Through the examination of 171 electrocardiograms (ECG) of 101 patients with primary pulmonary hypertension (PPH), the following conclusions were obtained.
Arrhythmias were found in 27 (26.7%) of the 101 patients. Among the surviving cases, arrhythmias were found in 8 (17.8%) out of 45 patients, but among the deceased cases, the figure was higher, 19 (33.9%) out of 56. There were instances of more than one kind of arrhythmias in the same patient and a total of 34 types of arrhythmias were noted. The main types of arrhythmias were sinus tachycardia (13 cases), sinus bradycardia (6 cases), and first degree A-V block (5 cases), which accounted for 70% of the total. Sinus tachycardia was observed in only 2 of the survivors but in 11 of the deceased cases, which showed a significant difference (p<0.05). First degree A-V block were all induced by digitalis. Wenckebach type of second degree A-V block was noted in only 1 case and it was also induced by digitalis. Since severe attacks of ventricular arrhythmias were very rare in these cases with PPH, it is difficult to consider the Adams-Stokes syndrome as the cause of syncopal attacks or sudden death. However, it is necessary to further investigate nodal functions by means of continuous ECG monitoring, the overdrive suppression test and His bundle ECGs.

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For the quantitative analysis of the effect of sodium balance on renin secretion, plasma renin activity (PRA) was measured in 9 healthy young males in the respective 3- or 4-day periods of sodium repletion, mild sodium restriction, moderate and severe sodium depletion. In the latter 2 periods, sodium balance was made negative by low salt diet and furosemide administration (120mg/day, p.o.) for 1 or 3 days. Blood samples for PRA determination were obtained at supine position (8:00 a.m.) and after 1-, 2-, and 4-hour's upright posture. PRA was also measured after furosemide stimulation (80mg, p.o.) plus 2-hour's upright posture in the period of sodium repletion.
Change in the supine PRA was directly correlated with that in hematocrit (r=0.81) and inversely with that in body weight (r=-0.64). The PRA rose significantly from 1- to 2- and 4-hour's upright posture in the period of mild sodium restriction, whereas it reached the maximum level at 1-hour's upright posture and remained unchanged thereafter in either period of negative sodium balance. The upright PRA after furosemide stimulation in the period of sodium repletion was almost identical to 2- and 4-hour's upright PRA in the period of mild sodiom restriction, and less than 1-hour's upright PRA in either period of negative sodium balance.
These data suggest that 1-hour's upright posture is enough to evaluate PRA when sodium balance is negative.

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The electrophysiologic effects of verapamil, a slow channel blocker, were investigated during diagnostic cardiac catheterization in 24 children premedicated with lytic cocktail. The ages ranged from 50 days to 12 years. Twenty had congenital and 4 had rheumatic heart disease. Surface EKG, high intra-atrial and His bundle electrograms were obtained in all before and 5min after a single dose of verapamil (0.15mg/Kg, max 5mg iv). In 14 cases complete electrophysiologic studies were performed using the atrial pacing and extrastimulus technique. Due to variability of the resting heart rates and the effect of cycle length on refractory periods each patient was paced with identical S1-S1 interval before and after verapamil, thus allowing each case to serve as his own control. Verapamil prolonged the corrected AH interval in all (mean±SD; from 116±37 to 152±41 msec, p<0.01) and shortened the HV interval in 15/24 (mean±SD: from 55±13 to 47±9.9 msec, p<0.05). The effective and functional refractory periods of the total conduction system, the AV node (ERPAVN) and atrium (ERPA) increased significantly in 10/14. The most profound effect was on ERPAVN and ERPA (25.54±29 and 19.27±21.81 percent mean percent increase±SD respectively, p<0.01 and p<0.02). Our findings show that verapamil prolongs the effective and functional refractory periods of the cardiac conduction system with maximal effects on the AV node, thus suggesting the mechanism of its effectiveness in the treatment of reentrant supraventricular arrhythmias.

