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Monomorphic sustained ventricular tachycardia (MSVT) was revisited in relation to the electrophysiologic findings and their relation to the drug efficacy. Old myocardial infarction is less common cause of MSVT in Japan, and the majority (about 2/3) of MSVT is unrelated to coronary artery disease but, the mechanism shared a common mechanism: reentry with an excitable gap as others. The reentrant mechanism was supported from the inducibility, the terminability of VT by electrical stimulation, and by the ability to entrain with rapid pacing. In MSVT associated with underlying heart diseases, diseased myocardium showed low amplitude and fragmented electrograms and the area was considered to participate as the central common pathway of reentrant circuit. The area of slow pathway showed a decremental conduction or all-or-nothing conductive property. The width of the excitable gap seemed to be determined by the maximal conductive frequency but not by the duration of action potential: effective refractory period. As to the drug efficacy, there was no baseline characteristics in predicting the efficacy. However, the significant narrowing of the width of the excitable gap was associated with the drug efficacy and VT became non-inducible after addition of the same drug. The response pattern of the excitable gap to specific drug including class III, was not predictable. Further electropharmacological studies will be warranted.

The purpose of this study was to investigate the incidence of multivessel coronary spasm and compare the clinical characteristics between patients with and without multivessel coronary spasm. In variant angina, it is controversial whether coronary hyperreactivity to vasoconstrictor stimuli is localized to a segmental lesion in only one coronary artery. Moreover, the clinical characteristics of patients with multivessel coronary spasm have never been investigated. Sixty-three patients (51 men and 12 women; mean age, 56 years; range 35-72 years) with variant angina and documented ST-segment elevation during a spontaneous attack underwent spasm provocation testing with selective intracoronary injection of ergonovine. All but 4 patients who experienced spontaneous attacks during cardiac catheterization had induced coronary spasm associated with ST-segment elevation and chest pain. Multivessel coronary spasm was found in 27 (43%) of 63 patients. By univariate analysis, a high frequency of angina (> or = 3 times/week), occurrence of a spontaneous attack within 24 hours after withdrawal of medication, a long history of angina and a progressive course of angina were significantly associated with multivessel coronary spasm. Multivariate analysis indicated a positive correlation between multivessel coronary spasm and progressive angina. Multivessel coronary spasm was found in 43% of patients with variant angina. Patients with multivessel coronary spasm have some unique clinical features. These results may increase the understanding of the pathophysiology and natural course of variant angina.

The purpose of this investigation was to evaluate the effect of digoxin on aerobic performance in mildly symptomatic patients with congestive heart failure and sinus rhythm. Ten patients (8 men and 2 women) with idiopathic dilated cardiomyopathy (ejection fraction 17 to 33%, mean 27 +/- 4%) who were stable and mildly symptomatic with maintenance digoxin and diuretic therapy were studied. All patients underwent maximal symptom-limited ergometer exercise with analysis of respiratory gases during maintenance digoxin therapy, 4 weeks after digoxin withdrawal, and 4 weeks after digoxin readministration. Exercise capacity was assessed by peak oxygen uptake and anaerobic threshold. Serum digoxin concentration was 1.0 to 1.8 (mean 1.3 +/- 0.2) ng/ml during digoxin therapy, and less than the detectable level after digoxin withdrawal. No patients showed clinical deterioration after digoxin withdrawal. Peak oxygen uptake after digoxin withdrawal (23.7 +/- 3.0 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (23.8 +/- 2.5 ml/kg/min) or after digoxin readministration (24.1 +/- 2.9 ml/kg/min). The anaerobic threshold after digoxin withdrawal (14.9 +/- 2.5 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (15.0 +/- 2.1 ml/kg/min) or after digoxin readministration (14.9 +/- 2.2 ml/kg/min). No differences in heart rate and diastolic blood pressure were observed during exercise, but systolic blood pressure during exercise was significantly higher with digoxin therapy (p < 0.05). These results suggest that digoxin has no effect on aerobic performance in mildly symptomatic patients with idiopathic dilated cardiomyopathy and sinus rhythm.

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

An extremely rare case of hypereosinophilic syndrome is reported. The patient had congestive heart failure due to left ventricular obliteration by a giant thrombus in the apex. Arteriosclerosis obliterans resulted in serious lower extremity gangrene. Combination therapy with a corticosteroid and hydroxyurea caused a marked reduction in eosinophil count, and heart failure recovered in stages. Although the patient was discharged, he returned to our hospital 3 months later with acute myeloblastic leukemia and subsequently died of respiratory failure with pneumonia.

