Frank lead electrocardiograms (VCG_S) were recorded from 970 young subjects in order to establish normal limits for pediatric VCG_S. In 245 children and 231 adolescents, the thoracic electrodes were located at the levels of the 4th and of the 5th intercostal space with subjects in supine position. Pairwise comparisons of 211 linear and angular parameters were made, using the 4th interspace as the reference.
In children, there were 155 parameters with statistically significant differences and 56 parameters without significant dierences between levels 4 and 5. In adolescents, corresponding figures were 158 parameters with significant differences and 53 without.
Results for selected measurements showed an increase of the amplitude of Q and R waves in leads X and Y, a decrease of Q and R waves in lead Z and an increase of maximal spatial and planar QRS vectors, with the QRS loop being more anteriorly oriented by shifting the electrodes from level 4 to level 5.
The mean differences in amplitude and orientation were generally small and of little practical value. However, the percentile distribution of the differences indicated that substantial changes in either direction can occur in some subjects. Thus, quantitative analysis of the pediatric Frank VCG_S can be critically affected by modification of electrode placement. It is suggested that normal limits should be determined for each recording level and that criteria for analysis should be applied only to VCG_S recorded at the same specified level.

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We have studied the endocardial ventricular evoked response which follows delivery of a unipolar stimulus down the sensing electrode. The system uses the same lead for both pacing and sensing and permits recordings of the evoked T wave representing a dominantly local repolarization which follows a pacing-induced depolarization at the same site. In 12 animal experiments and in the course of electrophysiological investigations in 19 patients, we evaluated changes in the morphology and duration of the paced evoked response following drug interventions which alter myocardial refractoriness and repolarization time. These changes paralleled results obtained by simultaneous, paced monophasic action potential recordings, and suggest that myocardial repolarization can be accurately assessed by this new technique, which could overcome some of the difficulties in comparing 'in vivo' experiments with the clinical effects of drugs in man.

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A new practical method of computer digital image processing of two-dimensional echocardiograms was developed for the quantification of the left ventricular regional contractility.
Short axis, cross-sectional images of the left ventricle at the levels of the mitral valve, papillary muscle and apex were recorded by a phased array sector scanner. The echo data recorded on video tape were transfered to a minicomputer through the interface circuits and digitized and processed automatically. Automatic edge detection of the endocardial and epicardial walls was performed by applying sequential steps, including smoothing, dynamic thresholding, region growing and filling small holes. The rationale for edge detection depended upon the assumptions that the abrupt changes of the gray levels occurred at the boundaries and that the points with the maximum gradient values are boundaries of the left ventricular wall. Best-fit contours of endocardial and epicardial edges were drawn by fitting a spline.
The short axis cross-sectional left ventricular wall at each level was divided into eight segments, with the center of gravity of end-diastolic left ventricular cavity and the axis connecting this with the posterior end of the right side of the septum being used as the reference point and line. The segmental hemiaxis, area and wall thickness were measured every 33 msec from end-diastole during the cardiac cycle and the systolic percent changes were calculated automatically by a computer. Regional contractility of the left ventricle was evaluated by systolic percent changes of the segmental hemiaxis, area and wall thickness.
The measured values in a patient with dilated cardiomyopathy were lower than those of a normal subject, probably reflecting myocardial damage of the left ventricle. Although there are some points to be improved, including a better system for transferring echo data to the computer and the evaluation of the validity of this fixed reference system, it is likely that computer analysis of the short axis cross-sectional echocardiogram of the left ventricle will be useful in a clinical setting.

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Negative contrast echocardiograms of two-dimensional long axis view of the right ventricle and the atrium were compared with the results of cardiac catheterization and surgical findings in 33 adults with atrial septal defects. Contrast echocardiographic evidence of atrial communication was noted in 30 cases (91%), and, in 28 cases, the negative contrast during one cardiac cycle could be measured. This could be applied even in cases with a small left-to-right shunt or with Eisenmenger's syndrome. No obvious difference in the behavior of negative contrast was documented among the cases with distinct types of septal defects.
The maximum negative contrast area and the duration of appearance in one cardiac cycle were related to the pulmonary-to-systemic flow ratio. However, a significant overlap and considerable effects of transducer angulation on measurements were documented. Thus, negative contrast echocardiography may be widely used for the noninvasive identification of a left-to-right shunt in atrial septal defects. However, the method is not appropriate for a precise quantification of three-dimensional shunt flow.

