverse vasoconstrictive stimuli known to provoke coronary spasm. Ergonovine, hyperventilation, handgrip, cold pressor, and exercise-tests, were carried out in all 28 patients. In the last 15 patients histamine was also administered. Spasm was provoked by ergonovine in 96% of patients, by hyperventilation in 54%, by histamine in 47%, by exercise in 46%, and by the cold pressor and handgrip tests in 11% and 7%, respectively. No significant differences were found in the responses to provocative tests of patients with normal coronary arteries or nonsignificant stenoses and those with significant lesions. In the same individual, spasm was induced by at least two vasoconstrictive stimuli, although with a different mechanism of action, in 82% of patients and spasm was induced by three or more stimuli in 39%. Tests were repeated in at least 23 patients and short-term reproducibility paralleled sensitivity. These results suggest that in patients with variant angina, a local nonspecific supersensitivity rather than an abnormal specific agonist-receptor interaction plays a major role in the genesis of coronary arterial spasm.

Adult↗
PubMed1989

Silent myocardial ischemia in patients with variant angina.

Twenty-four hour ambulatory electrocardiographic recording was performed in 56 patients with variant angina admitted to the coronary care unit in order to evaluate the incidence and pathophysiology of silent episodes of ST elevation. Of 696 episodes of ST elevation of more than 0.1 mV identified during a recording period of 141 days, 531 (76%) episodes were completely silent. The incidence of silent episodes increased as the number of total ischemic episodes per day increased. Silent ST elevation revealed a significantly shorter duration and a lower intensity than symptomatic ST elevation. However, there were wide overlaps in the duration and intensity of ST elevation between silent and symptomatic episodes. In some patients, silent and symptomatic episodes of similar duration and intensity were observed. Arrhythmias during ischemic episodes such as premature ventricular contractions, ventricular tachycardia, high grade atrioventricular block, and sinus arrest were observed in 32 of 56 patients, 57% of cases and 9% of the total episodes. Arrhythmias were more common during symptomatic episodes (29%) than during silent ones (9%, p less than 0.01), but serious arrhythmias such as ventricular tachycardia, high grade atrioventricular block and sinus arrest occurred even during silent episodes. In both silent and symptomatic episodes, the duration and intensity of ST elevation were significantly lower in ischemic episodes with arrhythmias than in those without arrhythmias. These results suggest that 1) the majority of ischemic events are silent in patients with variant angina; 2) the severity of ischemia seems to be an important factor as the cause of anginal pain, but additional factors may be involved; 3) arrhythmias were more common during sympatomatic than silent episodes.

Adult↗
PubMed1992

A study on coronary hemodynamics during acetylcholine-induced coronary spasm in patients with variant angina: endothelium-dependent dilation in the resistance vessels.

The epicardial coronary artery of patients with variant angina is hyperreactive to the constrictive effect of acetylcholine, but it is not known whether the coronary microvasculature also constricts in response to acetylcholine. Incremental doses of acetylcholine were injected into the left coronary artery of 57 patients with variant angina and with spasm in this artery. By measuring coronary sinus blood flow, coronary hemodynamic status just before angiographic documentation of spasm was examined. Acetylcholine induced spasm in the left coronary artery in all patients. It also decreased the diameter of the nonspasm artery by 36 +/- 19% from baseline. For all patients, coronary sinus blood flow was 89 +/- 38 ml/min at baseline and increased to 104 +/- 61 ml/min during an acetylcholine-induced anginal attack (p less than 0.01). In 10 patients with spasm in both the left anterior descending and left circumflex arteries (that is, multivessel spasm), coronary sinus blood flow decreased from 84 +/- 21 to 52 +/- 26 ml/min (p less than 0.01). In the other 47 patients with spasm in only one of these two arteries (that is, single-vessel spasm), coronary sinus blood flow increased from 90 +/- 41 to 115 +/- 61 ml/min (p less than 0.01) without change in the rate-pressure product. It is concluded that in patients with variant angina, acetylcholine induces spasm and constriction in the epicardial coronary artery, whereas it dilates the resistance vessels presumably through the release of the endothelium-dependent relaxing factor.

Acetylcholine↗
PubMed2000

Intravascular ultrasound findings of negative arterial remodeling at sites of focal coronary spasm in patients with vasospastic angina.

