We analyzed non-sustained ventricular tachycardia (VT) observed during ambulatory electrocardiographic (ECG) monitoring in 21 subjects. The rate of VT was 160.7±2.3 beats/min and showed a moderate positive correlation (r=0.61, p<0.01) with the preceding heart rate (81.8±1.0 beats/min). The prematurity index of VT was 1.118±0.015 and showed a moderate inverse correlation with the rate of VT (r=-0.64, p<0.01). The vulnerability index was 0.713±0.009. These indices of prematurity showed a wide distribution and the prematurity of ventricular ectopic beats may not be so significant as previously documented. The incidence of VT was higher in the morning and the evening and was reduced by sleep. The most frequent type of VT (25-/day) was observed only inpatients with VT predominantly occurring during the day. We have therefore postulated that these diurnal variations in the frequency of VT may have important therapeutic and prognostic implications. In this study, we used the classification of VT based on the focus, the diurnal variation and the frequency of the tachycardia. Ambulatory ECG monitoring is useful in distinguishing the various types VT and it is important to separate the various types of VT into several subgroups in order to classify grade the severity of VT.

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In a patient with mitral stenosis we previously found a negative periphero-central pressure gradient (P-C PG) despite a forward peripheral venous blood flow velocity (PVBFV) during supine leg exercise. The present study was undertaken to confirm this finding and elucidate its mechanism. In 6 patients with congestive heart failure, P-C PG was reversed from -2.4 to -18.7 cm H₂O for 1 to 5 minutes during exercise. PVBFV, measured simultaneously with peripheral venous pressure (Pv) in 8 subjects, remained positive; 5 of these were patients with a negative P-C PG. the effect of intravenous lidocaine (1-26 mg) was studied in 13 patients: In 4 of 13 patients the change in Pv by saline injection was smaller than that after lidocaine (2-5 mg) injection (-0.5 ±0.5, 3.9±0.8 cm H₂O, mean ±SE, respectively) (p<0.02). In 13 patients Pv rose after a small dose of lidocaine. After a larger dose the rate of rise of Pv decreased on Pv dropped. No significant change was observed in the central venous pressure. In 6 patients who performed Valsalva's maneuver, the rate of rise of Pv during the test decreased or unchanged after lidocaine injection. The probability of a pumping mechanism in superficial human arm veins was discussed.

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In order to evaluate the pulmonary embolism as a complication of transfemoral arteriography, we performed lung perfusion scintigrams before and after arteriography in consecutive 120 patients. On the initial 60 patients who did not receive subcutaneous low-dose heparin, 19(32%) demonstrated new pulmonary perfusion defects. There was no significant difference in regard to the incidence of new defects with or without right hear catheterization. On the other hand, in the latter 60 patients who received prophylactic heparin, the incidence of new defects decreased to 10%, without increasing clinically important bleeding. We believe that the source of emboli is from the leg vein thrombosis due to compression of the groin and subsequent bed rest. These data suggest that pulmonary embolism is a more common complication of transfemoral arteriography than previously appreciated and low-dose heparin is useful in reducing this complication.

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In order to define quantitatively the histological characteristics of the hypertrophied myocardium of the right ventricular outflow tract in patients with congential heart disease, a light-microscopic study of biopsy specimens obtained from 20 cases with tetralogy of Fallot (TOF) and 14 cases with muscular obstruction of the right ventricular outflow tract (RVOTO) was performed using a semi-automatic sampling counter. As the controls, the crista supraventricularis of 11 autopsied cases without cardiac disease were used. The TOF patients were divided into two groups; those with (9 cases) or without (11) a history of hypoxic spells. The myocyte diameter was calculated according to Chalkley's²⁷ and Arai's method.²⁸ The areas of myocardial fibrosis and myocyte disarray were determined quantitatively by the point count method. Myocardial fibrosis was classified into five types: focal, mild perimysial, severe perimysial, perivascular and plexiform. In the control group, the myocyte diameter and area of fibrosis and disarray tended to increase with age. In the obstructive groups, the myocyte diameter and area of disarray were greater than those of the control in any age group. Myocyte diameter tended to increase with age in all groups, except for the TOF cases with a history of hypoxic spells. The latter also had the largest area of myocardial disarray (25.3%) (p<0.01), and a largest area of fibrosis (20.5%) than the TOF cases without spell (14.4%), but severe perimysial fibrosis was observed in only five out of the nine patients with spells. The lack of a relation between the pressure and the presence of an increased area of the myocardial disarray in TOF with spells implies that his myocardial change is brought about by myocardial abnormality accompanied by cardiac malformation.

