Intravenous infusion of graded doses of α-human atrial natriuretic polypeptide (α-hANP) resulted in a dose-dependent decrease in blood pressure and an increase in heart rate in 11 healthy male volunteers. However, there were no significant changes in urine output or in the urinary excretion rate of sodium. Glomerular filtration rate did not change, while renal blood flow decreased, leading to significant increases in filtration fraction and renal vascular resistance. Although plasma renin activity (PRA) and plasma concentration of norepinephrine (PNE) increased during infusion of α-hANP (both p<0.001), plasma concentrations of aldosterone (PA) and cortisol (PC) decreased (both p<0.001). Plasma concentration of arginine vasopressin (PAVP) did not change during the infusion, but greatly increased after cessation of the infusion. The hematocrit increased slightly, but significantly, during the infusion. These results show that, although α-hANP has a potent hypotensive action and inhibits the secretion of aldosterone, cortisol, and probably arginine vasopressin, it does not dilate renal vessels in normotensive persons, and likely increases vascular permeability. The lack of consistent diuretic and natriuretic responses to α-hANP may be related to the predominance of the hypotensive effect over the renal effects of the peptide in normotensive persons, or a diurnal change may have served to obscure such a response.

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To study the factors controlling the release of atrial natriuretic factor (ANF), we analyzed the peripheral plasma ANF concentration in 34 patients with heart disease who underwent cardiac catheterization.
A significant positive correlation between plasma ANF concentration and pulmonary arterial pressure (systolic, r=0.87; diastolic, r=0.75; mean, r=0.85; each p<0.001) was found in all the patients examined. There were significant positive correlations between plasma ANF concentration and systolic right ventricular pressure (r=0.86, p<0.001), pulmonary capillary wedge pressure (r=0.50, p<0.01) and mean right atrial pressure (r=0.39, p<0.05). A weak but significant negative correlation was found between plasma ANF concentration and stroke volume index (r=-0.43, p<0.05). The correlation coefficient between plasma ANF concentration and mean pulmonary arterial pressure was significantly stronger than those between plasma ANF concentration and pulmonary capillary wedge pressure, and between plasma ANF concentration and mean right atrial pressure (p<0.05 and p<0.01, respectively).
In 10 patients with mitral valvular disease, significant correlations with plasma ANF concentration were also found for pulmonary arterial pressure (systolic, r=0.80; diastolic, r=0.82; mean, r=0.82; each p<0.01).
These findings suggest that pulmonary arterial pressure may play an important role in the mechanism of release of ANF from atrial cardiocytes.

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The effects of postextrasystolic potentiation (PESP) on systolic time intervals and left ventricular wall motion were studied during diagnostic cardiac catheterization in 20 patients (4 normal individuals, 11 patients with coronary artery disease and 5 patients with idiopathic dilated cardiomyopathy). Postextrasystolic changes in the aortic pressure and systolic time intervals were measured from the electrocardiogram and aortic pressure tracing. After a micromanometer-tipped catheter was positioned in the ascending aorta just above the aortic valve, a single ventricular premature beat was introduced using an R-wave coupled stimulator. PESP was then studied during left ventriculography which was undertaken simultaneously in the right anterior oblique 30° and left anterior oblique 60° positions. Following two or three normal sinus beats, a right ventricular extrastimulus was delivered again under the same stimulating condition. PESP in all patients caused a decrease in the ratio of the preejection period to the left ventricular ejection time (PEP/ET). The average percent decrease was 21% (from 0.429±0.162 to 0.339±0.102, p<0.001). The left ventricular ejection fraction (EF) increased in all patients with PESP from 0.52±0.20 to 0.61±0.17 (p<0.001). The postextrasystolic changes in the PEP/ET ratio and EF were greater in patients with low cardiac performance. There was a good correlation (r=-0.85, p<0.001) between the changes in the EF and those in PEP/ET in PESP. Thus, it is possible to determine left ventricular residual function (the postextrasystolic change in the global EF) using the postextrasystolic change in PEP/ET in patients with coronary artery disease and dilated cardiomyopathy.

