In order to evaluate coronary artery disease quantitatively we recorded body surface maps before and after treadmill exercise in 27 patients suspected of having coronary artery disease.
Electrocardiograms were recorded from 87 points on the anterior and posterior chest wall. The pre-exercise ST level was subtracted from postexercise ST level at each lead point and an ST difference MAP was constructed. The ST level at 60 msec from J point was used for the construction of the ST difference MAP.
By means of ST difference MAP, the area with ST changes which was induced by treadmill exercise could be evaluated. The size of the ST-depression area in the ST difference MAP was considered to be proportional to the severity of the coronary artery disease and the ST-elevation area was closely correlated to the motion abnormality of the corresponding left ventricular wall.
Treadmill exercise test using body surface mapping has provided a measure of quantitative diagnosis of coronary artery disease especially in symptomatic patients

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The influences of pregnancy on the pulmonary circulation in mitral stenosis (MS), were studied.
1) Twenty-two cardiac patients underwent serial right heart cath-eterization with the use of flow-directed catheter without X-ray fluoroscopy during the course of pregnancy. 2) In 23 cases of MS, in whom cardiac catheterization had been performed before pregnancy, clinical courses during the pregnancy were studied.
In the 26-32 weeks' gestation: in MS (Group I), an elevation of peak systolic pulmonary arterial pressure (s-PAP) (mean+14.9mmHg, p<0.001) was seen; in contrast, in atrial septal defect (Group II), s-PAP remained constant. Right atrial pressure rose in the 26-32 weeks' gestation in both the groups. Infusion of 200ml of dextran in 12-16 weeks' gestation induced an elevation of s-PAP in Group I, especially in those who fell into heart failure in the succeeding courses of pregnancy; but not in Group II.
In MS, in 12 cases, whose s-PAP before the pregnancy was below 35mmHg, no heart failure occurred during the pregancy; in 6 of 8 cases with s-PAP between 35 and 50mmHg, mild heart failure occurred; and in 2 cases with s-PAP over 50mmHg, severe heart failure occurred during the pregnancy.
In conclusion, in MS, PAP rises during pregnancy, and s-PAP be-fore pregnancy and the reaction to dextran infusion can give suggestions for allowing pregnancy

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The mathematical analysis of thallium-201 (Tl-201) kinetics showed that the uptake level reached a plateau in several minutes and the level was related to the blood level of Tl-201 and the blood-myocardium partition coefficient. The regional perfusion rate was suggested to cause an enhanced uptake only in the early phase but not in the final equilibrium state. On the other hand an increase in the partition coefficient was shown to raise the level of equilibrium. Since the clinical imaging data are assessed in the equilibrium or near equilibrium state, a role of regional perfusion may be small for Tl-201 uptake unless it causes an ischemia.
In the clinical data, the dependency of the uptake level upon the blood level of the isotope was confirmed especially when the blood-tissue transport was assumed to be constant. An alteration of uptake count was observed when heart rate was changed in the pacemaker-implanted patients. This change in Tl-201 uptake was suggested to be brought about by the change of the blood-tissue transport activity; hence the partition coefficient, not by the change in the perfusion rate, as suggested in the analysis of Tl-201 kinetics

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Antihypertensive effect of an orally active angiotensin I-converting enzyme inhibitor, SQ 14225 (Captopril), was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r=-0.64, p<0.01 systolic, r=-0.60, p<0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r=0.64, p<0.05). The serum potassium elevated from 4.2±0.4 to 4.8±0.9mEq/L (p<0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r=-0.71, p<0.02), while serum sodium slightly decreased from 140±2 to 138±3mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension

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Inosine at the dose of 200mg was administered via central vein to 16 cases of various cardiac diseases, including effort angina pectoris, myocardial infarction, valvular disease, idiopathic cardiomyopathy, and congenital heart disease. Left ventricular performance was assessed by the time-course of various hemodynamic parameters (pulmonary wedge pressure, heart rate, LVP, LVEDP, max dp/dt, dp/dt/P, and cardiac output) including ejection fraction in some cases.
Inosine caused significant decrease in pulmonary wedge pressure ranged from -7% to -47% during 5min period following injection. Significant decrease in LVEDP ranged from -4% to -67% was also observed. Meanwhile significant decrease in systolic left ventricular pressure (LVP) was observed. In patients with relatively low value of max dp/dt (less than 1, 500mmHg/sec), the increase ranged from l00 to 300mmHg/sec (6% to 38%) except 1 case with hypertrophic obstructive cardiomyopathy. In all cases, increase in dp/dt/P ranged from 4% to 44% during 5min period following injection. In addition, the ejection fraction increased slightly in 2 out of the 3 cases studied. Cardiac output increased in all cases except a normal case by 1% to 31%, during the period of 5 to 10min following injection. Change in the heart rate was not significant.
Quantitative evaluation disclosed the beneficial effects of inosine on the left ventricular function through the remarkable load-reducing effect and the unequivocal positive inotropic effect, particularly in the cases of disturbed functions. In addition, mild coronary vasodilation action was also noted

