Conduction system was histologically examined in a total of 8 cases of complete left bundle branch block (LBBB). All 8 cases showed excellent correlation between electrocardiogram (ECG) and pathological changes in the left bundle branch (LBB), though the mode of interruption had rather wide variety. Seven cases had fibrotic interruptions of the LBB, one case had interruption by fatty metamorphosis in its anterior radiation and one case showed acute interstitial edema.
Concerning the pathogenesis, degeneration and extension of the central fibrous body (CFB) at the left side which was associated with myocardial hypertrophy were assumed to produce secondary damages to the conduction cells in 3 cases. Coexistence of ischemic septal fibrosis advocated for effects of ischemia itself on the LBB, or increased mechanical strain on the LBB in sandwiched state between fibrous tissues in other 3 cases. The other 2 cases were idiopathic cardiomegaly and uremia, respectively.

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Two patients (group 1) with relatively normal left ventricles who had never been in left ventricular failure, and 4 patients (group 2) with abnormal left ventricles who had previously been in left ventricular failure, underwent right and left heart catheterization. Cardiac pressures and cardiac output were measured before and at various time intervals during the continuous administration of 0.3mg. per min. of phentolamine.
Among the subjects in group 1, phentolamine produced only minimal changes in the measured hemodynamic parameters. Among the subjects in group 2, phentolamine produced marked increases in the cardiac index and stroke index. A striking fall in the pulmonary artery pressure and left ventricular end-diastolic pressure was also observed.
Phentolamine is ideally suited for the treatment of patients in left ventricular failure. It is very effective, rapid in action, devoid of side effects and produces no arrhythmias.

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Two cases of benign Duchenne type of progressive muscular dystrophy with myocardial involvement were presented. In one case, congestive heart failure was the predominant clinical feature and severe impairment of the left ventricular function was demonstrated by hemodynamic and cineangiocardiographic studies. Analysis of the cineangiocardiogram demonstrated a systolic expansion of the posterolateral portion of the left ventricular wall in both cases, which corresponded to the site of severe myocardial damage of the left ventricle in one autopsied case. A possible relationship between the site of myocardial damage and electrocardiographic and vectorcardiographic abnormalities was also discussed.

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In order to confirm a possibility of cell division in the heart muscle, chemical and microspectrophotometric determination of the DNA content and histometrical estimation of the cell count of human heart muscle obtained at autopsy were performed. The following conclusions were obtained.
(1) The DNA content per single nucleus of heart muscle cell and of interstitial cell was the same, regardless of difference of cell kind, age, and heart weight. The absolute DNA content per each nucleus was 0.950-1.083×10^-11Gm.
(2) The DNA content per 100mg. of heart weight ranged from 60μg. to 136μg., but was proportional to the cell count estimated in an unit heart muscle volume.
(3) The heart weight was normal or less in malignant tumor group. The cell count in an unit muscle volume increased and the DNA content also increased. On the contrary, the cell count in an unit muscle volume was unchanged in renal and cardiovascular groups (so-called hypertrophied hearts), and the DNA content was rather constant even with the increase in heart weight. These results seem to substantiate our view that the cellular hyperplasia rather than hypertrophy occurs in these so-called hypertrophied hearts.

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An electronic circuit for servocontrolled computation of instantaneous aortic blood flow i(t) from instantaneous aortic blood pressure p(t) is devised with equation: i(t)=p(t)/R+C•dp(t)/dt, where the arterial system is regarded as a Windkessel (compression chamber), R is its resistance and C is its compliance. In this circuit, R is resistance of a photocell (CdS) and its value is servocontrolled by the light of a lamp which is controlled to make computed i(t) zero at the end of each diastole (at R wave of EKG). Its biological application in dogs resulted in satisfactory agreement of computed i(t) with that measured by an electromagnetic flowmeter.

