Acetylcholine-induced coronary spasm with a history of Kawasaki disease: case report.

A 21-year-old woman without any known coronary risk factors was found at coronary catheterization to have normal coronary angiograms, but demonstrated acethylcholine (ACh)-induced coronary spasm. She had a history of Kawasaki disease (KD) at 19 months of age and, although coronary angiography was not performed at that time, no coronary aneurysms were detected by echocardiography. To the best of our knowledge, this is the first case report of ACh-induced coronary spasm associated with normal coronary angiograms in a young person with a history of KD. The findings suggest that subclinical, persistent coronary endothelial dysfunction may exist in this patient; furthermore, the dysfunction appears diffuse and might be unrelated to coronary aneurysm formation. The long-term significance of coronary endothelial dysfunction in patients with KD, as suspected by coronary spasm, remains unknown but may be an important risk factor for future atherosclerosis.     

Successful catheter interventional therapy for acute coronary syndrome secondary to kawasaki disease in young adults.

Acute coronary syndrome occurred in 2 young adults who had a history of Kawasaki disease (KD), but few other coronary risk factors. The first patient was a 27-year-old male with acute myocardial infarction without stenosis detected by coronary arteriography 4 years earlier. Emergency coronary arteriography showed occlusion of the right coronary artery. Aspiration-thrombectomy and rescue balloon angioplasty were successfully performed. The second patient was a 32-year-old male with unstable angina. Right coronary arteriography showed total occlusion with severe calcification. Left coronary arteriography showed 99% stenosis at the proximal site of the circumflex artery, and a directional coronary atherectomy was performed. Histological examination of a specimen from this site revealed a lipid core, macrophages, and smooth muscle cells. Restenosis was not observed on follow-up coronary arteriography after 5-6 months in either case. The coronary stenosis in each case was probably caused by accelerated atherosclerosis at the site without aneurysm as it seemed to be 'normal' on arteriography. Conventional catheter intervention was effective treatment. The sequelae of KD should be recognized as independent coronary risk factors.     

An unusual cause of chest pain: Acute coronary syndrome following administration of ergotamine tartrate

For many years, ergotamine has been used for the acute treatment of migraine. Ergotamine may produce coronary vasospasm, which is often associated with ischemic electrocardiography changes and angina pectoris. A 62-year-old woman who was admitted to the emergency department because of chest pain is described. She had a history of severe migraine attacks and started to use ergotamine tartrate 0.75 mg daily the day before. Electrocardiography revealed sinus tachycardia with left anterior hemiblock and T wave inversion in the precordial leads. Cardiac biomarker levels were elevated. After discontinuation of the drug and initiation of vasodilator treatment, her chest pain resolved. Patients with migraine may have an underlying vasospastic disorder predisposing them to coronary artery spasm. Physicians should be alerted to potential cardiac vasospastic effects of low-dose ergotamine in the treatment of migraine.     

Investigation of flow-mediated dilation response in normal coronary angiographic patients

Normal findings from coronary angiography do not always show normal endothelial functions. An impaired flow-mediated dilation (FMD) can be a useful marker of the presence of endothelial dysfunction. Hypertension, left ventricular hypertrophy, hypercholesterolemia, and vasospastic angina pectoris can negatively affect FMD response. FMD responses of normal subjects and patients with coronary artery pathology were compared in a prospective cross-sectional study. Patients were divided into 3 groups. Group I patients had a positive exercise stress test and angiographically normal coronary arteries. Group II patients had angiographically significant coronary artery stenosis and stable angina pectoris. Group III had normal results from an exercise stress test and no chest pain. It was concluded that flow-mediated dilation response cannot predict coronary angiographic results. Patients with normal findings from coronary angiography may have impaired endothelial functions.     

Two adults requiring implantable defibrillators because of ventricular tachycardia and left ventricular dysfunction caused by presumed Kawasaki disease.

