The effects of Dipyridamole (Persantin) on the coronary blood flow (the great cardiac vein flow and coronary sinus ostial flow), the femoral arterial pressure, the coronary vascular resistance and the heart rate were measured continuously in man.
The newly devised method of the continuous local thermodilution method enabled us to perform the exact measurement of the above mentioned variables in man.
The increase of the coronary blood flow was seen definitely in the non-ischemic group and, therefore, the decrease in the coronary vascular resistance occurred in 30 sec and continued for more than 20 min. In the myocardial ischemic group, some patients showed the similar response to the non-ischemic group. However, some patients showed no increase of the flow, even though the coronary vascular resistance decreased in all cases in this group. The heart rate increased slightly in all cases.

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Forty patients with systemic hypertension were classified into 4 types based on the left ventricular echocardiographic findings. Patients with normal left ventricular echogram, type I, showed little clinical symptoms and signs of hypertensive involvement. Higher systolic pressure and marked hypertensive retinal and renal changes were observed in patients with symmetric hypertrophy of the left ventricle, type II. Congestive heart failure was dominantly present in those with dilatation of the left ventricle, type IV. High voltages and marked ST-T changes in electrocardiogram were usually found in patients with asymmetric septal hypertrophy, type III, while retinal and renal damages were mild. Left ventriculograms obtained from 6 cases in type III also revealed hypertrophy of the interventricular septum and one of them demonstrated left ventricular outflow tract obstruction. These cardiac features in type III, which are quite similar to those in hypertrophic cardiomyopathy, seemed to be a secondary change induced by systemic hypertension on the basis of some predisposition.

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Fifteen patients with ventricular aneurysm were selected based on the following 3 criteria: 1) electrocardiographic evidence of old myocardial infarction, 2) presence of abnormal precordial impulse, 3) presence of dyskinesis or akinesis with diastolic bulging of the ventricular cavity by angiocardiogram. Eight patients had anterior left ventricular aneurysm and 7 apical aneurysm. The characteristic abnormal precordial impulse was diminished or absent A wave, pre-upstroke retraction, late systolic bulge, and diminished rapid filling wave, all of which were recorded over the restricted area of the broad precordial impulse.
M-mode echocardiogram revealed increased or normal excursion of the posterior left ventricular wall. However, abnormal motion of the anterior left ventricular wall was detected in all, if the transducer was located over the abnormal precordial impulse or slightly inside of it. Compound M-mode echocardiographic scan toward the abnormal precordial impulse was able to detect asynergy of the anterior left ventricular wall and the apex, and distinguish it from motions of the interventricular septum and the anterior right ventricular wall. Abnormal motion of the anterior left ventricular wall was paradoxical in 13 patients and flat in the others. Systolic posterior mortion of the posterior left ventricular wall was detected in 2 patients with apical aneurysm. Cardiac ultrasonogram scanning over the abnormal precordial impulse demonstrated the bulging of the ventricular cavity in either systole or diastole depending on the site of lesion. There was a good correlation between cardiac ultrasonography and angiocardiography with respect to the site of lesion.
Our study indicates that this method is useful in the diagnosis of anterior and apical aneurysm which ordinary technique failed to detect.

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The responses of blood pressure, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) to infusion of either angiotensin II (10ng/Kg/min) or norepinephrine (100ng/Kg/min) were observed in 25 patients with essential hypertension. The difference in modes of response between low renin essential hypertension and normal or high renin essential hypertension was analyzed. For comparison, 5 patients with Conn's syndrome, 4 with renovascular hypertension, and 5 normotensive subjects were also studied.
Following infusion of angiotensin II the changes in diastolic blood pressure (DBP) were +24±3.0mmHg in low renin essential hypertension and +25±3.1mmHg in normal or high renin essential hypertension, in PRA -0.28±0.06ng/ml/h in low renin essential hypertension and -0.69±0.02mg/ml/h in another and in PAC +3.7±1.4 and +7.6±1.8ng/100ml respectively. There was a significant difference in magnitude of response in PRA between the 2 groups of essential hypertension (p<0.05).
Norepinephrine induced rise in DBP with decreases both in PRA and PAC. The mean changes in DBP were +6±1.4mmHg in low renin essential hypertension and +16±2.2mmHg in another and the pressor response in the later was significantly greater (p<0.01). The changes in PRA were-0.14±0.07ng/ml/h in low renin essential hypertension and -0.67±0.26ng/ml/h in normal or high renin essential hypertension, and in PAC -4.9±1.3 and -3.3±1.9ng/100ml respectively. The greater fall in PRA in normal or high renin essential hypertension was observed but the difference between the 2 groups of essential hypertension was not significant. The changes in PAC did not parallel the changes in PRA.
Angiotensin II induced essentially similar effects on blood pressure in both groups but the greater feedback inhibition of PRA was produced by this peptide in normal or high renin essential hypertension than in low renin essential hypertension. Norepinephrine induced significantly greater pressor effect in normal or high renin essential hypertension. The adopted dose of norepinephrine suppressed both PRA and PAC and atendency to the greater fall in PRA was observed in normal or high renin essential hypertension. There was no difference in responses of PAC to both agents between the 2 groups of essential hypertension.

