In order to clarify the clinical significance of left ventricular outflow tract obstruction, 11 infants with coarctation of the aorta and ventricular septal defect were subjected to cineangiography (or autopsy) analysis.
Three infants without left ventricular outflow tract obstruction were salvaged by aortoplasty using a subclavian flap or a Dacron patch with concomitant pulmonary artery banding. The remaining 8 infants died surgically or nonsurgically, and were confirmed retrospectively to have had left ventricular outflow tract obstruction.
It seems worthwhile to stress that the presence of an abnormal muscle bundle in the left ventricle can be demonstrated angiographically, especially by the axial technique.
From our present study, though the number of cases examined is limited, we have an impression that left ventricular outflow tract obstruction may be a determining factor with regard to the appropriateness of pulmonary artery banding in the two-stage operation for infantile coarctation associated with a large ventricular septal defect.

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The effect of aging on histological changes of the conduction system was studied by serially sectioning 55 autopsied hearts weighing less than 300Gm. None of the hearts showed evidence of cardiovascular disease nor were there any abnormalities in the clinical findings and ECG taken during the last 3 months of life. A reduction in the number of muscle cells and an increase in the number of collagen fibers were apparent in hearts taken from patients over 70 years of age. These findings were most evident in the S-A node and less so in A-V node, bundle of His, and left and right bundle branches. Deposition of amyloid substances was not observed in any portion of the conduction system.

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Exercise tests were performed in 14 patients with untreated variant angina with frequent spontaneous attacks and in 15 patients after treatment abolished the attacks. (1) Anginal attacks associated with ST elevation were induced by exercise in 79% of untreated patients. By contrast, ST elevation was not observed in treated patients and ST depression was induced in 53% of the cases. (2) Exercise-induced ST elevation in untreated patients was shown in the same leads as the spontaneous attacks. (3) Exercise-induced ST elevation appeared initially during the recovery phase after exercise in 36% of untreated patients. Exercise-induced ST depression appeared during or immediately after exercise. (4) The reproducibility of exercise-induced ST elevation was low with repeated tests at different stages, but exercise-induced ST depression was consistently observed. (5) The exercise-induced ST depression and lack of ST changes in treated patients were highly suggestive of the presence and absence of organic coronary artery disease, respectively. However, the exercise-induced ST elevation in untreated patients did not differentiate between the presence or absence of organic stenosis of the coronary arteries. The results of exercise tests vary with the stage of variant angina. It is suggested that a coronary arterial spasm is a trigger mechanism for exercise-induced angina in cases of variant angina with frequent spontaneous attacks.

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Mitral and aortic regurgitation was evaluated by X-ray, dye dilution bolus, and ¹³³Xenon infusion methods in 24 patients with mitral, aortic or both valve lesions. Good reproducibility was found using the ¹³³Xenon infusion method. The regurgitant fraction estimated by ¹³³Xenon constant infusion method correlates well with the results of the dye dilution method in mitral regurgitation as well as in aortic regurgitation. The ¹³³Xenon infusion method is well-suited for quantitative evaluation of mitral and aortic regurgitation. For its simplicity, it is therefore recommended for further clinical evaluation in pharmacodynamic and preoperative studies.

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A correlative study of transmembrane potential characteristics, surface morphological features of human atrial muscle, and cardiac hemodynamics was carried out in 41 patients, who were divided into 2 groups based on the level of the mean maximum diastolic potentials (MDP). Group A consisted of 19 patients with MDP values ranging from -60.0 to -82.0mV (mean±S.D.=-65.70±6.63mV). Group B included 22 patients who had abnormally low MDP (range -36.0-58.5mV, mean±S.D.=-48.14±6.72mV). The differences in electrophysiological data were statistically significant. However, there were no significant differences in the hemodynamic data between the 2 groups. Furthermore, there was poor correlation between the electrophysiological and hemodynamic data in both groups. In group A, scanning and transmission electron microscopy revealed either no changes or only mild alterations in the surface morphology of the atrial myocardium. Various degrees of surface morphological changes, including a focal loss of the endothelium which was always associated with endocardial fibrosis, irregular thickening and lamination of the glycocalyx, disruption of the sarcolemma and complete destruction of the surface membrane structures were more often observed in group B.
These results provide valuable evidence that sarcolemmal changes may underlie the electrophysiological alterations in diseased human atria. We suggest that the principal pathogenetic mechanisms leading to the transmembrane potential changes are the altered sufrace morphology of atrial myocardial cells, resulting from underlying disease processes.