There is an adult patient population in Japan with undiagnosed coronary artery lesions caused by Kawasaki disease (KD) occurring before 1967, the time at which KD was first described. Two adult patients presented with a low left ventricular (LV) ejection fraction and ventricular tachycardia (VT) caused by presumed KD. A 43-year-old man with rapid VT had a history of an acute febrile illness with desquamation of the fingertips at the age of 10 months. Coronary angiography (CAG) showed segmental stenosis of the right coronary artery (RCA) and occlusion of the left anterior descending artery with a giant aneurysm. The other patient was a 48-year-old man with a history of ischemic cardiomyopathy diagnosed after a previous myocardial infarction when he was 32 years old. He had segmental stenosis of the RCA on CAG. Non-sustained VT with transient unconsciousness was observed during 24-h Holter electrocardiography. Rapid VT with syncope was induced in both patients in the electrophysiologic studies and an implantable defibrillator was required to prevent sudden death. Physicians must be aware that VT can occur in older patients with LV dysfunction many years after KD.     

A change in the pattern of vasospasm after stenting in a patient with vasospastic angina

We report an unusual case of a male patient with vasospastic angina in whom the pattern of coronary artery spasm changed after coronary stenting. The patient was admitted to our hospital with an acute coronary syndrome. Coronary angiography revealed an intermediate grade stenosis in the right coronary artery, and focal coronary spasm was provoked by intracoronary acetylcholine. A diagnosis of vasospastic angina was made, and the patient was followed medically. He subsequently was readmitted with refractory vasospastic angina and underwent coronary stenting. He was pain-free after stent implantation. Repeat angiography 6 months later showed no restenosis in the stented segment; however, coronary spasm was provoked in all areas except the stented segment by intracoronary acetylcholine injection.     

Relation of basal coronary tone and vasospastic activity in patients with variant angina.

OBJECTIVE: To examine the vasoconstrictor response to ergonovine and the vasodilator response to isosorbide dinitrate in spastic and non-spastic coronary segments from 31 patients undergoing serial angiographic follow up of variant angina. METHODS: Coronary angiograms and ergonovine provocation tests were repeated at an interval of 45 (SD 15) months apart. While all 31 patients showed a positive response to ergonovine initially, vasospastic responsiveness persisted in only 16 patients at follow up (group 1) and not in the other 15 patients in whom symptoms of variant angina had resolved (group 2). Mean luminal diameter of 170 normal or near normal entire coronary segments (American Heart Association classification) were measured (a) at baseline, (b) after the administration of ergonovine, and (c) after the administration of isosorbide dinitrate, during both the initial and follow up angiograms using a computer based quantitative angiography analysis system (CAAS II). RESULTS: In vasospastic patients (initial and follow up angiograms in group 1, and initial angiogram in group 2), basal tone was significantly higher in spastic segments compared to adjacent segments or segments in non-spastic vessels. The diagnostic sensitivity and specificity at 20% increase in basal coronary tone for the prediction of vasospasm were 77% and 73%, respectively. CONCLUSIONS: Coronary artery tone may change in proportion to the activity of variant angina over several years. Contrary to some previous reports, the estimation of basal coronary tone may be useful in the assessment of vasospastic activity in patients with variant angina.     

Variant angina associated with coronary artery endothelial dysfunction and myocardial bridge: a case report and review of the literature

The association of variant angina (VA) and myocardial bridges is a rare finding. We describe a case of VA with recurrent coronary spasm triggered by different stimuli at the site of a myocardial bridge. The interplay of endothelial dysfunction, coronary vasoconstriction and myocardial bridging was detected by intracoronary acetylcholine test and IVUS. We speculate that mechanical stimulation at the bridge site caused endothelial dysfunction and enhanced local susceptibility to vasoconstrictor stimuli. Variant angina should always be suspected in cases of ST-elevation acute coronary syndrome without any significant angiographic coronary stenosis.     

Interventional treatment for very young adults with acute myocardial infarction. Clinical manifestations and outcome

Direct percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is now established as a standard therapy for older patients. However, experience with PCI in very young adults with AMI has been limited. In this report we retrospectively evaluated the effectiveness of PCI for very young adults with AMI and estimated their clinical characteristics and outcome. Of the 502 patients with AMI, 5 were 35 years old or younger (1.0%) during a period of 4 years (2000--2004). We assessed the utility of PCI in these five consecutive patients under the age of 35 presenting with a first AMI. Five AMI patients, ranging in age from 20 to 34 years (median, 27+/-5 years) underwent direct PCI for the culprit lesions. The lesions targeted for PCI were located in the left anterior descending artery in 3 patients and in the right coronary artery in 2 patients. One patient had a past history of Kawasaki disease (KD). In all of the patients, PCI were angiographically effective at the acute phase without complication. In hospital course, a subacute stent thrombosis occurred in one patient. Follow-up angiograms performed 6 months after the procedure revealed no restenosis, but identified a new coronary aneurysm in one patient with a past history of KD and a regressed giant coronary aneurysm probably due to atypical KD in another patient, which were confirmed by intravascular ultrasound. There was one death ascribed to heart failure 8 months after the initial PCI. The findings of this report suggest that PCI for very young adults with AMI can be safe and effective in the short-term.     

