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A 75-year-old woman presented with recurrent ventricular tachycardia (VT) compatible with torsades de pointes (TdP) based on sinus bradycardia and QT prolongation. Previously she had received pirmenol, at a serum concentration within therapeutic range, for her paroxysmal atrial fibrillation. Emergent cardiac catheterization identified a ventricular aneurysm of the anteroapical and inferior wall along with angiographically normal coronary arteries. A right ventricular endomyocardial biopsy revealed postmyocarditic change. The left ventricular contraction improved after 5 weeks of conservative treatment. A follow-up echocardiogram revealed transient thickening of partial left ventricular wall consistent with the segment of the aneurysm. Several months later, almost all abnormal findings had improved except for sustained deep negative T waves in precordial leads. Acute myocarditis was primarily suspected as the cause of her clinical presentation.

To clarify the mechanism and the predictors of the reduction in left ventricular mass (LVM) induced by antihypertensive drugs, forty hypertensive patients were classified according to the presence of left ventricular hypertrophy (LVH) as a defined by echocardiographic LVM findings (LVH group: 27 patients, non-LVH group: 13 patients) and according to the presence of negative U-waves (NU) (NU group: 10 patients, non-NU group: 30 patients). Negative U-waves appeared in the LVH group only (10 of 27 patients). The hemodynamic determinants were investigated as a mechanism of LVM reduction in 38 of these patients who were treated for 2 years with antihypertensive drugs. In the LVH group, thickness of interventricular septum (IVST), posterior wall thickness (PWT) and LVM increased significantly compared to the non-LVH group. In the NU group, the left ventricular end-diastolic dimension (LVDD) was significantly larger and the relative wall thickness was significantly smaller compared to the non-NU group in the LVH group, with no difference in LVM between the two groups. Negative U-waves disappeared in all cases after treatment. Significant decreases in LVDD and LV wall thickness were observed in the NU group and significant decrease in LV wall thickness in the non-NU group. LVM index was reduced by 24.0% in the NU group and 9.5% in the non-NU group. The disappearance of negative U-waves was an independent predictor of the reduction of LVH.

Dobutamine stress echocardiography has become a diagnostic tool for the evaluation of coronary artery disease and the detection of myocardial viability. In the diagnosis of significant coronary artery disease, it provides similar accuracy to exercise stress thallium-201 myocardial perfusion scintigraphy. Dobutamine stress echocardiography is also a promising modality for predicting the recovery of hibernating myocardium from contractile dysfunction after coronary angioplasty or bypass surgery. This article, reviews our recent clinical experience with the detection of coronary artery disease and viable myocardium by dobutamine stress echocardiography.

To determine whether syncope predisposes to sudden cardiac death, variant angina patients with syncope during cardiac attacks were compared with those without syncope. There were 240 consecutive patients (193 males and 47 females) diagnosed with variant angina pectoris. Thirty patients had a history of syncope during cardiac attacks while the remaining 210 had none. The incidence of cardiac events in the former group was 10.0% (3 of 30) and 10.5% in the latter. There were 3 cases of sudden cardiac death, all in the latter group. Significant clinical variables in the syncope patients included inferior ST-segment elevation and serious arrhythmias. We conclude that there is no relationship between syncope during variant angina and sudden cardiac death.

We investigated the role of myocardial ischemia in acute myocardial infarction and cardiac death in 253 patients with asymptomatic coronary disease (206 men, 47 women, mean age: 55 +/- 8 years). Patients were divided into two groups: those with angina pectoris with no history of myocardial infarction (AP group, 93 patients) and those with a history of myocardial infarction (MI group, 160 patients). We also examined the usefulness of exercise electrocardiographic and Holter electrocardiographic findings as prognostic indicators of cardiac events. After 24-hour Holter electrocardiograms were obtained in both groups, patients were assigned to subgroups with or without silent myocardial ischemia (SMI) based on the presence or absence of transient ST-segment depression. Prognostic indicators were evaluated by multiple regression analysis. Cardiac events occurred in 26 (10.3%) of 253 patients; in 6 patients these events were fatal. The incidence of cardiac events was significantly higher in the SMI group than in the non-SMI group (16.4% versus 5.6%, p < 0.05). SMI was identified as a significant prognostic indicator in the overall population (p = 0.0088), as were the number of diseased coronary arteries in the AP group (p = 0.0152), and SMI (p = 0.0022) in the MI group. There were 3 deaths related to cardiac events in each group. The mean time from onset of angina pectoris to death was 73 +/- 41 months compared with 33 +/- 43 months in the MI group. Our findings suggest that the severity of the coronary lesion and SMI were important predictors of major cardiac events, and that the mechanism of the onset of cardiac events was different in the AP and MI groups.