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Pulsed Doppler echocardiography was performed in 17 subjects who had clinically uncomplicated porcine bioprosthesis in the mitral position. A positive initial diastolic flow wave was present in all patients; end-diastolic A waves were seen in the sinus rhythm of every patient. The peak of the diastolic wave was delayed when compared with the normals in our laboratory. This wave had clearly demarcated ascending, mid- and descending segments. When contrasted with normal subjects, the slope of the diastolic wave was mildly reduced in all patients. Fine to coarse indentations on the descending and mid-segments were seen in 15/17 (88%) of the patients. We conclude that the diastolic flow profile of the clinically uncomplicated mitral bioprosthesis resembles mild mitral stenosis. Reduced orifice size and/or the physical properties of the bioprosthesis are the likely mechanisms for these alterations.

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Echocardiography was performed on 10 patients with suspected acute pulmonary embolism. In 3 patients with normal echocardiograms, the diagnosis was excluded by pulmonary angiography. Two with small emboli on angiography had a pulmonary arterial pressure≤35mmHg and normal echocardiograms. Five had an increased right ventricular end-diastolic dimension (RVEDD) and 4 had a left ventricular end-diastolic dimension (LVEDD) below normal or in low normal levels. The RVEDD/LVEDD ratio was increased in 4 patients, 3 of whom had paradoxical interventricular septal motion. The mitral valve E-F slope and left atrial dimension changed variably. The posterior aortic wall O-V excursion (PAW-OV-Ex) decreased in 5 and was correlated with LVEDD (r=+0.92, p<0.01) and the RVEDD/LVEDD ratio (r=-0.87, p<0.025). Follow-up echocardiography in 3 cases after recovery showed a decreased RVEDD/LVEDD ratio, normal septal motion and improved LVEDD and PAW-OV-Ex.
The PAW-OV-Ex seems to mirror the abnormalities in volume changes of the left side of the heart resulting from pulmonary embolism. An entirely normal echocardiogram would be unlikely in the presence of a hemodynamically significant pulmonary embolism.

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This study compared responses of blood pressure, plasma concentrations of norepinephrine (PNE) and aldosterone (PA), plasma renin activity (PRA) and urinary excretion of aldosterone during a 5-day period of high salt intake in 11 untreated patients with essential hypertension and 11 age-matched normotensive control subjects. The hypertensive patients all had blood pressures that had been above 160 systolic and/or 90mmHg diastolic before admission and had decreased to below 150/90mmHg with only bed-rest and mild salt restriction (6Gm per day). Sodium balance was also measured before and after high salt intake (16Gm per day). The hypertensive patients showed both a significant reduction in blood pressure after hospitalization and a significant blood pressure elevation when salt intake was increased. In contrast, no obvious changes in blood pressure were observed in the normotensive subjects. Sodium retention and decreases in PNE and PRA during the high salt period were similar in both groups. However, the reduction in PA and urinary aldosterone excretion in response to excessive salt intake was less pronounced in the hypertensive patients than in the normotensive subjects. The ratio of percentage changes in PA to percentage changes in PRA after salt loading was significantly lower in the hypertensive patients than in the normotensive subjects. In addition, the changes in PA during salt loading were inversely proportional to changes in blood pressure (r=0.66, p<0.01). Thus, it is suggested that the sensitivity of blood pressure to increased dietary salt intake in hypertensive patients may be related to altered aldosterone dynamics, and that the blunt responses of the PA and urinary excretion of aldosterone can be attributed to reduced sensitivity of the adrenal cortex to changes in circulating angiotensin.