Evaluation by high-resolution ultrasonography of endothelial function in brachial artery after Kawasaki disease and the effects of intravenous administration of vitamin C.

Previous studies in patients with a history of Kawasaki disease (KD) have focused on the endothelial function of the coronary arteries and that of the systemic arteries is not fully understood. Furthermore, the effect of vitamin C on systemic vascular endothelial function after KD has not yet been elucidated. In the present study, 39 patients (age, 7.1 +/- 2.7 years) at 1-10 years after acute KD were compared with 17 matched healthy subjects (7.0 +/- 3.1 years). High-resolution ultrasonography was used to analyze brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilation) and sublingual nitroglycerin (causing endothelium-independent dilation) after KD, and to investigate whether the acute administration of vitamin C can restore systemic endothelial dysfunction. The percent change in diameter of the brachial artery induced by reactive hyperemia in the patients with a history of KD (6.2 +/- 3.9%) was significantly less than that in the control group (14.1 +/- 6.8%, p < 0.0001). No significant difference could be found in the percent change in diameter induced by sublingual nitroglycerin between the controls (33.2 +/- 13.7%) and the patients (30.6 +/- 9.2%, p = 0.49). There was no significant difference in percent change in diameter of the brachial artery induced by reactive hyperemia between the patients who received gamma globulin (6.0 +/- 4.0) and those who did not (7.9 +/- 3.3, p = 0.33). Intravenous infusion of vitamin C significantly increased the percent change in diameter of the brachial artery induced by reactive hyperemia in 19 patients with history of KD (6.6 +/- 3.5% to 13.0 +/- 5.5%, p < 0.0001). After placebo administration in 20 patients with history of KD there was no significant increase in the percent change in the diameter of the brachial artery induced by reactive hyperemia (6.5 +/- 4.5% to 7.3 +/- 4.9%, p = 0.20). The decreased percent change in the diameter of the brachial artery induced by reactive hyperemia in patients with a history of KD compared with the healthy children indicates that systemic endothelial dysfunction exists after KD. Although it is not influenced by early treatment with high-dose gamma globulin in the acute stage of KD, systemic vascular endothelial function can be restored by acute intravenous administration of vitamin C.     

Clinical characteristics of female patients with coronary spastic angina: comparison with male patients

There are many patients with vasospastic angina who have minor atherosclerosis, and in Japan the majority of them are male. No data exist concerning sex differences in patients with coronary spastic angina, so the present study sought to clarify the clinical characteristics between male and female patients with vasospastic angina. Between April 1991 and June 1998, 204 consecutive patients were diagnosed with vasospastic angina and of these, 26 (12.7%) were female. An acetylcholine test was performed with incremental doses of 20, 50, and 80 microg injected into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Ergonovine was injected in a total dose of 40 microg into the right coronary artery and 64 microg into the left coronary artery. Coronary spasm was defined as 99% or more luminal narrowing accompanied by ischemic changes on ECG. Compared with male patients, female patients had less organic stenosis (12 vs 33%, p<0.05), less history of smoking (15 vs 85%, p<0.01), and fewer focal spasms (31 vs 64%, p<0.01). There were no other differences between the 2 groups. In conclusion, Japanese female patients with vasospastic angina had the characteristics of diffuse provoked spasm, less organic stenosis, and less history of smoking, but only 1 in 10 of all patients with vasospastic angina are female.     

