Biomedical subjects
Publications and source records attributed to C M Cottrill.
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Myocardial sinusoids communicating with the coronary systems occur in pulmonary atresia with intact ventricular septum. To test the hypothesis that the extent of ventriculocoronary connections correlates with the degree of right ventricular outflow obstruction as evidenced by clinical, angiographic and gross anatomic findings, a serial section study of six human autopsy hearts representing a spectrum of hypoplastic right heart was undertaken. Slides were evaluated for the presence and extent of ventriculocoronary connections, associated developmental abnormalities and secondary changes in the ventricular walls. Whereas extensive blind-ended deep sinusoids were a feature of all five cases with unrelieved obstruction, ventriculocoronary connections were identified in three. Changes that suggested ongoing remodeling provide new evidence for the postnatal temporal evolution of these anomalous communications. The regional distribution of myofiber disarray in hypoplastic right heart supports the concept that vascularization parallels myocardial organization in the developing human heart.
Evaluation of pulmonary arterial pressure in small laboratory animals requires surgical catheter implantation. However, even this modest surgical procedure is known to retard weight gain, alter various biochemical parameters and may exert other deleterious actions which could complicate data interpretation. To obviate these adverse effects of surgery and to permit better staging of experimental procedures, a method for non-invasive detection of pulmonary hypertension would be desirable. The present study examined the utility of m-mode echocardiography to detect increased pulmonary arterial pressure and right ventricular hypertrophy in rats with monocrotaline-induced pulmonary hypertension. At various times after administration of monocrotaline (105 mg/kg), rats were anesthetized lightly with sodium pentobarbital (30 mg/kg) and m-mode echocardiograms were generated using a 7 mHz transducer with the animals in the supine position. Mean pulmonary arterial pressure was then determined by closed-chest catheterization of the pulmonary artery. At sacrifice, the extent of right ventricular hypertrophy was determined as the ratio of the weight of the right ventricular free wall to that of the left ventricle plus septum. Right ventricular systolic time intervals, determined from the echocardiogram, correlated significantly with the extent of right ventricular hypertrophy (p = 0.05; r2 = 0.39) but not with mean pulmonary arterial pressure (p = 0.2; r2 = 0.14). Echocardiography may provide a simple, non-invasive means to detect cardiopulmonary abnormalities in rats and may thus be useful in staging subsequent experimental procedures without need for prior surgical catheter implantation.
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Echocardiograms were performed on parents of five infants with Pompe disease (glycogen storage disease, type II). Three of the infants had presented with congestive cardiomyopathy and two with dynamic muscular subaortic stenosis. No heart murmurs were audible in any of the parents of the five infants. The parents of the three infants without left ventricular outflow tract obstruction had normal echocardiographic results, whereas one parent of each of the infants with left ventricular outflow obstruction had asymmetric septal hypertrophy. The association between left ventricular outflow obstruction and parental asymmetric septal hypertrophy suggests that both septal hypertrophy and glycogen storage disease were inherited by these two infants.
A newborn with partial deletion of the long arm of chromosome six presented with cyanosis at birth. Initial studies suggested the diagnosis of tetralogy of Fallot and the infant underwent a Waterston shunt procedure with subsequent clinical improvement. The infant subsequently died of unrelated causes. Autopsy revealed a ventricular septal defect and a dysplastic pouchlike structure related to an anomalous tricuspid valve leaflet which obstructed right ventricular outflow. Classical anatomic findings of tetralogy of Fallot were absent. Clinical and echocardiographic findings that would be expected to aid early diagnosis of future cases are presented.
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Two patients with anomalous origin of the left main coronary artery from the pulmonary artery had an associated defect (one, critical pulmonary stenosis; the other, ventricular septal defect). They presented with signs and symptoms of the associated defect and the coronary anomaly was unrecognized. Both cases at autopsy lacked the usual large right coronary artery seen with this anomaly. The pathophysiologic features of the combined defects are described, their differences from the isolated anomaly are noted and their relation to surgery is discussed.