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PTCA (percutaneous transluminal coronary angioplasty) was performed on 44 patients with angina pectoris during the 18-month period from April 10, 1981 to September 30, 1982. It was successful in 36 o the 44 patients (82%), resulting in a subsidence of the symptoms and a considerable increase in exercise tolerance. Successful dilatations were achieved in 30 of 35 left anterior descending arteries (86%) and 7 of 11 right coronary arteries (64%). Five patients had complications: myocardial infarction in 2, unstable angina pectoris in 1, and dissection of the coronary artery in 2. One of these patients underwent an urgent A-C bypass operation. The patients were followed up for 0.5 to 18 months (average: 7.4±0.9 months). Stenosis recurred in 6 patients (16.7%), but repeat PTCA disclosed successful dilatations of stenotic lesions in 3 patients. No deaths occurred throughout the study period including the follow-up period. Our experience suggests that PTCA is of use in the treatment of certain groups of angina pectoris patients if case selection is appropriate.

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Age-related changes of the muscle fiber diameter of the left ventricle were studied in 20 autopsied specimens of tetralogy of Fallot (TOF) and in 34 normal autopsied hears. According to the amount of pulmonary blood flow, two groups were defined: In Group 1, TOF with a markedly decreased pulmonary blood flow. In Group 2, TOF with a moderately decreased pulmonary blood flow. In Group 1, the muscle fiber diameter was nearly normal at birth, but increased slightly and remained constant after one year, so that it was significantly less than normal. Moreover, histological observation revealed underdevelopment of the left ventricular muscle fibers in this group. In Group 2, the diameter increased with age in a manner similar to normal and, histologically, the muscle fibers were not different from normal ones except for those in one heart with left ventricular hypertrophy. The growth of muscle fibers in the left ventricle seems to depend on the volume of pulmonary blood flow, or the left ventricular inflow volume. If the left ventricular functional capacity correlates with the growth of muscle fibers, left ventricular functional capacity correlates with the growth of muscle fibers, left ventricular dysfunction after the corrective operation may originate in the underdevelopment of muscle fibers. Surgical intervention is advisable before the retardation of muscle fiber growth has become apparent.

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In ten patients with familial amyloid polyneuropathy (FAP), the effects of atropine and isoproterenol on the cardiac conduction system were studied using surface electrocardiogram (ECG) and His bundle electrograms. Intravenous administration of atropine sulfate, 1mg, prolonged the sinus cycle length (SNCL) in 6 of 8, sinus node recovery time (SNRT) in 3 of 6, automaticity recovery time of the atrioventricular (A-V) node in one, A-H interval in 4 of 7, effective refractory periods of the atrium and A-V node in 4 of 6 and in 3 of 7 patients, respectively. Continuous intravenous administration of isoproterenol, 0.5 μg/min, shortened the SNCL, SNRT, A-H interval and refractory periods of the atrium and A-V node in all patients. We conclude that the therapeutic does of atropine may be useless or potentially detrimental for bradyarrhythmias or conduction blocks in some patients with FAP, but that isoproterenol may have beneficial effects on those arrhythmias in FAP.

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Body surface isopotential maps were compared between 52 normal children and 47 normal adults. While sequential changes in body surface potential distribution were similar, 4 significant differences in body surface maps were observed between them: 1) Surface maps of normal children showed less smooth contour of isopotential lines than did those of normal adults. For example, breakthrough minimum was recognized more frequently in children (100%) than adults (65%). 2) Breakthrough minimum appeared earlier in normal children (23.2±5.0 msec) than in normal adults (29.2±4.3 msec), and more leftwards on the chest. 3) Forty-seven percent of the children showed positive potentials on the upper and right portions of the anterior chest in the terminal phase of QRS, but this pattern was not observed in normal adults. 4) The maximum at the time of the peak of the T wave appeared more leftward in normal children than normal adults.