To investigate the usefulness of nicorandil as an antianginal drug, we compared the coronary vasodilatory response in nonstenotic coronary artery segments and the hemodynamic response in 26 coronary artery disease patients. Both responses were studied prior to sublingual administration of 10 mg of this drug and 10, 30 and 60 min afterward. The plasma nicorandil concentration was determined up to 120 min after administration. The mean coronary dilating ratio of nicorandil was 117% 30 min after administration (p less than 0.01) and showed a good correlation to the plasma nicorandil concentration. The mean maximum dilating ratio of each patient was 125%. There was no difference between individual coronary arteries or between proximal and distal segments in terms of the coronary artery dilating ratio. The plasma nicorandil concentration required for 120% dilation of the coronary arteries was 26 ng/ml, 89 ng/ml and 142 ng/ml for those cases with variant angina, exertional angina and postinfarction angina, respectively. Hemodynamic changes due to administration of this drug included a decrease in blood pressure, and a reduction in total peripheral resistance, rate-pressure product, pulmonary capillary pressure and stroke-work index. These results indicate that the antianginal effects of nicorandil are derived from its coronary vasodilatory action and an inhibitory effect on myocardial oxygen consumption.

The extremely prominent negative U wave occasionally appears during a cardiac attack in variant angina pectoris. The clinical profile of the negative U wave was therefore studied in 80 patients with variant angina pectoris (VA) and 33 controls with resting angina pectoris (RA). The prominent negative U wave appeared in 55 of the patients with VA (68.8% of patients) and in 10 of the patients with RA (30.3%); thus, there was a significant difference in the appearance of the wave between the 2 groups of patients (p less than 0.001). The leads in which the negative U wave appeared were mostly consistent with those in which the ST segment was elevated. The negative U wave began to appear at about the time when ST-segment elevation began to improve; the wave then gradually became very prominent and then eventually disappeared. The patients with VA and also those with RA on whose ECGs the negative U wave appeared during exercise testing also had negative U waves during spontaneous episodes of angina. An investigation of the frequency of appearance of ST deviation and negative U waves during exercise testing, regardless of the type of angina pectoris, disclosed that the negative U wave appeared in 14 of 20 patients with ST-segment elevation (70% of patients), while the negative U wave appeared in only 52 of 519 patients with either no ST change or ST-segment depression (10.4%); thus, there was a significant difference in the appearance of the negative U wave between these 2 groups (p less than 0.001). Coronary cinearteriography failed to disclose any apparent difference between the appearance of the negative U wave and the presence of stenosis. The prognosis of VA and RA in patients with negative U waves was less favorable compared to those without negative U waves. In particular, we noted that of the 10 patients with RA associated with negative U waves, 4 died. Although the mechanism of the negative U wave is not yet known, we believe that the above findings contribute to its elucidation.

A 48-year-old man had histologically demonstrated cardiac involvement associated with progressive muscular dystrophy. On coronary arteriography, numerous vascular communications between the coronary arteries and the left ventricular chamber were found. These vascular communications are considered to be the arterioluminal vessels. This is the first report of a case of progressive muscular dystrophy with numerous arterioluminal vessels.

In order to clarify the clinical significance of a persistent negative U wave in patients with myocardial infarction, the clinical features and prognosis of a group of such patients were compared with a group without negative U waves. The persistent negative U wave was defined as the presence of a negative U wave at the time of discharge. The subjects were classified into 2 groups: group A--55 patients (50 males and 5 females, 59 +/- 10 years) with negative U waves; group B--70 patients (55 males and 15 females, 61 +/- 9 years) without negative U waves. The average follow-up periods were 49 +/- 21 months in group A and 42 +/- 18 months in group B. Negative U waves appeared in leads where r or R waves were present, but were not observed in leads with a QS pattern. The incidences of a diseased left anterior descending artery, multi-vessel disease, left ventricular wall motion abnormality and left ventricular ejection fraction below 50% were higher in group A than in group B. The recurrence of myocardial infarction was 18.2% in group A and 7.1% in group B, and the number of patients treated with antianginal drugs was higher in group A than in group B. The rate of recurrence of myocardial infarction at 1, 3 and 5 years was 6%, 17% and 26%, respectively in group A and 6%, 8% and 11%, respectively in group B. Thus, it was concluded that patients in group A require more active treatment than those in group B.