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In order to evaluate how taurine relates to the pathogenesis of essential hypertension, the taurine content of plasma, whole blood and urine was measured in 18 normals and in 79 hypertensive patients. The patients included 32 untreated cases of essential hypertension, 32 treated cases and 15 cases with labile hypertension. There were no statistically significant differences between normals and essential hypertensives in either plasma or whole blood taurine content. However, in comparison to urinary taurine excretion in normals, 1594.0±143.7μmol/day (mean±SE), that for untreated essential hypertensives, 708.1±57.1μmol/day (p<0.001), and for treated essential hypertensives, 953.6±94.3μmol/day (p<0.001), were significantly lower. Those with labile hypertension showed almost the same value, 1478.3±134.3μmol/day, as normals. Taurine clearance and the taurine/creatinine ratio were also markedly decreased in essential hypertensives without treatment. For all subjects, taurine clearance had a positive correlation (r=0.327, p<0.01) with creatinine clearance, but there were significant negative correlations between systolic blood pressure and daily urinary taurine excretion (r=-0.472, p<0.01) and between diastolic blood pressure and daily urinary taurine excretion (r=-0.382, p<0.01). There were also significant positive correlations between daily urinary taurine excretion and serum high-density lipoprotein cholesterol (r=0.559, p<0.01) and between the former and cardiac index (r=0.547, p<0.01). These results suggest that a deficiency of taurine plays an important role not only in elevating blood pressure in essential hypertension but also in atherogenesis as well.

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This study was designed to determine whether coronary collaterals have preventive effects on tachycardia-induced myocardial ischemia under partial restriction of proximal coronary artery inflow. Studies were carried out in dogs with developed coronary collaterals and control dogs. ST-elevation in epicardial and intramyocardial electrograms was used for assessing the degree of regional myocardial ischemia. In control dogs with coronary constriction (80% reduction of i.d.) pacing-induced tachycardia produced significant ST-elevation, 1.48±0.17mV in the inner layer and 0.79±0.29mV in the middle layer at a cardiac rate of 150/min, 3.58±0.38mV in the inner layer, 2.73±0.38mV in the middle layer, and 1.93±0.36mV in the outer layer at a rate of 180/min. In dogs with moderate collaterals ST-segment elevation was only 1.41±0.18mV in the inner layer and 0.96±0.24mV in the middle layer at a rate of 180/min. In dogs with abundant collaterals there was no significant ST-elevation during tachycardia. These findings indicate that blood supply to the affected myocardium via developed collaterals is sufficient to meet graded increases in metabolic requirements under the condition of limited coronary flow reserve in an experimental model simulating angina pectoris.

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We developed a canine model with coronary stenosis produced by intraluminal obstruction with a micro-balloon occluder to assess the role of vasomotor tone of a large coronary artery with a preexisting fixed stenosis in the genesis of myocardial ischemia. Hemodynamic and electrocardiographic responses to ergonovine, an agent capable of provoking coronary spasm, were evaluated. In the absence of coronary stenosis, intracoronary infusion of 4μg/min ergonovine had no systemic and coronary hemodynamic effects. Similarly, with various degrees of external obstruction created by a screw-type metal constrictor, ergonovine had little hemodynamic effects. By contrast, with a stenosis greater than 28.4±5.0mmHg in pressure gradient, created by intraluminal obstruction which preserved active arterial vasomotion, ergonovine-induced vasoconstriction produced a marked decrease in coronary blood flow and distal coronary pressure, followed by ST-elevation. These deleterious effects of ergonovine on coronary hemodynamics were reversed completely by intracoronary infusion of nitroglycerin. Our results indicate that the effects of normal coronary arterial vasomotor activity on a stenosed vessel can cause myocardial ischemia.

