To twenty six patients with angina at rest (including 13 patients with Prinzmetal's variant angina), propranolol 40-50 mg, dilitiazem 60-90 mg, dipyridamole 50 mg, atropine sulfate 0.6 mg and phenoxybenzamine 10-20 mg were given at 9:00 p.m. and 2:00 a.m. (except phenoxybenzamine which was given only at 9:00 p.m.) to examine the effect of these drugs on the attack. Propranolol was not only ineffective in suppressing the attack but rather tended to aggravate it in all the cases of Prinzmetal's variant angina. It was effective to some degree in 5 of 13 cases of angina at rest other than Prinzmetal's variant angina. Diltiazem suppressed the attack completely and dramatically in all the cases of angina at rest (including Prinzmetal's variant angina). Dipyridamole was ineffective in all the cases except one in suppressing the attack. Atropine sulfate and phenoxybenzamine suppressed the attack in 13 of 21 cases and in 6 of 12 cases respectively. Coronary arteriography was done before and after the intravenous administration of 10 mg of diltiazem in 8 patients and it was demonstrated that diltiazem dilates large coronary arteries in all these patients. It is concluded that diltiazem, a calcium antagonistic drug, is specifically effective in suppressing the attack of angina at rest by dilating large coronary arteries and that the cautonomic nervous system plays a role in the genesis of the attack probably by constricting large coronary arteries by way of alpha adrenergic receptors.

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Quantitative one-plane cineangiocardiography in right anterior oblique position for evaluation of LV performance was carried out in 62 patients with various heart diseases and in 13 subjects with normal LV. Parameters for evaluating both pump and muscle performances were derived from volume and pressure measurements. Of 31 patients with either systolic hypertension or LV myocardial diseases (coronary artery disease or idiopathic cardiomyopathy), 14 had clinical evidence of LV failure before the study. It was found that mean V_CF and EF were most sensitive indicators of impaired LV performance among the various parameters. There was a close correlation between mean V_CF and EF, yet discordant changes of both parameters were noted in some patients. Furthermore, wall motion abnormalities were not infrequently observed in patients with coronary artery disease or primary cardiomyopathy. Therefore, assessment of at least three ejection properties (EF, mean V_CF and wall motion abnormalities) are considered to be essential for full understanding of derangement of LV function in heart disease. This is especially true of patients with coronary artery disease. LV behavior in relation to different pathological stresses or lesions, such as chronic pressure or volume load, myocardial disease and mitral stenosis, was also studied and possible cause of impaired LV myocardial function in mitral stenosis was discussed.

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Mice were inoculated with recently isolated Coxsackie virus B-3 and B-4 intraperitoneally. Severest lesions in the hearts were observed in mice between the age of 7 and 14 days. Grossly, yellow-white patches were seen on the hearts of mice from the 7th day to the 6th month after virus inoculation. Microscopically, the hearts showed extensive myocardial necrosis, inflammation with small mononuclear cells and calcification on the day of 7. There were myocardial fibrosis and calcification at the 6th month after inoculation with Coxsackie virus B-3, and at the 3rd month after inoculation with Coxsackie virus B-4, but generally pathologic changes were less severe in the latter. Myocardial fibrosis in the present experiment was most prominent among the experiments we have studied. It was confirmed that chronic myocardial fibrosis follows acute Coxsackie virus myocarditis in mice. Possible role of Coxsackie virus myocarditis in the development of cardiomyopathy was briefly discussed.

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We stressed the importance to check consequent voltage change dependent on the etiopathogenetic varieties of the disease. The voltage showed rapidly increasing curves in cases with non-specific pericarditis, which would mean the myocardium showing inflammatory enlargement resulted from supermyocarditis after affection. Contrastly, those of secondary ones were not significantly changed. Those findings on voltage change are very useful guidline to diagnose the disease particularly in cases with vague synptoms and/or cases without obvious finding in the eary stage, besides to lend making differential diagnosis on the varieties of the disease.

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The purpose of this experimental and clinical study was to evaluate the utility of body surface maps in detecting the preexcitation site of WPW syndrome. By using the electrical bypass tract, the electrocardiographic patterns of WPW syndrome were simulated by the fusion beat between pre- and normal excitation of the in situcanine ventricle. A comparison was made between the body surface and the epicardial maps of the same fusion beat. Throughout the ventricular activation serial body surface maps represented well the activation sequence on the epicardium. The following three points seem to be important for the detection of the preexcitation site of WPW syndrome through the use of body surface maps; 1) the location of the initial minimum, 2) the time of appearance of the voltage concavity (or the saddle) in the right anterior chest wall (in posterior preexcitation), 3) and in addition, the sequential changes in the pattern of positive and negative areas throughout the ventricular activation. In clinical use, body surface maps also localized well the preexcitation sites of the patients with WPW syndrome who underwent the operation.

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