The purpose of the present study was to clarify the characteristics of myocardial ischemic attacks in patients with exertional angina (EA, 56 cases), exertional and rest angina (ERA, 28 cases), rest angina (RA, 4 cases), and variant angina (VA, 39 cases). The Holter electrocardiographic findings were compared among the four types of angina pectoris. The frequency of symptomatic ischemic attacks in descending order was 46.0% in EA, 29.0% in ERA, 28.1% in RA, and 21.6% in VA, while the frequency of asymptomatic ischemic attacks was in the reverse order. The maximal heart rates during symptomatic ischemic attacks were in descending order, EA, ERA, RA, and VA. The maximal heart rate during ischemic attacks was significantly lower in patients with spontaneous angina than in those with exercise-induced ischemia for all types of angina (p less than 0.05, respectively). Further, the difference in maximal heart rate during ischemic attacks between the ambulatory electrocardiogram and exercise test was greater in patients with RA and VA than in those with EA. Therefore, this suggests that increased coronary vascular tone is a cause of spontaneous ischemic attacks in each type of angina pectoris.

The effects of drugs were evaluated in 47 cases with variant angina (VA), 19 with resting angina showing ST depression (RA), and 84 with unstable angina (UA). In VA patients, calcium antagonists were effective in 87.1% of the cases, while other drugs were effective in 56.3%. The difference was statistically significant. In RA patients, calcium antagonists were effective in 80.0% of the cases and other drugs in 44.4%. Nifedipine was effective in all 5 cases with coronary stenosis of more than 75.0%. All cases of RA had multiple vessel disease and nifedipine was effective in 80.0% of the patients. Nifedipine was effective in 83.3% of VA cases showing ST elevation during an exercise test, and was particularly effective in all patients having attacks only at rest. The effects of nifedipine were confirmed in 83.3% of UA cases. These results indicate that calcium antagonists are effective in VA, RA, and UA.

The purpose of this study was to clarify the factors influencing the clinical course and prognosis in variant angina. Also, the mechanism of acute myocardial infarction in variant angina is reviewed. The subjects were 110 patients with variant angina who, after the initial visit or admission, were observed for a period of at least 2 months, the average observation period being 68 +/- 49 months (range: 2 months-16 years). The incidence of acute myocardial infarction was 21.8% of these patients and 87.5% of the infarctions occurred within 1 month of the initial visit or admission. In variant angina, the average rate over 1 year was 2.2%; however, in classical angina the rate was 3.7% and in postinfarction angina 5.0%. The mortality rate was 5.5%, with death in the majority of cases occurring within 1 month, as in myocardial infarction. When treatment was stopped, spontaneous remission occurred in at least 26 of the 110 cases (23.6%). Beyond 3 months, the remission continued in 19 of these 26 cases. Seven cases had acute myocardial infarction in spite of the suppression of anginal attacks with administration of calcium antagonists. Apparently coronary spasm is the cause of anginal attacks, and the cause of acute myocardial infarction in patients with variant angina appears to be coronary thrombus formation.

The purpose of this study was to investigate the efficacy, effective dose, administration frequency and antianginal effect of a new antianginal agent, nipradilol, in 12 patients with stable effort angina. A single blind design was employed; the test consisted of an observation period (1 week) and a treatment period (1-2 weeks). Twenty four hour Holter monitoring was performed on the penultimate day of each period. Nipradilol was administered twice a day at a daily dose of 3-12 mg (mean 7.9 +/- 3.3 mg). The mean frequency of ST-segment depression was 7.1 +/- 6.7 times per day at baseline and 3.1 +/- 2.7 after drug administration, showing a significant reduction (p less than 0.05). The suppression of ST-segment depression and decrease in heart rate due to this drug persisted for 12 hours following administration. The plasma drug concentration at a daily dose of 12 mg peaked at 9.5 +/- 2.4 ng/ml 1 hour after administration and the 12 hour value was 2.3 +/- 1.2 ng/ml. No side effects were observed. Therefore, it seems that, when administered twice a day (total daily dose 6 mg) this drug is effective in effort angina and that the antianginal effect is mainly attributable to beta-adrenoceptor blockade.