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An orifice equation is demonstrated which is independent of the symmetry and kinetic state of the left ventricle. The expression allows calculation of the cardiac output in conditions of mitral stenosis when the mitral valve area is known. This equation is Q=(1/21) R A T², where Q=cardiac output in ml/min, R=heart rate, A=mitral valve area and T=diastolic filling period in sec/min. Ten patients whose gynecologic or obstetric exam suggested a diagnosis of mitral stenosis were evaluated by conventional cardiac catheterization and M-mode echocardiography. Cardiac output computed using the new equation and the Fick principle corresponded at r=0.95, SE=340ml, N=10. These results suggest that cardiac output may be conveniently estimated for serial studies by the readily measurable echographic variables of heart rate and diastolic filling period once the mitral valve area has been measured by conventional catheterization or bi-dimensional echographic methods.

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The epidemiology of hypertension was studied on the basis of total community surveys in defined urban (mostly non-agricultural) and rural (agricultural) populations of Haryana, using WHO criteria. A total of 4, 068 subjects, comprising 95% of the eligible populations, were examined. Hypertension was found to be almost twice as common in the urban (64.3/1, 000) as in the rural group (35.7/1, 000). The prevalence of hypertension as well as the mean pressures were greater in men than in women in the 3rd and 4th decades, after which the pattern was reversed in all the subsequent age groups. The regression lines intersected at approximately 45 years of age. However, there was no appreciable sex difference in either group in the overall prevalence of hypertension.
The mean systolic and diastolic pressures rose significantly with increasing age. These were generally lower in rural than in urban subjects and there was a difference of almost one decade group. Only one out of every four hypertensives detected during the survey was aware of his disease, and even among these three-fourths were either untreated or inadequately controlled.
The lower prevalence of hypertension was associated with lesser mean pressures in the rural community, and both these observations are ascribed to a much larger proportion of rural people (compared to city dwellers) being thinner in size, engaging in hard physical activity, and belonging to a lower socio-economic group. The data have also been compared with other studies from India and abroad and the possible reasons for the observed differences discussed.

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The biological actions of angiotensin III (AIII) in animals have been reported to be stimulation of aldosterone secretion and vasoconstriction. However, the biological actions of AIII in human essential hypertension (EH) have not been evaluated. Twenty ng/Kg/min of AIII was infused intravenously for 30 min into 6 normal subjects and 24 patients with EH. The systolic blood pressure was elevated significantly, from 116±5 (mean±SD)/68±4 to 137±9/74±5mmHg in normal subjects and from 155±29/95±17 to 176±26/106±20mmHg in EH patients. The elevation in systolic BP of low-renin EH patients was significantly larger than that of normal-renin EH patients. Plasma renin activity (PRA) decreased significantly from 1.64±1.07 to 1.21±1.05ng/ml/hr in normal subjects and from 0.88±0.66 to 0.76±0.63ng/ml/hr in EH. Plasma aldosterone concentration (PAC) increased significantly from 57±34 to 116±34pg/ml in normal subjects and from 66±56 to 91±24pg/ml/ in EH. There was no significant difference between the increase of PAC in low-renin EH and in normal-renin EH. Plasma cortisol concentration (PCC) did not change in these subjects. There were no significant relationships between the changes of PRA and PAC or PRA and blood pressure. These results suggest that the pressor action of AIII appeared in relation to the basal PRA in EH. In EH, PRA is suppressed by the direct action of AIII in the kidney and neither by increased PAC nor by increased blood pressure. The small changes in blood pressure caused by AIII infusion suggest that a test using an AIII infusion for aldosterone stimulation would be preferable to an angiotensin II infusion.