A new noninvasive method of diagnosing vasospastic angina based on dilation response of the left main coronary artery to nitroglycerin as measured by echocardiography

Objectives.The purpose of the present study was to evaluate the feasibility of diagnosing vasospastic angina based on coronary artery tone as assessed by M-mode echocardiographic measurement of the dilation response of the left main coronary artery to nitroglycerin.Background.The definite diagnosis of vasospastic angina is done by a coronary spasm provocative test using ergonovine maleate or acetylcholine during cardiac catherization. Current noninvasive, nonpharmacologic diagnostic methods are not sensitive enough for the diagnosis of vasospastic angina.Methods.Thirty-eight patients who had an angiographically normal left main trunk were studied. These patients were classified into four groups based on the presence or absence of more than 50% stenosis in the coronary arteries except for the left main trunk and the results of the acetylcholine or ergonovine provocative test. At 7 a.m. and at noon on the same day, the left main trunk diameter was measured by M-mode echocardiography before and after sublingual administration of nitroglycerin (0.3 mg), and its percent dilation was calculated to assess coronary artery tone.Results.The percent dilation of the left main trunk diameter induced by sublingual nitroglycerin at 7 a.m. and at noon was 22.4 ± 4.7% (mean ± SD) and 18.1 ± 4.0% in 11 patients with vasospastic angina and without coronary stenosis, 14.9 ± 7.1% and 11.2 ± 6.9% in 9 patients with vasospastic angina and coronary stenosis, 6.1 ± 3.5% and 7.0 ± 5.1% in 8 patients without vasospastic angina but with coronary stenosis and 8.1 ± 5.6% and 7.8 ± 5.7% in 10 control subjects. The percent dilation at 7 a.m. was significantly greater in the vasospastic angina without coronary stenosis group than in the remaining three groups, and in the vasospastic angina groups, the percent dilation at 7 a.m. was significantly greater than that at noon. When percent dilation at 7 a.m. exceeding 15% was defined as positive for the diagnosis of vasospastic angina, the sensitivity was 80% and the specificity 94%.Conclusions.Basal tone of the left main trunk is elevated in the early morning in vasospastic angina. Dilation of the left main trunk diameter exceeding 15% induced by sublingual nitroglycerin in the early morning as measured by M-mode echocardiography is a highly sensitive and specific criterion for the diagnosis of vasospastic angina.     

Combined cardiac surgery and total thyroidectomy: a case report

A 65-year-old woman with aortic stenosis, ischemic heart disease, and Graves' disease had complained of effort angina. She then suffered from liver dysfunction due to treatment with antithyroid drugs. One year after the start of radioiodine administration, she demonstrated unstable angina with palpitation and sweating. Laboratory studies revealed a recurrent hyperthyroid state, and a second coronary angiogram revealed progressive ischemic heart disease. Combined coronary artery bypass grafting, aortic valve replacement, and total thyroidectomy were performed. The postoperative course was uneventful without any problems associated with hyperthyroidism or hypothyroidism. Combined cardiac surgery and total thyroidectomy can be performed safely if the perioperative levels of thyroid hormone are maintained at euthyroid or hypothyroid levels.     

Long lasting spasticity in controlled vasospastic angina

OBJECTIVE: To evaluate changes in coronary artery spasticity in patients with vasospastic angina who had been stable for years under continuous drug treatment. METHODS: Follow up coronary angiography was performed under intracoronary ergonovine provocation in 27 well controlled patients with vasospastic angina and no organic stenosis; the tests were done > 24 months after the initial coronary angiography, in which occlusive spasm had been induced by the same regimen of ergonovine provocation. RESULTS: The mean (SD) follow up period was 47.2 (21.6) months. All patients had been free from angina attack for more than 24 months under treatment with antianginal drugs. During this follow up period, organic stenosis developed in only one case. Occlusive spasm was observed during follow up coronary angiography in 23 patients. Spasm with 90% narrowing was observed in three other patients, and diffuse significant narrowing was seen in the final patient. No significant difference was found in spasticity (p = 0.75) between the initial and the follow up tests. CONCLUSIONS: Repeated ergonovine provocation during coronary angiography after a controlled period of several years showed that coronary spasm remains inducible in most patients. Discontinuance of drug treatment during the remission from anginal attacks achieved by medication may put the patient at high risk.     

Ultrastructural characteristics of myocardial and coronary microvascular lesions in Kawasaki disease.