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In the present study, the effects of morphine and pethidine on coronary vessel resistance (CPP), blood pressure (BP), and experimental myocardial infarction-induced cardiac arrhythmia were investigated. Both morphine and pethidine induced a fall in CPP and BP and inhibited the cardiac arrhythmia. The morphine effects on CPP and BP were largely blocked by mepyramine. The effects of pethidine, on the other hand, were not blocked by mepyramine, propranolol, or atropine. An interesting dose dependent inhibition of cardiac arrhythmia was observed with pethidine.

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To evaluate the role of brain prostaglandins in the regulation of blood pressure, we examined the effects of intracerebroventricular injections of prostaglandin D₂, angiotensin II and indomethacin on blood pressure in conscious rats. Intraventricular administration of prostaglandin D₂, the major prostaglandin synthesized in the rat brain, did not elicit a significant change in blood pressure. On the other hand, intraventricular injection of angiotensin II resulted in an increase in blood pressure in a dose-related manner. However, this central pressor effect of angiotensin II was not affected by intraventricular pretreatment with indomethacin. Indomethacin per se did not induce any change in blood pressure. These results suggest that prostaglandin D₂ in the brain does not play an important role in the regulation of blood pressure in conscious rats. It is also suggested that the central pressor effect of angiotensin II is not mediated by prostaglandin biosynthesis in the central nervous system.

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Angiotensin-converting enzyme activity in six areas of the brain (cerebral cortex, midbrain, thalamus, hypothalamus, striatum, and cerebellum) and subcellular fractions of the aorta (homogenate, mitochondria, microsomes, and supernatant) was determined in both normotensive and renal hypertensive rats [Goldblatt one-clip, one-kidney (1-c, 1-k) and one-clip, two-kidney (1-c, 2-k) hypertensive, and two-clip, two-kidney (2-c, 2-k) hypertensive rats]. Converting-enzyme activity was relatively high in the thalamus and relatively low in the cerebellum in normotensive and renal hypertensive rats. The enzyme activity in the hypothalamus of Goldblatt 1-c, 2-k rats was significantly higher than that of normotensive and other renal hypertensive rats. However, there was no significant difference in the enzyme activity in each brain area among normotensive, Goldblatt 1-c, 1-k hypertensive and 2-c, 2-k hypertensive rats. The enzyme activity of the supernatant from aortic subcellular fractions was extremely high in normotensive and renal hypertensive rats, However, the enzyme activity in all aortic fractions from Goldblatt 1-c, 2-k rats was significantly higher than that of normotensive and other renal hypertensive rats. There was no significant difference in the enzyme activity among normotensive, Goldblatt 1-c, 1-k hypertensive and 2-c, 2-k hypertensive rats. Therefore, it is likely that increased angiotensin-converting enzyme activity in the brain and the aorta may play a role in the initiation or the maintenance of hypertension in Goldblatt 1-c, 2-k hypertensive rats.

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Although mucolipidosis, a fatal metabolic storage disorder, is associated with cardiovascular abnormalities, detailed, non-invasive cardiac examinations have not been well documented. We studied 4 children with type II and type III mucolipidosis, 3 of whom had unequivocal evidence of aortic regurgitation characterized by phonocardiography and M-mode echocardiography. Two-dimensional echocardiography showed an aortic valve prolapse in 3, a mitral valve prolapse in 2 and a tricuspid valve prolapse in 1. The QT interval was prolonged in 2 cases.
In 1 autopsy case, we found considerably thickened and retracted aortic, mitral, and tricuspid valves, and an accumulation of the foam cells in the myocardium. Echocardiography revealed similar findings in another 3 cases.
We conclude that cardiac manifestations in this disorder should be examined carefully particularly by the use of echocardiography which is an excellent technique for detecting cardiovascular abnormalities in mucolipidosis.

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