A formula to estimate heart weight was derived using a theory of quantification which employed the measurements of cardiac silhouette taken from routine postero-anterior projection chest X-ray film. The films obtained in 73 necropsied cases of essential hypertension, renal hypertension, mitral and aortic valvular diseases, and 62 necropsied cases with other diseases were used for derivation of the formula. The measurements of the horizontal distances from the midsternal line to the intersecting point of the lower margin of each rib along the left cardiac border, and of the greatest distance along the right cardiac border were employed; body height, age and sex were also included.The heart weight estimated by this formula coincided with the heart weight measured at necropsy with a high correlation coefficient of 0.81. The correlation rate in 34 external samples was also significantly high, being 0.72. These results indicate the practical usefulness of this formula.

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Clinical, echocardiographic, hemodynamic, and angiographic features of 7 patients with midventricular obstruction, aged 12-51 years, are described. All had cardiac catheterization and left ventricular cineangiography with special care to eliminate catheter entrapment. Simultaneous biventricular cineangiography was performed in 2 subjects and autopsy in another. Carotid upstroke was brisk in all but 1. Echocardiogram, available in 6 patients, showed septal thickness in all, however systolic anterior motion of the mitral valve was absent in 5 individuals. A resting gradient ranging from 58 to 185mmHg (mean 117mmHg) was detected across the midventricular narrowing in 6 patients. In 1 patient with no resting gradient, 40mmHg pressure difference was provoked between the apex and inflow tract following intravenous administration of isoproterenol. Midventricular obstruction, distinctly different from subaortic narrowing observed in hypertrophic obstructive cardiomyopathy (HOCM) was present in cineangiogram. Midbiventricular bulging of the septum was present in 2 patients with simultaneous biventricular cineangiogram and another at autopsy.Disappearance of gradient following intravenous administration of propranolol and its return after sublingual administration of nitroglycerine favor the dynamic nature of the obstruction. Midventricular obstruction must be distinguished from HOCM by its characteristic hemodynamic and angiographic features for proper surgical approach, consisting of midventricular myectomy with or without papillary muscle resection and mitral valve replacement.

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One hundred and eight patients with ventricular septal defect (VSD) including 20 operated patients were studied with real time cross-sectional echocardiography combined with M-mode echocardiography.
The subjects were divided into 3 groups according to the cross-sectional echocardiographic findings. Group 1 included 34 patients in whom the defect area of interventricular septum (IVS) was demonstrated and they were diagnosed as VSD solely with this method. The majority of the patients in this group showed marked pulmonary hypertension and severe cardiac symptoms. Group 2 consisted of 13 patients who showed abruptly posterior movement of IVS toward the left ventricular cavity at early diastole and were suspected of VSD. Group 3 consisted of 41 patients with VSD showing normal cross-sectional echocardiograms without echo discontinuity of IVS. This group had a small defect of IVS with near normal pulmonary artery pressure.
The analysis of cross-sectional echocardiogram combined with M-mode echocardiogram and the data of other cardiac examinations revealed that group 1 showed a larger left-to-right shunt at the ventricular level, severer pulmonary hypertension and more marked heart enlargement than groups 2 and 3.
The patients with visualized defect of IVS had severe cardiac signs and symptoms and were indicated for the cardiac surgery.
In the postoperative patients, the patch echo was clearly recognized as a linear strong echo.
Real time cross-sectional echocardiograpy is available to visualize directly the defect of IVS in the majority of the patients with VSD and to estimate the condition of patients with this lesion.

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Thirty patients (22 males and 8 females, aged 64 to 89 years) with chronic bifascicular block were studied electrophysiologically and prognosis was assessed. Three had RBBB with LPH, 17 had RBBB with LAH, and 10 had LBBB.
AH interval was prolonged in 12 (43%) of 28 patients and HV interval was prolonged in 11 (37%) of 30 patients. Of 16 patients with first or second degree AV block, 11 (69%) had prolonged AH interval and 8 (50%) had prolonged HV interval. Effective refractory period of the right atrium was prolonged in 8 (50%) of 16 patients and that of atrioventricular node was prolonged in 9 (64%) of 14 patients. Second degree AV block was observed at lower rates of atrial pacing (130 beats/min or less) in 14 (74%) of 19 patients. Sinus node dysfunction was present in 16 (62%) of 26 patients. During the follow-up period (37.1±6.1 months), advanced or complete AV block developed in 2 of 27 patients (2.4% per year) and a patient died of acute myocardial infarction (1.1% per year).
The present study showed that prolongation of AH interval was observed more frequently than that of HV interval, and the presence of widespread lesions in the conduction system was suggested in chronic bifascicular block, and in spite of these facts prognosis was not so unfavorable as reported previously.