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Quantitative assessment of left ventricular function in patients with coronary artery disease was made by computer analysis of two-dimensional echocardiography performed during a cold pressor test. Short-axis cross-sectional images of the left ventricle at the levels of the mitral valve and chordae tendineae were recorded by a phase array sector scanner in 12 patients with coronary artery disease and 11 normal controls. Endocardial outlines at enddiastole and end-systole were traced and analyzed by a computer system. The short-axis cross-sectional images were divided into octants and were analyzed. The segmental area and its changes during the cardiac cycle were measured and calculated for each octant. Regional function of the left ventricle was evaluated by percent changes of segmental area. The regional segmental area changes in patients with coronary artery disease were compared with those in normal controls. Similar increments were achieved in rate pressure product in the 2 groups. In relation to the perfusing coronary arteries, 8 segments were integrated arbitrarily into 3 walls (anteroseptal wall, lateral wall, and posterior wall and posterior septum). The cold pressor test induced wall motion abnormalities in 12 of 16 walls which were supplied by stenosed coronary arteries. In contrast, wall motion abnormalities were detected in only 5 of 38 walls which were supplied by coronary arteries without significant stenotic lesions. The sensitivity of cold pressor test-induced wall motion abnormalities in detecting coronary artery disease was 75% and the specificity was 87%. No serious complications were encountered in this study.
In conclusion, computer-aided cold pressor two-dimensional echocardiography is a safe and sensitive method for the assessment of left ventricular function and diagnosis of coronary artery disease.

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The levels of serum estradiol, testosterone and progesterone were determined in 13 cases of acute myocardial infarction. Thirteen intensive care patients without coronary, hepatic or renal disease, 13 cases of unstable angina and 15 normal subjects. The patients were males ranging from 24 to 56 years of age, the average being 40.4 years. The levels of serum estradiol in the acute myocardial infarction and unstable angina groups were significantly higher than in the normal group, and no difference was found between the normal and intensive care patient. The testosterone levels were significantly lower in the acute myocardial infarction and unstable angina groups than in the normal group. Progesterone levels increased in acute myocardial infarction patients. The estradiol: testosterone ratio was considerably elevated in the acute phase of myocardial infarction, and in unstable angina patients. No difference was found between the intensive care patient and normal groups.

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PG I₂ stimulating plasma factor was measured in patients with ischemic heart disease and age-matched controls. The plasma factor measured by bioassay using rat aorta was 3.2±0.6 (n=21), 2.7±0.8 (n=7), 1.6±1.5*** (n=18) and 2.2±0.06** (n=3) PG I₂ng/mg rat aorta (mean±SD; *p<0.05, **p<0.01, ***p<0.001) in control, angina pectoris, acute myocardial infarction and old myocardial infarction with angina pectoris groups, respectively. The plasma factor measured by radioimmunoassay was 43.5±19.5 (n=11), 35.4±13.1 (n=4), 38.5±18.0 (n=9), 26.0±20.1* (n=7) and 59.5±31.2 (n=5)ng/mg rat aortic protein/15 min in control, variant angina, stable angina, acute myocardial infarction and old myocardial infarction groups, respectively. The factor in deproteinized plasma of the acute myocardial infarction group was also smaller than that of the control group. PG I₂ synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A₂. The plasma factor was not inactivated by heating. The results indicate that a heat-stable plasma factor which acts on phospholipase A₂ or on its surrounding reaction systems is deficient in the early stage of acute myocardial infarction. A decrease in the factor may cause PG I₂ deficiency, resulting in coronary thrombosis or vasospasm and consequently in acute myocardial infarction.

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The index of the baroreceptor reflex sensitivity (BRS) was measured noninvasively by monitoring the arterial pressure (AP) of the finger and R-R interval on the EGG during a Valsalva maneuver. An indirect finger AP measurement system was newly designed on the basis of the so-called vascular unloading technique. The BRS index was determined as the slope of the linear regression equation between the R-R interval and the virtual brachial AP which was evaluated from the finger AP. The data on both parameters were taken from the second period of the fourth phase in the Valsalva maneuver. The measurement was carried out on 24 inpatients (29-65 years) with essential hypertension. The conventional invasive method using phenylephrine or nitroglycerine was also performed on the same subjects. The correlation coefficient between the invasive and noninvasive methods was 0.81 when phenylephrine was used and 0.90 with nitroglycerine (p<0.001). The present method was found useful in routine clinical examination because of its easy and repeatable noninvasive application to patients without causing stress.

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Abnormality of the circulatory reflexes has been reported in patients with primary aldosteronism. However, changes in blood pressure, heart rate, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) after head-up tilting in primary aldosteronism have not yet been reported. Seven patients with primary aldosteronism were tilted to a 65 degree head-up position which was maintained for 30 min. Systolic blood pressure decreased significantly 5 min after tilting and remained at this level during the period of tilting. Diastolic blood pressure did not change during the tilting. Heart rate increased after 5 min of tilting and this level of heart rate was maintained for 30 min. Plasma renin activity was low and did not change during tilting. However, plasma aldosterone concentration increased significantly 20 min after tilting. Plasma cortisol concentration and plasma ACTH concentration also increased significantly. These results suggest that primary aldosteronism causes abnormalities of the circulatory reflexes. The increase of endogenous ACTH may increase plasma aldosterone concentration in patients with primary aldosteronism.