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Mitochondrial oxidative phosphorylation, calcium transport activity and calcium content were investigated in dog hears injured by excessive noradrenaline (NA). Diffuse cardiac injury was produced by a 5-hour infusion of NA (2 or 5 μg/kg/min), and the injury was evaluated based on ECG and hemo-dynamic changes. Mitochondrial calcium uptake and binding activities measured in the presence of ATP showed no significant differences between the control and NA groups. However, the calcium content of hear mitochondria isolated from the NA groups, state 3 respiration and the respiratory control index were significantly depressed without any change in the ADP/O ratio. These results suggest that excessive NA causes the intracellular calcium overload and the depression of mitochondrial respiration, and the both of these changes may play a key role in the pathogenesis of myocardial injury through the insufficient control of cytosolic calcium levels.

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The left anterior descending coronary artery of a dog was occluded for 15 min followed by a 5 min reperfusion in order to investigate the mechanism responsible for the paradoxical exacerbation of heart mitochondrial dysfunction caused by reperfusion. the mitochondrial function was assessed and the concentration of Ca⁺⁺, phospholipids and free fatty acids (FFA) were determined. The relative importance of mitochondrial lysophospholipids was also investigated. Eleven dogs (30.6%) developed "resperfusion arrhythmia" (arrhythmia group) but 23 did not (control group). Although mitochondrial dysfunction was observed in the reperfused area even in the control group, a greater impairment of mitochondrial function was observed in the reperfused area in the arrhythmia group. There was no significant difference in the contents of FFA and phospholipids in the mitochondria from the normal area of both groups and from the reperfused area of the control group. However, a marked increase in eight FFA and a significant decrease in phospholipids were observed in the mitochondria from the reperfused area of the arrhythmia group. A significant increase in Ca<++> content both in the myocardium and the mitochondria from the reperfused area was observed in the arrhythmia group but not in the control group. In separate experiments, the mitochondria prepared from dog left ventricle were incubated with either phospholipase C (PhC) or phospholipase A₂ (PhA₂). Both phospholipases induced severe mitochondrial dysfunction. PhC induced a significant increase in FFA, quite analogous to the changes in mitochondrial FFA caused by reperfusion in vivo. PhA₂ also induced a tremendous increase in FFA but only in the content of unsaturated FFA. Although PhC did not affect the lysophospholipid profiles, PhA₂ induced lysophosphatidyl choline. These results indicate that mitochondrial damages characteristic of the early phase of coronary reperfusion may be caused by the action of PhC, activated by increased intracellular Ca⁺⁺, which in turn induces degradation of the mitochondrial membrane.

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Long-term (35 days) effects of thyroid hormone on the number of myuocardial β-adrenergic receptors and the c-AMP concentration were studied in the rat. The ventricles from triiodothyronine-administered rats (T₃ rats) showed an increase in the number of β-receptors compared to controls (54.3±3.1 vs 39.3±1.8 fmole of [¹²⁵I]-iodohydroxybenzylpindolol (IHYP) binding sites/mg protein p<0.001) on the 35th day. Conversely, the ventricles from thiouracil-administered rats (TU rats) showed a decrease in the number of β-receptors compared to controls (31.4±1.6 vs. 38.4±2.6 fmole/mg protein, p<0.05). The equilibrium dissociation constants (Kd) for the interaction of receptors with IHYP did not differ significantly (0.10 to 0.15 nM). The myocardial concentration of cyclic AMP was not significantly different (T₃ rats, 1.09±0.09 nM/g wet weight tissue; T₃ controls, 1.12±0.07; TU rats, 1.13±0.07; TU controls, 1.16±0.12) on the 35th day. On serial effects of tri-iodothyronine from the first to the 35th day, the number of β-receptors of T₃ rates increased significantly on the 24th and the 35th day, but the c-AMP concentration was not significantly different from that in control rats. These results demonstrated that thyroid hormone affects the number of myocardial β-receptors in rats, and suggested a different mechanism of action of thyroid hormone on the myocardium from that of catecholamines.

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