Kawasaki disease (KD) is an acute febrile mucocutaneous lymph node syndrome with multisystemic vasculitis affecting mainly infants and children. Although several studies on cardiovascular lesions in KD have been done at the light microscopic level, the ultrastructural characteristics and incidences of these lesions have not been well defined. In order to investigate the myocardial and coronary microvascular sequelae in KD, we performed an ultrastructural study on endomyocardial biopsy specimens obtained during follow-up from 54 patients who had typical clinical manifestations of KD, of whom 47 had associated coronary aneurysms as demonstrated by coronary arteriography (CAG) or two-dimensional echocardiography in the acute or healed stage. The average age of onset was 2.2 years old and the duration of illness was from 2 months to 23 years. Follow-up CAG showed that the coronary aneurysms persisted in 33 of the 47 patients (8 with associated stenosis) and resolved in the remaining 14 patients. Ultrastructurally, the myocardial changes revealed hypertrophy, various degrees of degeneration, proliferation and abnormality of mitochondria, infiltration of a small number of lymphocytes, and fibrosis. The coronary microvascular lesion was characterized by microvascular dilatation, endothelial cell injury, platelet aggregation with thrombosis, and stenotic lumen with thickened walls in the small arterioles. It persisted after convalescent stage even up to 23 years and closely correlated with the myocardial sequelae. Moreover, significantly increased incidences of myocardial and coronary microvascular lesions were found in patients with coronary artery lesion. These findings suggest the coronary microvascular lesion as a possible underlying factor of persistent sequelae in KD.     

Does quinapril improve coronary vasoconstriction in vasospastic angina?

OBJECTIVES: Endothelial dysfunction is one of the important mechanisms of coronary spasm. Recently, the angiotensin converting enzyme (ACE) inhibitor quinapril, which has a high affinity for vascular ACE, has improved endothelial dysfunction in coronary artery disease. This study investigated whether quinapril improves coronary vasoconstriction induced by acetylcholine in vasospastic angina. METHODS: Twenty-four patients with vasospastic angina without significant organic stenosis diagnosed by the acetylcholine provocation test (vessel with spasm defined as > or = 90% stenosis provoked with chest pain and/or ischemic ST change) were enrolled in this study. Patients were randomly assigned to 2 groups: the quinapril group (receiving quinapril 20 mg/day, n = 12), and the non-quinapril group (not receiving quinapril, n = 12). All patients received calcium antagonist. Six months later, coronary angiography was repeated and changes in coronary spasm were compared between the groups. Seven patients were withdrawn from this study, so 17 patients were evaluated (the quinapril group: 8 patients, the non-quinapril group: 9). RESULTS: Angina symptoms were completely or almost suppressed in all patients during the study period. Angiographically, the number of patients with improvement of spasm, patients with deterioration of spasm and patients with stability of spasm were 1, 0, 7 in the quinapril group versus 0, 1, 8 in the non-quinapril group, respectively. There was no significant change between the 2 groups. Quantitative angiographic analysis showed that the coronary spasm rate (percentage of minimal lumen diameter at the site of spasm after administration of acetylcholine to minimal lumen diameter after administration of isosorbide dinitrate) at the first and second angiography were 71 +/- 10% and 62 +/- 21% in the quinapril group versus 73 +/- 14% and 67 +/- 15% in the non-quinapril group, respectively. There were no significant interval changes between the 2 groups (p = 0.60). CONCLUSIONS: Our results did not indicate that quinapril had improved coronary vasoconstriction induced by acetylcholine in patients with vasospastic angina.     

Lesion severity and hypercholesterolemia determine long-term prognosis of vasospastic angina treated with calcium channel antagonists.

Although patients with medically treated vasospastic angina have a good outcome, few data exist regarding the role of underlying lesion severity associated with or without hyperlipidemia in the prognosis. Therefore, the aim of the present study was to assess the relationship between the long-term outcome of vasospastic angina and the factors influencing its prognosis. A total of 256 patients (219 men, 37 women; mean age, 54.1+/-9.2) who had coronary spasm with or without underlying lesions and were being treated with calcium channel antagonists were enrolled and followed for 13.6+/-3.7 years. Cardiac events consisted of cardiac death and ischemic events, which included acute myocardial infarction and unstable angina. Cox analysis selected coronary artery stenosis (CAS, >/=50%) and risk factors such as age, hypertension, diabetes mellitus, low-density lipoprotein-cholesterol (LDL-C), sex and smoking. There were 19 cases of cardiac death (7.4%) and 58 of ischemic events (22.7%) during the follow-up period. The presence of significant CAS was an independent predictor of event-free survival (hazard ratio (HR) =2.84, 95% confidence interval (CI) =1.79-4.52, p<0.0001). In 193 patients without significant CAS, there were 10 cases of cardiac death (5.2%, p<0.05) and 34 of ischemic events (17.6%, p<0.01). In that group, high LDL-C was the independent predictor of event-free survival (HR = 3.89, 95% CI = 1.20-12.6, p=0.02). Kaplan-Meier survival analysis revealed significantly lower event-free survival in patients with than in those without lesions (p<0.0001 by log-rank test). These results demonstrate that the most important factor for long-term prognosis of vasospastic angina treated with calcium channel antagonists is significant CAS. High LDL-C, which might alter the underlying coronary endothelial function and/or accelerate atherosclerotic lesions, could also contribute to the occurrence of cardiac events, particularly in patients without significant CAS.     

