[Comparison of the circadian variation of the time of onset of acute myocardial infarction and of attack of vasospastic angina without significant stenosis].

OBJECTIVES: To study the involvement of vasospasm as the trigger of acute myocardial infarction without significant stenosis, the circadian variation of the time of onset of acute myocardial infarction was compared with that of vasospastic angina without significant stenosis. METHODS: The subjects consisted of 3 groups, 64 patients with acute myocardial infarction without significant stenosis, 101 patients with acute myocardial infarction with one vessel disease and 98 patients with vasospastic angina without significant stenosis. The times of onset of acute myocardial infarction and spontaneous attack of vasospastic angina were recorded and classified according to the 4 periods (0:00-6:00, 6:00-12:00, 12:00-18:00, 18:00-24:00) and the pattern of distribution was compared between the 3 groups. RESULTS: The time distribution of acute myocardial infarction without significant stenosis showed a double peaked pattern at 6:00-12:00 and 18:00-24:00 and was similar to the pattern of acute myocardial infarction with one vessel disease(p = 0.93). Only a single peak in 0:00-6:00 was found in the pattern of distribution of vasospastic angina without significant stenosis and differed significantly from acute myocardial infarction(p < 0.01). CONCLUSIONS: The circadian variation of the time of onset of acute myocardial infarction was similar in patients with or without significant stenosis, and differed significantly from that in patients with vasospastic angina.

[Multi-vasospastic angina refractory to medical therapy caused by hyperthyroid stage of chronic thyroiditis and hypereosinophilia: a case report].

A 49-year-old woman with bronchial asthma was followed up at our hospital. After 3 years, she experienced an attack of chest pain with ST elevation in the precordal leads of electrocardiography. After admission, the chest pain and ST elevation disappeared, but the chest pain recurred after 6 days. Coronary angiography revealed no significant stenosis in the coronary arteries. After discharge, she had the chest pain repeatedly. ST elevation in the II, III, aVF leads was recorded. The diagnosis was coronary multispasm. The chest pain was refractory to medical therapy. Hypereosinophilia developed and bronchial asthma worsened. After steroid administration, the angina and bronchial asthma ceased. She has lost about 15 kg during 1 year. Laboratory data revealed low thyroid-stimulating hormone, high thyroid hormone, positive thyroglobulin antibody, and negative thyroid-stimulating hormone receptor antibody. The diagnosis was chronic thyroiditis. The multi-vasospastic angina refractory to medical therapy was caused by the hyperthyroid stage of chronic thyroiditis and hypereosinophilia.

[Cardiac events in vasospastic angina: site and morphology of coronary artery spasm is related to the long-term prognosis of vasospastic angina].

To determine whether the site and morphology of coronary artery spasm provoked with acetylcholine can predict the long-term prognosis of vasospastic angina, coronary artery spasm (more than 90% narrowing) provoked with acetylcholine was studied in 66 consecutive patients (56 males, 10 females, mean age 56 +/- 9 years) with vasospastic angina. All patients were followed for 6.7 +/- 0.9 years and the incidence of cardiac events such as sudden death, myocardial infarction or worsened unstable angina was compared with the site and morphology of provoked spasm. The site of spasm was regarded as proximal when spasm occurred in the proximal site of 3 major coronary arteries which was designated as segment 1, 6 or 11, according to the classification of the American Heart Association, and distal in other segments. The morphology of spasm was classified into 3 types, focal (12 cases, localized more than 90% narrowing with adjoining parts constricting less than 25%), diffuse (17 cases, diffuse more than 90% narrowing), and intermediate (37 cases, localized more than 90% narrowing with adjoining parts constricting 25-90%). The site of spasm was classified into 2 types, the proximal group (24 cases) and the distal group (42 cases). Cardiac events occurred in 7 patients during the follow-up period: sudden death in 2, myocardial infarction in 2, and worsened unstable angina in 3. As to the site of spasm, the incidence of cardiac events was 21% (5/24 patients) in the proximal group, significantly higher than 5% (2/42) in the distal group (p < 0.05). As to the site of spasm, the incidence of cardiac events was 41% (5/12) in the focal group, significantly higher than 3% (1/37) in the intermediate group and 6% (1/17) in the diffuse group (p < 0.001). The presence of proximal and focal coronary artery spasm was associated with a significantly higher incidence of cardiac events. The site and morphology of coronary artery spasm provoked with acetylcholine is related to the long-term prognosis of vasospastic angina.

[Reproducibility of spasm in patients with long-term remission of vasospastic angina by medical treatment].

The reproducibility of coronary vasospasm was assessed in nine patients with complete remission of vasospastic angina by medical treatment by reexamination at intervals of mean [+/-SD] 5.7 +/- 0.9 years. Twenty-one segments were defined as spastic, demonstrating more than 90% narrowing after acetylcholine injection at the initial angiography. The degree of spasticity, type of spasm (diffuse or focal) and coronary artery diameter in these segments at the initial and follow-up studies were compared. Of the 21 segments, 17 (81%) still had some spasticity (> 25%) at the follow-up study and 8 (38%) of these 17 showed spasticity with greater than 90% narrowing. On the other hand, spasm was not reprovoked in 4 (19%) segments. Luminal diameter of the spastic segments decreased significantly at the follow-up study (2.52 +/- 0.83 vs 2.26 +/- 0.62 mm, p = 0.01), but percentage stenosis was not different between the initial and follow-up studies (9.1 +/- 7.2 vs 10.3 +/- 8.0%, NS). The reproducibility of the type of spasm provoked was 83%. Coronary vasospasticity persists to some extent in spite of complete remission of angina by medical treatment, and the type of spasm provoked has high reproducibility. Therefore, the cessation of drug treatment should be done carefully.