A 46-year-old Japanese woman, who had been diagnosed as having aortitis syndrome 4 years earlier, was admitted to our hospital in May 1989. The diagnosis of aortitis syndrome was confirmed by intravenous digital subtraction angiography which showed stenotic lesions in each subclavian artery, the left common carotid artery, and the descending aorta. Coronary arteriography revealed diffuse and prominent dilatation of entire coronary artery segments. Moreover, a left ventriculogram showed complete obstruction of the mid-ventricle during systole. Thus, we diagnosed this case as aortitis syndrome complicated by coronary artery ectasia and mid-ventricular obstruction. The causal relations of these findings are discussed.

We report a case of a 44-year-old male with variant angina who developed acute anterior myocardial infarction 2 weeks following demonstration of normal left coronary artery. This experience provides inferential evidence that myocardial ischemia resulting from coronary spasm may progress into myocardial infarction.

To investigate the relationship between mechanical and metabolic deterioration in the ischemic myocardium following a decrease of coronary blood flow, the patterns of regional myocardial contraction and myocardial adenosine triphosphate (ATP) content were analyzed simultaneously in canine left ventricles with constriction of the left anterior descending coronary artery (LAD). The patterns of contraction in the ischemic region were monitored by means of ultrasonic dimension gauges implanted in the endocardial surface and were classified into 5 types; Type 0 = normal, Type I = late systolic lengthening, Type II = early and late systolic lengthening with end diastolic length elongation, Type III = systolic bulge with early diastolic shortening, and Type IV = holosystolic bulge. Type I developed in 6/8 dogs with 1-49% LAD flow reduction, Type II in 6/8 dogs with 50-74% reduction, and Types III and IV in all dogs with 75-100% reduction. The myocardial ATP content (microM/Gm tissue) at the sites of the patterns of myocardial contraction measurement was analyzed. No differences in ATP content were noted between Type 0 and Type I (3.70 +/- 0.51 vs. 3.60 +/- 0.36). In contrast, the ATP content in Type II was significantly reduced (2.94 +/- 0.20) compared to Type I (p less than 0.005). In Types III + IV with systolic bulge, the ATP reductions were severer (2.59 +/- 0.36) than in Type II (p less than 0.05). In conclusion, it can be said that as the LAD flow reduction advanced, the patterns of myocardial contraction were transformed from Type 0 to Type IV with accompanying ATP reductions.

The effects of supervised mild aerobic exercise at the work load of the blood lactate threshold for 10 weeks on serum lipids and apolipoproteins were studied in 24 patients with essential hypertension. Significant reduction in both systolic and diastolic blood pressure and increased maximal oxygen uptake were observed in both men and women. The high density lipoprotein cholesterol increased significantly following mild aerobic exercise in women. Apolipoprotein A-II was significantly elevated at the 4th week in women. No significant differences in total cholesterol, triglyceride, low density lipoprotein cholesterol, apolipoproteins A-I, C-II, C-III, B and E were observed in either men or women following an exercise program. These data demonstrate the different effect of mild aerobic exercise therapy on high density lipoprotein in hypertensive men and women.

The effects of mild aerobic exercise on serum lipids, apolipoproteins and lecithin-cholesterol acyltransferase (LCAT) activity were examined in 11 male patients with coronary artery disease and 4 healthy male controls. The mild aerobic exercise program involved exercise intensity at 50% of maximal oxygen uptake, as determined from the blood lactate threshold, for 60 min periods 3 times per week for 10 weeks. Following mild aerobic exercise, serum levels of high density lipoprotein cholesterol (HDL-C) were increased significantly from 50 +/- 7 mg/dl to 59 +/- 11 mg/dl (p less than 0.05) with a simultaneous increase in apolipoprotein A-I (apo A-I) in normal controls. The LCAT activity was significantly increased from 65 +/- 22 nmol/ml/hr to 99 +/- 30 nmol/ml/hr in normal controls (p less than 0.05). Furthermore, maximal oxygen uptake (VO2max) was significantly increased in normal controls. In contrast, no significant changes were found in HDL-C, apo A-I, apo B, VO2max and body weight in patients with coronary artery disease. There was significant correlation between the initial HDL-C level and the change in HDL-C level following the exercise program in the combined group of normal controls and patients with coronary artery disease.