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Using the canine heart-lung preparation supported by a donor, the effects of ethyl adenosine-5'-carboxylate (EAC) on the heart and coronary circulation were studied and compared with those of adenosine. EAC produced qualitatively similar effects to adenosine in this preparation. Aminophylline inhibited the effects of EAC as well as those of adenosine. Dipyridamole did not potentiate the effects of EAC, while it produced a definite potentiation of the effects of adenosine.

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Deviation of systolic time intervals (STI) from the regression lines obtained from 122 normal subjects was studied in 22 healthy adults (Group 1), 18 N.Y. functional class I cardiac patients (Group II) with ischemic (IHD) or primary myocardial disease (PMD), and 15 similar patients (pts) but N.Y. functional class II with prior heart failure (Group III).
STI_c (corrected for heart rate) were normal in Groups I and II. Supine exercise caused shortening of pre-ejection period PEP_c and prolongation of left ventricular ejection time ET_c in both groups. Group III pis had a significantly longer PEPc and shorter ET_c at rest. Supine exercise caused further prolongation of PEP_c and a slight prolongation of ET_c in this group.
In 8 mongrel dogs, the effect of controlled changes of hemodynamic variables on STI was studied with intact hearts and repeated after myocardial impairment has been induced by pentobarbital. Doubling of venous return while the heart was intact produced changes in STI similar to the effects of supine exercise in Groups I and II human subjects. With myocardial impairment, comparable increase in venous return had an effect on STI similar to the effect of supine exercise in Group III patients. Controlled increase in each of heart rate or blood pressure, with other hemodynamic variables kept constant, produced changes in STI different from the effect of supine exercise on human subjects.
The study suggests that the value of supine exercise induced changes in STI in reflecting left ventricular performance is attributable primarily to increased volume load. In this respect supine exercise is probably superior to other forms of exercise in disclosing impaired left ventricular performance.

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Kidney extract from rats which were adrenalectomized and given tap water was dialyzed, salted out, ultrafiltrated or heated. A given dose of each extract or fractionized material was administered to uninephrec-tornized rats subcutaneously every 12hours for 10days. The relationship between renin content of each sample and final blood pressure level following repeated injections as an index of its hypertension-inducing potency was analyzed. There was no apparent discrepancy between the two of each sample. No evidence was obtained for the existence of other renal substance than renin which might be implicated in producing hypertension.

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Slow cyclic fluctuations were frequently observed in blood pressure of the distal portion of the partially constricted coronary artery of anesthetized dogs. Lowering the mean peripheral coronary blood pressure below 50% of the control value was required for initiation of fluctuations. Each fluctuation in pressure was composed of 2 phases; the phase of rise and phase of fall. Almost invariably, the phase of rise and phase of fall were accompanied by increase and decrease in coronary blood flow, respectively. When the mean peripheral coronary blood pressure fell below 20% of the control value during the phase of fall, systolic bulge and elevation of the ST segment of surface ventricular electrocardiogram occurred. Period duration of each fluctuation ranged from 30 sec to 14min. The cyclic fluctuations in pressure, flow, electrocardiogram and left ventricular wall motion were eliminated by nitroglycerin, but were not affected by phentolamine, propranolol, atropine, cervical vagotomy, and stellectomy.

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1) Patients with myocardial infarction constituted 2.36% of all the hospitalized patients during 1961-1968. The mortality of the hospital-ized patients with myocardial infarction during the same term was 19.1%. The ratio of the male to female patients with myocardial infarction was 5.2.
2) As the risk factors of myocardial infarction, the following items were considered to be of importance: 1. gout in past history, 2. angina pectoris in family history, 3. diabetes mellitus in family history, 4. cigaret smoking over 40 pieces per day, 5. diabetes mellitus in past history, 6. administrative occupation, 7. serum cholesterol level over 250mg/100ml, 8. obesity of 20% excess over standard body weight, 9. hypertension in family history.

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A family of Holt-Oram syndrome is reported. Twenty of 41 living members in the last 3 generations were examined. The propositus expressed typically the cardinal features of this syndrome: atrial septal defect, patent ductus arteriosus, cardiac arrhythmias and conduction block of various types, and hypoplasia of the left thumb. Two individuals were clinically diagnosed to have atrial septal defect without any upper limb anomaly, and 3 showed upper limb anomaly without any sign of congenital heart disease. Other 5 members showed only minor abnormalities, such as funnel chest or mild right ventricular hypertrophy on ECG and VCG. Some of the skeletal abnormalities observed were hitherto undescribed ones. These include generalized hypoplasia of left hand and downward displacement of right sterno-clavicular joint.

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