BACKGROUND: There are few data about the intravascular ultrasound (IVUS) findings in patients with vasospastic angina, especially regarding patterns of vascular remodeling. METHODS AND RESULTS: Coronary spasm was documented by angiography and electrocardiographic evidence of ischemia in 36 patients after administration of ergonovine (cumulative doses up to 350 microg). After relief of spasm with 1000 microg of intracoronary nitroglycerin, quantitative angiography and IVUS imaging were performed and analyzed by standard methods. The 36 focal spasm sites were compared with the proximal and distal reference segments. The angiographic baseline minimum lumen diameter measured 1.78 +/- 0.66 mm, which decreased to 0.66 +/- 0.38 mm with ergonovine provocation (P <.0001), increased to 2.66 +/- 0.64 mm after intracoronary nitroglycerin (P <.0001 compared with baseline and after ergonovine), and did not change after IVUS imaging (2.66 +/- 0.63, P =.9). By IVUS, atherosclerotic lesions were observed at all coronary spasm sites; the mean plaque burden measured 56% at the spasm site and 35% at the reference. Spasm site plaque composition was hypoechoic in 31 and hyperechoic, noncalcific in 5; there was no calcium. The mean eccentricity index (maximum divided by minimum plaque thickness) was 6.7. Positive remodeling (spasm site arterial area greater than proximal reference) was present in 5; intermediate remodeling (proximal reference greater than spasm site greater than distal reference arterial area) was present in 7; and negative remodeling (spasm site arterial area less than distal reference) was present in 24. CONCLUSIONS: Sites of vasospasm in patients with variant angina showed characteristics of early atherosclerosis, except for an unusually high incidence of negative arterial remodeling.

Adult↗
PubMed1995

Does prevalence of migraine and Raynaud's phenomenon also increase in Korean patients with proven variant angina?

BACKGROUND: The incidence of coronary artery spasm in oriental patients is higher than that in western patients. Oriental patients with variant angina (VA) frequently show normal or insignificant coronary artery stenosis by angiogram, compared with western patients. The prevalence of migraine and Raynaud's phenomenon in oriental patients with VA has not yet reported. OBJECTIVE: We did a prospective study on the prevalence of migraine and Raynaud's phenomenon in patients with proven VA compared with those in two control groups using a radioisotope technique following ice water exposure. Simultaneously, we studied lipid profiles of each group. METHODS AND RESULTS: migraine was diagnosed if the score in part A totalled 7 or more of 26, and Raynaud's phenomenon was diagnosed if the score in part B totalled 4 or more of 11 by Miller et al. Technetium-99m-labeled red blood cells (99mTc-RBC) radionuclide angiography was performed in all patients. Patients were included in a prospective protocol. Patients were grouped as follows: Group I: 20 patients with proven VA; Group II: 30 patients with coronary artery disease; Group III: 31 patients without heart disease. Age and sex of patients were not statistically different among the three groups. Migraine was diagnosed in 8 patients (40.0%) of group I and in 6 patients (20.0%) of group II and in 12 patients (38.7%) of group III. Raynaud's phenomenon was reported in 2 (10.0%) of the patients in group I and in 5 (16.1%) of the patients of group III. The mean index ratio of the digital blood flow of right over left hand on static image was 0.85 +/- 0.07 (mean +/- S.E.M.) of the patients of group I, 0.73 +/- 0.03 of the patients of group II and 0.74 +/- 0.04 of the patients of group III. The mean flow index ratio of right over left hand of the digital blood flow on dynamic study was 0.51 of the patients of group I, 0.43 of the patients of group II and 0.43 of the patients of group III. The score of migraine did not differ significantly among the three groups. The score of Raynaud's phenomenon of patients with variant angina did not differ significantly from that of patients in the non-coronary control group, although it differed significantly from that of patients in the coronary control group. But, the prevalence of migraine and Raynaud's phenomenon (questionnaire and radionuclide angiography) in patients of group I did not differ significantly from that in groups II and III. In the end, more patients with variant angina than coronary or non-coronary control group did not reach the predetermined point level for the diagnosis of migraine and Raynaud's phenomenon. Lipid profiles were not significantly different among three groups. CONCLUSIONS: This result suggests that variant angina may not be a manifestation of a generalized vasospastic disorder in Korean patients.

Adult↗