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Serum angiotensin converting enzyme (ACE) activity in patients with chronic renal failure (CRF) on regular hemodialysis (HD) was measured. The enzyme activity of these patients was significantly higher than that of an age-matched control group. Additionally, we found that an elevated activity was observed in patients who had a longer history of HD. The enzyme activity in patients with CRF caused by diabetic nephropathy was higher than that in patients with CRF caused by chronic glomerulonephritis, though this difference was not significant. We conclude that diffuse vascular damage might be the cause of the increased ACE activity seen in CRF.

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This study examines the responses of coronary collateral vessels to various vasoconstrictors and compares them with responses of 3 different divisions of the native coronary arterial trees in dogs. Only high concentrations of phenylephrine induced contractions in collateral vessels and medium coronary arteries, whereas even a high concentration of this agent did not affect small coronary arteries. Lower concentrations of serotonin or ergonovine elicited contractions in collateral vessels, and medium and large coronary arteries, but even a high concentration of these agents did not affect small coronary arteries. Angiotensin II (10^-7M) elicited prominent contractions in the following order : small vessels, collateral vessels, medium and large coronary arteries. These results indicate that well-developed collateral vessels behave like native medium diameter coronary artery, and that the tonus of collateral vessels is possibly influenced by various vasoactive substances.

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Right-heart cardiac output was determined in 10 dogs using a newly developed, highly accurate catheter-tip resistivity probe. A saline indicator was injected into the right atrium and the blood resistivity was monitored at the catheter tip in the pulmonary artery. The resulting dilution curves were calibrated electrically according to the manner in which blood resistivity changes with saline concentration and cardiac output values were calculated. Cardiac output values determined simultaneously by the direct Fick method were used as a reference.

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This study examined changes in cardiac myofibrillar ATPase activity during the development of hyperthyroidism and the relationships between changes in myofibrillar ATPase activity and hemodynamic parameters in rabbits. Calcium-stimulated, magnesium-dependent ATPase (Ca-ATPase) activity of cardiac myofibrils exhibited about a 30% increase after the first week of treatment with excess desiccated thyroid tissue powder (thyroid-treatment) and did not show further increase during thyroid-treatment. Development of cardiac hypertrophy and increases in systolic and diastolic blood pressure were dependent upon prolonged periods of thyroid-treatment lasting from 3 days to 4 weeks, whereas the maximal increase (about 55%) in heart rate was seen after the first week of thyroid-treatment. The elevated level lasted throughout subsequent thyroid-treatment. Lineweaver-Burk plots showed an increase in Km and Vmax values for Ca-ATPase activity of my-ofibrillar preparation from the thyrotoxic hearts of treated animals. Increased Ca-ATPase activity was correlated with thyroid-induced changes in heart rate. Propranolol partially reduced the thyroidinduced increase in Ca-ATPase activity and heart rate, suggesting participation of beta-adrenoceptors in the thyroid-induced increases of Ca-ATPase activity and heart rate.

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The interactions between coenzyme Q₁₀ (CoQ) and chlorpromazine (CPZ) were studied after CPZ-induced injury of cultured myocardial cells of new-born Wistar rats. Administration of 7.5×10^-6M of CPZ caused decreases in adenosine triphosphate (ATP) contents and beating rates by 77.4% and 54.2%, respectively. These changes were dependent on the dosage of CPZ. Histologically, many lamellated granules appeared in the cytoplasm and seemed to originate from mitochondria. The decreased density of the mitochondrial matrix and an irregular arrangement of cristae were also observed. Coincubation of the cultures with CPZ and CoQ led to a dose-dependent increase in ATP contents and beating rates. The appearance of increased number of granules in the cytoplasm was suppressed. Indomethacin, an inhibitor of prostaglandin synthesis, interfered with the effects of CoQ on the CPZ-induced myocardial cell injury. These findings suggest that CoQ may protect myocardial cells from CPZ-induced injury, and that prostaglandins may play an important role in the action of CoQ.

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A 22-month-old girl with Down's syndrome with a direct communication between the right pulmonary artery and left atrium leading to systemic desaturation is presented. She also had an atrial septal defect of the secondum type, which spontaneously closed. She underwent successful ligation of the abnormal communication. The literature is reviewed and, considering the high incidence of cerebral and systemic emboli, early surgical intervention is recommended.

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