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The present studies were performed to evaluate the protective effect of topical hypothermia on anoxic heart. The myocardial protection was assessed by myocardial contractility in the isolated blood-perfused electrically driven canine left ventricular muscle. The isometric tension and the rate of rise of tension development (dT/dt) were measured before and after hypothermic anoxic arrest and percent recovery of these values was used as a parameter of myocardial contractility. The percent recovery rates of 100, 95, 90, and 65 were obtained after acute anoxia of 90, 120, 150, and 180min, respectively at the myocardial temperature of 17°C. These data suggest that the safe limit of acute anoxia at the myocardial temperature of 17°C is defined as 90min in this experimental model and it can be extended to 120min at the myocardial temperature below 17°C.

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Left ventricular (LV) power output (PW) distribution during ejection period, and its relation to LV function were analyzed in 22 patients with valvular disease or cardiomyopathy, and also in 5 controls.
The PW was calculated from LV pressure and LV volume change by ventriculography at every 20msec of the ejection period.
The controls and those with idiopathic non-obstructive hypertrophic cardiomyopathy showed a higher PW in the early phase of ejection period, followed by a gradual decrease. In the cases of idiopathic obstructive hypertrophic cardiomyopathy, aortic insufficiency, and mitral insufficiency, greater PW was generated widely over the ejection period, but the distribution was greater during the middle phase of the period. The idiopathic congestive cardiomyopathy and combined valvular disease developed a greater PW in the late phase of the period. The peak PW was observed during the phase of greater PW distribution in each disorder.
Five controls (EF_??_60%, SWI_??_5600ml•mmHg/M2) showed a greater PW (49±4% of the total PW)in the early phase of ejection period, 9 with loaded but compensated LV function (EF_??_60%, SWI>5, 600) (41±10%)in the middle third, and 9 with failed LV function (EF_??_60%) (41±14%) in the late third.
An index (2/3PW) of PW distribution correlated with EF (r=0.73, p<0.05). Heart rate, systolic blood pressure, and LV end-diastolic pressure were not different among patients with different levels of EF.
Our investigation provides data which suggest that the main PW distribution probably shifts from the early to the middle phase adaptively to ventricular load, but may move from the middle to the late phase in cases of LV failure.

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Using ultrasound method, aortocoronary bypass patency was determined by means of bidirectional Doppler's flowmeter. In 8 (3%) of 302 subjects without aortocoronary bypass was recorded diastolic signal which might distort the results of postoperative evaluation of graft patency. Two-hundred and ninety-seven patients with 330 aortocoronary bypasses were studied at the mean time of 8 months after operation. The graft patency was 84.5%. Comparison of 89 ultrasound findings with angiographic results established considerable specificity (90%) and sufficient sensitivity (77%). Reproducibility of this method was also good. The method is inexpensive and not time consuming. The advantages are also its safety and convenience for the patient. In the present level of development it can be used mainly as screening test at long-term follow-up of aortocoronary graft patency.

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Eleven autopsy cases (average age of 71 years) with complete right bundle branch block were examined histologically with serial sectioning of the conduction system. The results were as follows: 1) moderate to severe reduction of conducting cells in the right bundle branch (RBB) by fibrous replacement in all 11 cases, 2) a preponderance of main lesions in the first portion of the RBB in cases with R configuration in leads V₁ and V₂, and in the second to the third portion without significant lesion of the Purkinje cell network in the right ventricle in cases with rsR', rSR', and RSR' configuration in these leads, 3) as to the etiology, 1 case was assumed to have had rheumatic myocarditis and an another case, 1 chronic ischemia. In cases in which the cause could not be clearly established, reduction of the conducting cells in the first portion of the RBB was thought to be due to fibrosis of the upper ventricular septum. Lesions in the second portion of the RBB may be due to mechanical strain effected by muscle crossing of the trabecula septomarginalis and RBB.

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Complete disappearance of ventricular parasystolic beats by cardiac pacing with the rates of near multiples of the parasystolic rate was observed in 2 patients with ventricular parasystole. This finding represents a clinical counterpart of recently demonstrated experimental and mathematical models of electrotonic modulation of the parasystolic discharge.