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Although many of its effects have not been clarified, it is well known that the carotid sinus reflex has a profound influence on the cardiovascular system. The purpose of this paper is to investigate the effect of the carotid sinus reflex on the canine heart.
The present experiments were performed on the in situ canine heart: 1) during sinus rhythm, 2) during electrically driven rhythm, and 3) during electrically driven rhythm after the administration of atropine. Before and during carotid sinus stimulation, the intracellular and surface electrograms, standard lead II electrocardiograms and aortic blood pressure were simultaneously recorded. The intracellular and surface electrograms were obtained from the epicardial surfaces of the right atrium and the left ventricle.
Atrium. The duration of the membrane action potential (MAP) shortened during sinus rhythm and electrically driven rhythm. There were no significant changes in the amplitude of the MAP and the membrane resting potential (MRP). The PQ interval in the standard lead II electrocardiogram became significantly prolonged during both types of rhythm. The P amplitudes decreased during sinus rhythm. The shortening of the duration of the MAP was almost entirely inhibited by atropine.
Ventricle. The duration of the MAP during sinus rhythm showedsignificant widening. The ST segment in the surface electrogram became significantly elevated during sinus rhythm and during electrically driven rhythm. The QT interval in the standard lead II electrocardiogram prolonged significantly during sinus rhythm, but less so during electrically driven rhythm. The RR interval became significantly prolonged during sinus rhythm. After atropine, the duration of the MAP widened very slightly during electrically driven rhythm.
The following possibilities are discussed: Electrical behavior in atrial muscle is mainly mediated by the cholinergic nervous system. The response of the sinoatrial node is caused by cholinergic activity as well as by the decrease in adrenergic activity.
The effect of carotid sinus stimulation on intracellular electrograms is more apparent in atrial muscle and in the sinoatrial node than in ventricular muscle.

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Variations of transthoracic electrical impedance and their relations with physiological events within the thorax were studied by using electrodes applying constant sinusoidal current at 55kHz on bilateral chest walls of anesthetized dogs during breath holding. The level of the impedance lowered during decrease of oxygen and elevated during ether gas evaporation in the lungs with steady pulmonary blood flow. The impedance decreased when concentrated saline was selectively infused into the pulmonary vasculature but not into the left heart and the great vessels. The impedance levels also were related inversely with the change of blood flow and resultant blood volume in the lung when the pulmonary blood flow was decreased as during occlusion of the venous return to the right heart, pulmonary trunk and unilateral pulmonary artery. The impedance levels on the bilateral chest walls varied independently by manipulations mentioned above which was employed in the individual lung of each hemithorax. These results clearly suggest that the current flux applied on the chest wall well penetrates through the chest cage and passes preferentially through the lung parenchyma, the conductivity of which depends on the changes in the amount of electrically conductive or resistive materials associated with physiological events within the lungs.

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(1) P wave and Ta wave of 35 open-chest dogs were recorded in high amplitude (100μV.=3cm.) after production of A-V block, and normal patterns of the waves were studied. Direct current amplifier which yielded no untoward deformity of P wave or Ta wave was used.
(2) P wave and Ta wave were always opposite in direction and the area of both waves was almost equal, i.e. atrial gradient was nearly zero. Consequently it is considered that the activation process and recovery process of atrial excitation have the same direction, and furthermore, the time sequence of both processes is very similar.
(3) There was good correlation between the amplitude of P wave and Ta wave. [Ta=0.21P+3(μV.)], i.e., the amplitude of Ta wave is about 24% of that of P wave.
(4) Duration of Ta wave was 2.4 times that of P wave on the average.
(5) There was good correlation between atrial rate (P-P interval) and P+Ta time. [P+Ta=0.31(P-P)+77(msec.)]
(6) Ta wave extends to ST segment over QRS complex for 0.06 msec. on the average. Consequently, determination of PR segment or ST segment deviation, especially in their depression must carefully be made. When the depression of PR segment or ST segment does not exceed the amplitude of Ta wave expected from that of P wave, the depression might safely be considered to be the influence of Ta wave. When the ST depression exceeds the amplitude of Ta wave expected from that of P wave, it may be the real ST depression.
(7) ST segment does not return to the isoelectric line completely even in normal condition, but deviates in the opposite direction of P wave by the influence of Ta wave.

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Two cases of unusual atrioventricular nodal bigeminal rhythm who had atrioventricular nodal parasystole on different occasions are presented, and several possible interpretations of the electrocardiograms are explained in detail. One of the more likely of these is non-paroxysmal nodal tachy-cardia with blocked reciprocal beats occurring every third contraction. The fundamental cause for the development of unusual A-V nodal bigeminy was considered to be digitalis intoxication. Similar findings have been encountered by other clinicians.

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Two patients with tetralogy of Fallot with previous functioning shunt developed obstruction of the right ventricular outflow tract. Preoperative diagnosis and total corrective surgery were successfully carried out. The acquired obstructions were clearly demonstrated by the series of angiocardiograms. Pulmonary atresia may be suspected clinically by disappearance of the systolic murmur. Acquired obstruction of the right ventricular outflow tract appears to be associated with angiocardiographic evidence of increase in the degree of overriding of the aorta. Prompt correction of the defect should be considered after angiocardiographic confirmation of the acquired atresia of the right ventricular outflow tract in such patients.

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