A dynamic study by right and left cardiac catheterization and phonocardiography was performed in 10 subjects with normal hearts and in 11 patients with complete left bundle branch block (LBBB). Comparison was made between the mechanical events of the 2 groups and, in each, between those of the right and those of the left heart.
The onset of ventricular contraction was found delayed in all cases of LBBB; that of right ventricular contraction in 3 out of 11. This indicated the possible occurrence of a right intraventricular block plus a complete LBBB.
The isovolumic period of the LV was found prolonged for either ventricle (more for the left) or only for the left.
Individual cases showed either delayed LV contraction or delayed biventricular prolongation.
In the majority of cases, LV contraction terminated after RV contraction but there were exceptions (either simultaneous or opposite sequence). In spite of this, in 7 out of 9 cases, the aortic incisura followed the pulmonary incisura and reverse splitting of the second sound took place.
These facts reveal the interrelationship of conduction delays, prolongation of the isovolumic periods, and peripheral factors affecting the timing of the incisuras and of the sound components.

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In 12 patients with nocturnal angina pectoris, all-night continuous polygraphic recordings were made, including electroencephalogram, electrooculogram, electromyogram, impedance pneumogram and electrocardiogram, and ECG was analyzed in relation to heart rate and sleep stages. Out of 58 episodes of ischemic ST, T changes which were recorded with the peak frequency between 4:00 and 6:00a.m., 24 were REM-associated and 21 occurred in awake state.The number of attacks per hour in individual sleep stages was most prominent in REM sleep stage. In 3 cases episodes were seen only in awake period, and in 1 case in NREM sleep stages alone.
The analyses of ECG and heart rate during sleep disclosed that the attacks were not likely to be induced by REM-associated increase of heart rate and, in individual episodes, heart rate increase did not precede the ST, T changes. The triggering mechanism of attacks remains to be investigated.
Two representative cases were presented.

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Fifty-five percent of 106 Japanese patients between 2 days and 5 years of age with Down's syndrome were found to have major congenital cardiac defects. Autopsy was performed on 18 cases. Of these, 11 had major congenital heart defects. In addition, all 18 autopsied cases revealed many minor cardiac abnormalities, such as nodular or diffuse hypertrophic valves, parachute formation of atrioventricular valves, hypoplastic papillary muscles, and abnormal attachment of chorda tendineae. It is postulated that minor cardiac abnormalities are secondary to abnormal endocardial and bulbar cushion formation.

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The effects of rubidium and potassium each in the concentrations of 2, 4, and 8mM, on the spontaneously beating right atria, and the excitability and contractility of the left atria and papillary muscles of the guinea-pig heart were investigated. Rubidium and potassium consistently produced a concentration dependent decrease in the S-A nodal automaticity. Potassium was more effective than rubidium in this respect. Both rubidium and potassium increased the excitability of the left atrium and papillary muscle in lower concentrations (2 and 4mM) and decreased it in high concentration (8mM). Rubidium was more effective than potassium in increasing the excitability, while potassium was more effective than rubidium in decreasing it. Potassium produced a concentration dependent decrease in the contractility in both the left atria and papillary muscles. Rubidium, on the other hand, increased the contractility in the concentrations of 2 and 4mM and decreased it in high concentration (8mM). Atrium was more sensitive than papillary muscle to the effects of rubidium and potassium on the excitability and contractility. These results suggest that rubidium might be a better antiarrhythmic agent than potassium because it does not depress the myocardial contractility in moderate concentrations although it has properties similar to potassium as far as the effects on automaticity and excitability are concerned.

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The hexose monophosphate shunt activity as well as the non-oxidative pentose pathway in nucleic acids synthesis was studied in the time course of the left ventricular hypertrophy of 63 male rats weighing 200 to 600 Gm. induced by cellophane perinephritis hypertension. Another 26 rats with same range of body weight were employed as control group.
(1) Ventricular hypertrophy was estimated by the ratio of the ventricular weight to body weight, and it revealed an apparent increase of the ratio in only left ventricle ranging all body weights from 4 to 34 weeks after operation.
(2) Left heart failure was not demonstrated by determination of the water content in lungs in this series of experiment.
(3) At the early stage of the left ventricular overload, total DNA content decreased, however, during continuous overload total DNA content returned to normal, and then, at the late stage of compensated hypertrophy or of this series, this value increased over normal level. This fact suggests the possibility of cellular damage at early stage and cellular hyperplasia at late stage of ventricular overload. The incorporation ratio of C14glucose into DNA increased tremendously at 4 weeks after operation, which was likely an increase in degradation and synthesis of DNA. The HMP shunt activity in DNA synthesis was not detected in all course of ventricular overload.
(4) RNA content increased through all course of experiment, however, the incorporation of C14-glucose into RNA increased rapidly at early stage of overload, and then returned to normal level during compensatory hypertrophy, and finally came down under normal level at late stage of compensatory hypertrophy. The HMP shunt activity in RNA synthesis was tremendously activated at early stage of ventricular overload, but disappeared even in the compensatory hypertrophy. Therefore, the HMP shunt may be considered to play some important roles in occurrence of cardiac hypertrophy and even cardiac failure.

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Plasma renin activity and serum electrolytes were measured in 20 normal and 22 hypertensive rabbits. Hypertension was produced by the clipping of one renal artery in animals with an intact contralateral kidney. The measurement was made during the period of 20 to 57 weeks after the clipping. Plasma renin activity was above normal in 11 of 22 hypertensive animals and serum potassium was below normal in 6 of 22 hypertensive animals. An inverse correlation existed in hypertensive animals between plasma renin activity and serum potassium (r=-0.77, p<0.01). No significant correlations were found in hypertensive animals either between plasma renin activity and serum sodium or between plasma renin activity and blood pressure. The present study indicates that plasma renin activity is increased in a half of animals with chronic renovascular hypertension when one renal artery is clipped and the other kidney is left intact. But there is not sufficient evidence to show that the renin-angiotensin system plays a role in maintenance of hypertension.

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Using a direct in situ perfusion technique of the AV node artery, the effect of bethanechol, a selective muscarinic stimulant, was investigated in 18 mongrel dogs and compared with other muscarinic stimulants, methacholine and carbachol which are used clinically. The injection of bethanechol into the AV node artery induced various degrees of AV block. The threshold dose was 1 to 3μg. for inducing a second degree of AV block. More than 10μg. of bethanechol induced long lasting complete AV block. When complete AV block was induced, a constant rate of 32±2.1 (mean±S.E.) beats/min. of nodal rhythm was obtained in 15 cases. During complete AV block, atrial fibrillation was occasionally induced and also ventricular tachycardia at a rate of 110±5.8 (mean±S.E.) beats/min. (n=11). These effects of bethanechol were similar to those of methacholine or carbachol.

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An example of atrial reciprocal rhythm and reciprocating tachycardia is presented. These arrhythmias were observed immediately after DC electrical conversion for atrial flutter. A His bundle electrogram recorded after the DC conversion demonstrated the prolonged conduction time through the A-V node, suggesting the basis of this reciprocation.

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Here was described a 38-year-old man with cerebellar ataxia who developed Adams-Stokes syndrome, abnormal electrocardiographic findings including various arrhythmias, and congestive heart failure. His parents were first cousins. One of his sisters manifested convulsive seizures and ataxia. The patient died of congestive heart failure. Autopsy revealed atrophy of cerebellar cortex and degeneration of dentate, olivary and pontine nuclei, but no spinal cord lesion. The heart showed extensive myocardial fibrosis and fatty infiltration. Coronary arteries appeared normal. The relationship between neurological and myocardial changes in cerebellar ataxia was discussed.

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