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Over the past 15 years 23 patients, aged 14-50, with aortic sinus-cardiac chamber fistulous communication have been operated upon. All were symptomatic and had angiographic evaluation before surgery. The last 5 were diagnosed by two-dimensional echocardiography. The origin of the fistula was the right aortic sinus in 22 and the non-coronary sinus in 1. The involved cardiac chamber was the right ventricle in 18, right atrium in 3 and left ventricle in 2. Associated lesions were ventricular septal defect (VSD) in 9, ventricular septal defect+atrial septal defect (VSD+ASD) in 1, ventricular septal defect+pulmonary stenosis (VSD+PS) in 1, atrial septal defect (ASD) in 3 and congenital aortic stenosis (AS) in 1. At surgery both the aorta and involved cardiac chamber were opened. No recurrence was encountered when the fistula was repaired using teflon felts on both ends. Three patients, 2 of whom had been operated upon before the use of cardioplegic arrest, died (13%).

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Recent reports suggest that prostaglandins play an important role in the beta-adrenergic receptor mechanism of renin release. However, the site of the action of prostaglandins has not yet been clarified. Superfusion of rabbit renal cortical slices was used to evaluate the beta-adrenergic receptor mechanism of renin release. Renin release was stimulated by isoproterenol, prostaglandin E₂, and dibutyryl cyclic AMP. Renin release stimulated by isoproterenol was inhibited by propranolol, whereas renin release stimulated by prostaglandin E₂ was not inhibited by propranolol. Isoproterenol stimulated prostaglandin E₂ release as well as renin release, and indomethacin inhibited these effects of isoproterenol. Propranolol inhibited prostaglandin E₂ release stimulated by isoproterenol. On the other hand, indomethacin did not affect renin release stimulated by prostaglandin E₂. Dibutyryl cyclic AMP did not stimulate prostaglandin E₂ release. Indomethacin did not affect renin release stimulated by dibutyryl cyclic AMP, however, it suppressed prostaglandin E₂ release during the superfusion with dibutyryl cyclic AMP. Finally, isoproterenol and prostaglandin E₂ stimulated cyclic AMP release. These data suggest that prostaglandins play an important role in the betaadrenergic receptor mechanism of renin release and the site of the action of prostaglandins is between the beta-adrenergic receptor and cyclic AMP.

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The body weight of the spontaneously hypertensive rat (SHR) during the suckling, birth to 3 weeks of age, and weanling period, through 6 weeks of age, is compared to that of its normotensive controls, the Wistar Kyoto (WKY) and Wistar (WR) rats. Litters were normalized to 6 pups per dam just after birth. The WR is larger than the SHR and WKY at all time points examined. The WKY is similar in weight to the SHR at birth but larger than the SHR at the other time points studied. These findings suggest the WR is inherently a larger rat than the SHR and WKY during the suckling and weanling periods while the development of a weight difference between the SHR and WKY after birth suggest an extrauterine influence.

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A 16-month-old girl with a diagnosis of severe valvular pulmonary stenosis, ventricular septal defect and unilateral absence of the right pulmonary artery proven by cardiac catheterization, angiography and surgery is presented. The right lung was smaller than the left one on chest X-ray, and aortography showed that it was supplied by a rudimentary circulation arising from intercostal branches of the descending thoracic aorta.

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An infant who died at 5 months with hypertrophic cardiomyopathy accompanied by QT prolongation was examined at autopsy. At the age of 16 days, serum IgM level was elevated (226mg/dl). Microscopic examination revealed characteristics of hypertrophic cardiomyopathy with myocardial cell hypertrophy with disarray and healed myocarditis with patchy fibrosis and mononuclear cell infiltration. The histological findings were compatible with those of postmyocarditic cardiomegaly developing during the fetal period.

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Recent epidemiologic and clinical studies have led to a much better definition of coronary heart disease risk factors and to the conclusion that an effective primary prevention program should begin in the pediatric age group. What remains unanswered is who should start the process in the pediatric age group and how? In view of the high degree of pediatric involvement in prevention and the family contacts, pediatricians are high on the list of suitable candidates for implementing coronary heart disease preventive measures in children. It nevertheless remains unclear as to how much counseling must be done by pediatricians and at what intensity, so as to avoid undue harm. There is, therefore, a clearcut need for guidelines to the general pediatrician for a sensible, effective and specific, yet harmless and cost efficient, approach.
Since eating habits in infancy establish the basis for lifetime eating habits, pediatricians can have a significant impact by encouraging a diet low in sodium, saturated fat and cholesterol, while adequate in calories and thoroughly meeting the nutritional needs of a growing child. Counseling regarding dietary moderation, avoidance of obesity and smoking, and regular exercise can and should become part of a pediatrician's counseling aimed at the prevention of coronary heart disease.

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