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Effects of local anesthetics (lidocaine and procaine) on the canine sinus node were studied using isolated right atrial preparations which were obtained from puppies and perfused with oxygenated Tyrode solution through the dorsal right atrial artery. Action potential of the sinus nodal area which was characterized by the slow rate of phase 0 and diastolic depolarization, was recorded using the conventional microelectrode technique, simultaneously with atrial contraction. Lidocaine (10-300μg) prolonged the cycle length and duration of action potential, decreased the rate of phase 4 depolarization and amplitude of action potential, and shifted the threshold potential and maximal diastolic potential to the depolarizing direction. The atrial contraction decreased simultaneously. In higher doses, sinoatrial block was occasionally observed in 8 of 55 experiments. Procaine (10-300μg) had similar negative chronotropic and inotropic effects and induced sinoatrial block in 7 of 57 experiments, but unlike lidocaine, procaine produced positive chronotropic and inotropic effects following the initial negative responses in 16 of 57 experiments. The sinus node acceleration was accompanied by an increase in the rate of phase 4 depolarization. Chronotropic changes of the sinus nodal cells by these drugs were accompanied by the changes in both the rate of phase 4 depolarization and duration of the action potential

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Effects of high plasma free fatty acids (FFA) on the free radical formation of myocardial mitochondria, isolated from normal and ischemic dog hearts, were studied by electron spin resonance (ESR) spectrometry.
Free radical concentrations in state 4 respiration were used for the evaluation of the function in the mitochondria in this study. High plasma FFA levels were induced either by intravenous injection of Intralipid and heparin, or by infusion of norepinephrine. Ischemic hearts were induced by inserting a Cournand's 7F catheter into the left coronary artery under fluoroscopic control.
Exogenous high plasma FFA induced by Intralipid and heparin caused the decrease of free radicals in state 4 respiration in the mitochondria isolated from normal and ischemic dog hearts. Endogenous high FFA induced by continuous infusion of norepinephrine also caused the decrease of free radicals. On the other hand, nicotinic acid prevented the decrease of free radicals as well as the rise of plasma FFA by the norepinephrine infusion.
These results suggest that high plasma FFA itself, whether it may be exogenous or endogenous, may impair the oxidative phosphorylation of the mitochondria isolated from normal and ischemic hearts

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Cardiohemodynamic effects of perhexiline were investigated in anesthetized open-chest dogs, measuring blood flow rates of the pulmonary artery (PAF), superior and inferior venae cavae (SVCF and IVCF), right atrial pressure (RAP), systemic blood pressure (SBP), and heart rate (HR). Sum of SVCF and IVCF was interpreted as venous return (VR). Perhexiline, 0.3-3mg/Kg, injected intravenously over 2min caused dose-dependent increases in PAF, VR, and RAP, followed by decreases in PAF and VR at higher doses. SBP and HR were depressed with perhexiline dose-dependently. Verapamil, 0.03-0.3mg/Kg, also increased PAF, VR, and RAP to a lesser extent than perhexiline. Verapamil decreased these variables except RAP more markedly than perhexiline. Treatment with propranolol (1mg/Kg) and phentolamine (1mg/Kg) which completely blocked cardiohemodynamic effects of 1μg/Kg of norepinephrine, markedly attenuated the effects of perhexiline on VR and PAF but not completely. It is concluded that the effect of perhexiline to increase VR and PAF is in most part mediated through the cardiovascular reflex control for blood pressure reduction by the drug, though a direct effect on capacitance vessels may be included

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The participation of coronary perfusion pressure in hemodynamic and transmural metabolic changes was examined in the open chest canine heart.
At a lower pressure than 50% of the control, reactive hyperemia disappeared and the coronary arterial inflow precipitously decreased. In 8 dogs, when the coronary arterial inflow was decreased to 47-49% of the control by coronary constriction for 15min, the coronary perfusion pressure fell in various degrees ranging from 39 to 73% of the control. At a lower pressure than 60% of the control, creatine phosphate (CP) content and its ratio of subendocardium (ENDO) to subepicardium (EPI) decreased, while lactate (LA) content and its ratio of ENDO to EPI increased depending on the degree of the fall in coronary perfusion pressure. A little decrease in ATP content was produced only in the subendocardium under the lower pressure than 50% of the control.
When the CP content decreased to below one-third of the control, the significant accumulation of lactate and the precipitous decrease in ATP occurred.
Our results suggest that the coronary perfusion pressure has an important role for a severity of the transmural energy metabolism in the hypoperfused ventricle