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Plasma renin substrate (PRS) was determined immediately before and 30min after the intravenous administration of 40mg of furosemide in 26 hypertensive subjects. PRS level after the administration of furosemide was found elevated by 30.5±4.7% which was statistically sigficant.

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From 1971 to 1977, a total of 43 cases with ventricular septal defect associated with pulmonary hypertension (VSD+PH), ranging from 3 months to 6 years of age, underwent VSD closure using cardiopulmonary bypass with a prophylactic dose of phenoxybenzamine (POB) 1mg/Kg. Twenty of these cases are included in the present study of the effect of POB on pulmonary hypertension. The ratios of pulmonary to systemic arterial pressures (Pp/Ps) and vascular resistances (Rp/Rs) were measured before, immediately after and 1 month after VSD closure. In all cases, the Pp/Ps before VSD closure was larger than 0.75. Both Pp/Ps and Rp/Rs markedly decreased immediately after VSD closure but rose again 1 month thereafter. These results suggest the possibility of pulmonary vasodilating effect of POB, which could be potentially useful in reieving the right ventricular load in the early postoperative period. The over all mortality was 3 out of 43 cases including 2 late deaths.

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A total of 25 cases (12 men, 13 women) of complete left bundle branch block (LBBB) were found among 1, 400 consecutive autopsy in the aged. Their ages ranged from 70 to 86 years (average 78.9). ECG was analyzed as for the occurrence of LBBB and myocardial infarction (MI). Pathological examinations included observations of the conduction system by serial sections. They were divided into group A with MI and group B without MI.
Duration of LBBB was 1 to 3 days in 4 cases, more than 1 month in 7, and more than 1 year in 14. From the temporal sequence of LBBB and MI in group A, cases were classified into (1) MI preceding LBBB in 5, (2) both coexistent in 5, and (3) LBBB preceding MI in 1. There were 8 cases of normal electrical axis, 17 left axis deviation, 7 first degree A-V block, and 2 atrial fibrillation. Various heart diseases were underlying in 21 cases, including hypertension, MI, mitral and aortic regurgitation, and primary myocardial disease, and there were 4 cases with no cardiac diseases. Cause of death was cardiac in 12; MI, congestive heart failure, and sudden death.
Heart weight was 410Gm on the average (240 to 550Gm). MI was found in 11, with stenotic index of 12/15, while it was 9/15 in group B. Lesions of the conduction system were slight to moderate (1.5 to 2.4) except left bundle branch, which showed marked changes in posterior (4.9) and anterior (4.8) fascicles. Site of interruption of the left bundle branch was the junction between the branching portion of the A-V bundle and the left bundle branch (Junctional type) in 17, and peripheral portion of the left bundle branch about 10mm or more below the junction in 8 (Peripheral type).
In conclusion, 2/3 of cases of LBBB belonged to the junctional type and most of them were not related to MI, but to the lesions caused by mechanical injuries at the septal summit. One third of the cases were as peripheral type, which was mainly related to the various types of lesions including septal ischemia (necrosis and fibrosis).

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The concentration of myocardial cyclic AMP was measured in 9 dogs by radioimmunoassay after the administration of aminophylline. Fourteen dogs served as control. The concentration of cyclic AMP in the left ventricle was the highest and the lowest value was obtained in the right atrium in the control dogs. Ventricular fibrillations were induced immediately after the injection of 30mg/Kg aminophylline in 3 dogs out of 9. The concentration of the left ventricular cyclic AMP in 6 dogs which tolerated aminophylline was significantly elevated compared with that of the control dogs (p<0.05). The left ventricular cyclic AMP in 3 dogs with ventricular fibrillation was significantly higher compared with that in the aminophylline tolerated dogs with non-fibrillating hearts (p<0.01).
These results showed that the concentration of cyclic AMP was elevated in the fibrillating heart.