Increased serotonin release across the coronary bed during a nonischemic interval in patients with vasospastic angina

Background: Platelet activation and coagulation abnormality have been observed during coronary spasm. It is crucial whether platelet activation occurs even during a nonischemic period. Hypothesis: This study was designed to determine whether platelets might be activated across the coronary bed during a nonischemic interval in patients with vasospastic angina. Methods: Plasma levels of serotonin, 6-keto-prostaglandin F1 α, and catecholamines in the aorta and the coronary sinus were simultaneously measured in 16 patients with vasospastic angina and 13 control patients with nonischemic heart disease. Results: None of these patients showed myocardial ischemia during sampling. The difference in transcardiac plasma levels of serotonin in patients with vasospastic angina was significantly higher than that in controls (1.48 ± 1.08 ng/ml vs. 0.07 ± 0.12 ng/ml, respectively, p<0.001). Coronary sinus plasma norepinephrine levels in these two groups were almost the same (204.8 ± 110.8 pg/ml vs. 190.4 ± 131.6 pg/ml, respectively). The ratio of 6-keto-prostaglandin F1 α in the coronary sinus and the aorta was not different between the two groups (1.17 ± 0.96 in patients with vasospastic angina vs. 1.15 ± 0.68 in controls). Conclusions: These data suggest that platelet activation across the coronary bed should be ascribed to endothelial dysfunction. Lack of compensatory enhancement of prostacyclin production might be concerned with dysfunction of coronary endothelial cells in these patients.     

Cardiac amyloidosis presenting as microvascular angina--a case report

Cardiac amyloidosis usually presents with heart failure, but rarely leads to coronary insufficiency. The authors report a case of a 69-year-old Japanese woman with cardiac amyloidosis presenting as microvascular angina. She had exertional angina with positive exercise test and normal coronary angiograms. However, heart failure developed, and she died 3 years after symptom onset. On autopsy, coronary arteries were patent. In contrast to that of the epicardial coronary arteries, histologic examination of the heart revealed severe obstructive alterations of the intramural coronary arteries with amyloid. Furthermore, amyloid was present mainly in the endocardium and the intramural coronary arteries, but there was little present in the myocardium. This case was a rare AL amyloidosis. There have been only 4 reported cases of cardiac amyloidosis that presented with exertional angina, a positive exercise test, and normal coronary angiograms and histologic examination.     

Long-term prognosis of spastic angina with normal or irregular coronary arteries. Apropos of 48 cases

Forty-eight consecutive patients (37 men, 11 women, mean age 49 +/- 8 years) were followed up regularly for a mean period of 7 years. All presented with spontaneous angina, documented coronary spasm and no stenosis greater than 50 p. 100 at coronary arteriography. The first attack of pain had taken place 3 days to 9 years previously; exertion angina was also present in 47 p. 100 of the cases and severe arrhythmia in 17 p. 100. Treatment was based on calcium antagonists in doses and combinations that varied with the course of the disease. The follow-up period lasted from 16 to 122 months (mean 85 +/- 24 months). 3 patients are now known to be alive but were lost sight of after 12 to 21 months. Major cardiac complications were 1 death (2 p. 100) and 3 cases of myocardial infarction (6.6 p. 100). None of the patients died suddenly. 70 p. 100 of the remaining 41 patients became asymptomatic; angina persisted in 15 p. 100 and 14 p. 100 had episodes of severe angina but with remissions of at least one year. No predictive factor of functional deterioration or major cardiac complications could be elicited. The long-term prognosis of vasospastic angina in patients with little or no coronary stenosis is favourable, but there is a very small risk of myocardial infarction or death.