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Effects of new inhibitors of thromboxane synthetase, (E)-3-[(1-imidazolmethyl)phenyl]-2-propenoic acid and (E)-3-[4-(pyridylmethyl) phenyl]-2-methyl-2-propenoic acid on cyclical reduction of flow in the partially constricted coronary artery were examined in anesthetized beagle dogs. Intravenous injections of both agents with a dose of 20mg/Kg eliminated the cyclical reduction induced by constriction in the majority of experiments. However, they failed to eliminate the cyclical reduction induced by indomethacin. Indomethacin-induced reduction was eliminated by prostaglandin I₂ in all experiments. It is suggested that thromboxane A₂ acted as an accelerator in the cyclical reduction of coronary flow induced by coronary constriction, but did not in the reduction induced by indomethacin

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The effects of imipramine were investigated on the blood pressure and heart rate in the intact dog and on the atrial rate and contractile force in the isolated atrial muscle perfused with arterial blood of the donor dog. A continuous infusion of small doses of imipramine (30μg/Kg/min, i.v., 30min) produced an increase in the blood pressure and heart rate of the donor dog and the positive chronotropic and inotropic effects in isolated atria. These responses were blocked by treatment with propranolol. When a large dose of imipramine (1mg/Kg/min, i.v., 15min) was administered to the donor dog, the blood pressure fell and the heart rate initially increased and then decreased (i.e., 15min later it decreased approximately 20% under the control level), and in isolated atria the developed tension initially increased and 15min later decreased but the atrial rate maintained over the control level. Examined doses of imipramine caused a potentiation of norepinephrine-induced action, and a large dose of imipramine significantly diminished norepinephrine-induced reflex bradycardia and/or frequently inverted to tachycardia. Moreover acetylcholine-induced reflex tachycardia was suppressed by imipramine treatment.
From these results, it is concluded that imipramine may cause a hypotension mainly due to peripheral vasodilation, and may induce a suppression of baroceptive reflex mechanism

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The role of the sympathetic nervous system in the mechanism of blood pressure rise in spontaneously hypertensive rats (SHR) was investigated by measuring plasma levels of adrenaline and noradrenaline in 5-week-old, 7-week-old, 6-month-old, and 12-month-old SHR. Age-matched normotensive Wistar-Kyoto rats (WKY) were used as control animals. Blood samples were collected through an indwelling catheter in a conscious state. In 5-week-old and 7-week-old SHR both plasma adrenaline and noradrenaline concentrations were significantly higher than those of WKY. In 6-month-old SHR plasma noradrenaline was significantly higher than that of WKY, while plasma adrenaline was not significantly different. In 12-month-old SHR the plasma levels of both adrenaline and noradrenaline were not different from those of WKY. This study indicated more distinct increase in plasma noradrenaline than in plasma adrenaline in young SHR, and also suggests that peripheral sympathetic activity and the adrenal medulla may play important roles in the development of hypertension in SHR

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An analog circuit was devised for real time determination of the left ventricular systolic pressure volume area (PVA), which we had recently identified as a reliable predictor of cardiac oxygen consumption rate per beat. PVA is the specific area in the pressure-volume diagram that is bounded by the end-systolic and end-diastolic pressure-volume relationship lines and the systolic segment of the pressure-volume loop trajectory of the left ventricle. The computed PVA was compared with PVA obtained as usual by planimetry. Correlation coefficient between the two PVA's was 0.997 (N=31, p<0.001) and the standard error of mean of the difference between the two PVA's was as small as practically negligi-ble 8mmHg ml in the PVA range from 0 to 2, 000mmHg ml. We concluded that this PVA analog computer can be used for real time determination of PVA, expediting the future studies of the relationship between PVA and cardiac oxygen consumption

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A 16-year-old high school boy showed various types of aberrant QRS complexes during supraventricular premature beats. The aberrant beats showed right bundle branch block pattern associated with varying degrees of left axis deviation
Rosenbaum et al explained it by slowing in conduction through the anterior fascicle in a bifascicular nature of human left bundle system. The alternative explantion might be possible if we consider a fanlike left bundle as proposed by Massing et al: namely incomplete or slight left axis deviation results from block of a small group of anterior parts of the fanlike left bundle, whereas marked left axis deviation results from block of a large number of fibers. The initial QRS force also changed to various degrees according to changes of the QRS axis
This case suggested the existence of an incomplete type of left anterior hemiblock, which produced not only an incomplete QRS axis change but also an incomplete change of the initial QRS forces

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