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New formulae for the estimation of change in water (ΔW) and salt (ΔNaGl) contents of the body from hematocrit, plasma Na, and protein concentrations were proposed based on a compartment model of body fluid regulation: ΔW=0.4(ΔVi/Vi₀)+0.2(ΔVe/Ve₀)litres/Kg of body weight; ΔNaCl=1.64[(ΔVe/Ve₀+1)/(ΔVi/Vi₀+1)-1]Gms/Kg of body weight; where ΔVi/Vi₀, and ΔVe/Ve₀ are relative increment of intra and extracellular fluid volume. ΔVi/Vi₀ is considered equal to ([Na]₀/[Na]-1) under the condition of normal cell membrane, where as ΔVe/Ve₀ may be a nonlinear function of relative increment of plasma volume and hematocrit or sodium concentration. Thus a nomograph was presented to obtain ΔdW and ΔNaCl simultaneously. This nomograph could predict ΔW and ΔNaCl with satisfactory accuracy in the experiments with the dogs to which fluid of various osmolarity was given intravenously. It was also confirmed in a case of mixed water depletion in which the clinical estimation agreed with that of the present method. The conventional formulae of calculation based on either pure dehydration or pure salt loss proved not to be applicable in the usual cases of body fluid disturbances.

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The effects of adenosine, nitroglycerin, noradrenaline, and isoproterenol on the myocardial oxygen tension were studied. The oxygen tension was measured by a polarographic method.
Adenosine and nitroglycerin (intravenous and intracoronary injections) did not produce a beneficial effect on the normal myocardium. Intravenous administration of noradrenaline produced an increase in subendocardial oxygen tension, while intravenous administration of isoproterenol decreased subendocardial oxygen tension. However, intracoronary administration of catecholamines increased myocardial oxygen tension.
These results suggest that in the absence of systemic hemodynamic changes, catecholamines produce a beneficial effect on the normal myocardium, but administration of adenosine and nitroglycerin (intravenous and intracoronary injections) have no beneficial effect.
The effects of several physiological parameters on the myocardial oxygen tension were studied. Pacing with a higher rate resulted in a decrease in subendocardial oxygen tension. When the perfusion pressure was lowered, subendocardial oxygen tension was decreased. When the perfusion pressure was raised, subendocardial oxygen tension was increased.

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Using the dog as experimental animal, effects on the cardiovascular system of a new vasodilator, 2-nicotinamidoethyl nitrate (SG-75), were studied.
In the heart-lung preparation, the compound produced a dosedependent increase in the coronary blood flow, which was associated with only a minimal increase in the myocardial oxygen consumption. There was essentially no change in the myocardial function. The myocardial redox potential was shifted to more positive values. In the isolated perfused heart preparation (Langendorff's preparation), SG-75 produced a dilatation of only the small resistive arterioles. However, it produced a dilatation of the large conductive artery in underperfused myocardium.
SG-75 produced a significant increase in the cerebral venous outflow, associated with an increase in the cerebro-spinal fluid pressure. It produced a reduction of the venous return, which was especially prominent in the lower half of the body.
In the isolated smooth muscle preparation of the coronary artery, high-doses of SG-75 induced calcium antagonistic effects and produced a relaxation of the lanthanum contracture.

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Necropsy findings in 3 cases of conjoined thoracopagus twins are presented. Conjoined hearts were seen lying in a common pericardial cavity. In 2 cases the common atrial complex was incompletely divided into the atrial cavities of the twins by ridges arising from the floor of the cavity. In 1 case the atrial division was better defined and the interatrial septal defect of septum secundum type was seen. Pulmonary veins opened normally into the atrial chamber only in 1 case, in the other 2 cases, these veins opened into the inferior vena cava and the liver respectively. Ventricular chambers were common in 2 cases with 3 rudimentary atrioventricular openings guarding the inlet and multiple VSD of muscular type. In 1 case one twin had 2 completely separated ventricular cavities and the other twin had partially separated ventricular cavities with a muscular VSD. Great vessels showed transposition in all the cases. In 1 case d-transposition of a rare variety was seen which was associated with a subaortic as well as subpulmonic conus. Persistent ductus arteriosus was a common feature and valvular type of pulmonic stenosis was seen in 2 cases.

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We report a case of a 44-year-old male with variant angina who developed acute anterior myocardial infarction 2 weeks following demonstration of normal left coronary artery. This experience provides inferential evidence that myocardial ischemia resulting from coronary spasm may progress into myocardial infarction.

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