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Compound 48/80 and Polymyxin B elicited prompt and sharp increases in histamine output from the isolated guinea pig heart and had no effect on norepinephrine output. Dextran decreased histamine output without affecting norepinephrine output. Bradykinin increased both histamine and norepinephrine output; the histamine output increased only after a latent period. Stimulation of both left and right stellate ganglia increased norepinephrine output, but only right ganglion stimulation increased histamine output, after a latency. Stimulation of the right but not the left vagus nerve decreased histamine output first, then increased it moderately, the peak of which came later than norepinephrine release. It was suggested that histamine release following nerve stimulation and bradykinin was secondary to norepinephrine release. Isoniazid decreased the output of both histamine and norepinephrine. Aminoguanidine increased histamine output but decreased norepinephrine output.

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We studied whether pulmonary arterial levels of plasma prostaglandin E rose following pressor effects of angiotensin II in the intact dogs. Furthermore, the modulation by indomethacin of the effect of angiotensin II, PGF_2α, and PGE₁ on pulmonary circulation was evaluated. Pulmonary arterial plasma PGE levels rose significantly from 0.52±0.10 (SE) ng/ml to 0.85±0.07 by the infusion of angiotensin II. This increase was not observed when indomethacin was given. The rise in pulmonary arterial pressure and total pulmonary resistance by angiotensin II was augmented significantly with pretreatment of indomethacin. These results showed that there was an augmentation of the pulmonary vasoconstrictor action of angiotensin II as indomethacin blocked an increase of pulmonary arterial PGE level. Thus, it was suggested that prostaglandins (especially PGE) modulated the pulnomary vasoconstrictor effects of angiotensin II.

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Effects of coronary constriction on the flow reserve of regional myocardium were studied in the anesthetized open-chest dogs. Regional mycocardial-blood flow (RMBF) was continuously measured using heated crossthermocouple method. Left circumflex coronary artery (LCX) was constricted gradually with a screw type constrictor. The coronary constriction decreased subendocardial myocardial blood flow, while subepicardial myocardial blood flow was not affected until reactive hyperemia in LCX nearly disappeared. Recovery and arrival to peak flow rate of RMBF following the release of 15-second's occlusion of LCX were progressively delayed with an increase in the constriction, especially in the subendocardial myocardium. Repayment of flow debt, however, was remained relatively well since the duration of reactive hyperemia in RMBF was prolonged by an increment of the constriction.
From these findings, it might be concluded that in the heart with coronary stenosis recovery from ischemia was caused by prolonged duration of reactive hyperemia, and is suggested that the time required for recovery from ischemia or isehemic abnormalities after the cessasion of stress might be an important marker for the severity of coronary insufficiency.

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Effects of triiodothyronine (T₃) on SA node pacemaker activity, atrial contractility and on chronotropic and inotropic responses to norepinephrine were investigated, using 9 isolated, blood-perfused dog atrium preparations. T₃ (0.001pg-0.1μg) did not cause a significant direct action injected into the cannulated sinus node artery. When T₃ (10pg/min, 40pg/min, 0.1μg/min, or 0.4μg/min) was continuously infused into the sinus node artery, both positive chronotropic and inotropic actions of norepinephrine (0.03μg-0.3μg) were not influenced.
From these results, it is concluded that T₃ has neither acutely direct chronotropic nor inotropic effects, and also T₃ does not have an acute effect on responses to norepinephrine in the isolated, blood-perfused canine atrium.

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During the prevalence of rubella infection in Japan in 1975, we experienced 2 cases complicated with cardiac involvement: a 40-year-old housewife and a 52-year-old man. These 2 cases showed enlarged cardiac silhouettes and bilateral pleural effusion on the chest X-ray films. Pericardial effusion was demonstrated by echocardiogram and cardiac RI pool scintigram. A myocardial biopsy specimen showed slight cell infiltration in Case 1. The anti-rubella antibody titer rose from 128× to 4096× in Case 1 and from 265× to 1024× in Case 2. From these findings Case 1 was diagnosed as rubella pancarditis and Case 2 as pleuropericarditis. Only 4 cases with the cardiac involvement of rubella was reported in the past.

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