Supravalvular aortic stenosis with a mean pressure gradient of 101 mm Hg was encountered in six patients aged 1 1/2 to 12 years. Three patients had Williams syndrome. In two other patients the stenosis was familial. The angiographic/anatomic subtype of deformity was hourglass in four patients, diffuse in one, and membranous in one. Four patients are alive following successful surgical repair; the other two died without surgery. Microscopically, disorganized medial elements with fibrotic intima sometimes containing lacunae were observed in five cases; the one other had valvelike tissue only. Ultrastructurally, thick irregular elastic fibers, abundant swirling collagen, hypertrophied smooth-muscle cells, and scant ground substance characterized the medial tissue defect. Although hemodynamics during intrauterine development may predispose to localization of the stenosis to the supra-aortic valvar region, the cause for the mural dysplasia remains uncertain.
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In 1973, standardized blood pressure measurements were obtained in 837 high school students in Bourbon County, Kentucky, a rural county with a high prevalence of individuals with systemic hypertension. In 1978, follow-up measurements of blood pressure were performed in selected individuals who were in the high, intermediate, and low ranges of the initial sex-specific blood pressure distributions. Relative rank order of initial blood pressure measurements over the five-year period was maintained. The results of this population-based study provided an opportunity to evaluate the cardiac status in young adults with relatively high blood pressures maintained over five years. Standard m-mode echocardiographic examinations were, therefore, performed over five years. Standard m-mode echocardiographic examinations were, therefore, performed at the time of follow-up. In individuals in the low and intermediate ranges for systolic blood pressure, indices of ventricular hypertrophy were directly correlated with blood pressure level. Among individuals with higher values for systolic blood pressure, after adjusting for the effects of relative body size, indices of ventricular hypertrophy were not significantly different from those noted in the intermediate group. Indices of cardiac performance and estimated left ventricular systolic wall stress were, however, significantly elevated in this "high" blood pressure group. Early in the course of systemic hypertension increased wall stress, rather than hypertrophy, appears to be the primary cardiac manifestation of elevated systolic blood pressure.
Twenty-one consecutive children (aged 3 to 14 months) with d-transposition of the great arteries were evaluated with standard M mode echocardiography at the time of hospital admission for routine preoperative cardiac catheterization. At catheterization, 6 of the 21 were found to have a systolic pressure gradient between the body of the left ventricle and the main pulmonary artery. Echocardiographic systolic anterior mitral valve motion was noted in nine patients, including five who did not have a left ventricular to pulmonary arterial systolic pressure gradient. Diastolic approximation of the anterior mitral leaflet to the septum was noted in 14 (9 without a gradient), pulmonary valve flutter was also present in 14 (9 without a gradient) and there was premature systolic pulmonary valve closure in 6 (3 without a gradient). Echographic left heart dimensions were not different in patients with a left ventricular outflow pressure gradient than in those without, but patients wit systolic anterior mitral valve motion and diastolic approximation of the mitral leaflet to the septum did have smaller left ventricular and pulmonary root dimensions than did those without these echocardiographic findings. Echocardiographic findings that have been described as suggesting left ventricular outflow obstruction in patients with d-transposition of the great arteries appear to be more related to size and configuration of the left ventricle than to the presence or absence of obstruction.
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The first stage of a repair of pulmonary atresia with intact ventricular septum (type I) was attempted in a 2-day-old infant. At surgery, decompression of the hypertensive small right ventricle was followed by a sudden loss of myocardial contractility and death. Postmortem examination revealed a fistula with a large orifice in the right ventricular infundibulum that communicated directly with the left main coronary artery. Severe hypertensive changes indicative of abnormally high perfusion pressure were noted in the distal left coronary artery branches. The clinical course suggests that the effect of relieving right ventricular outflow obstruction was a reduction of left main coronary artery blood flow, resulting in fatal intraoperative myocardial ischemia. This unusual case draws attention to the anomalous ventriculocoronary communications often present in pulmonary atresia and their potential for limiting a successful surgical repair.
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PRA is suppressed in approximately 25% of patients with essential hypertension. To determine if renin suppression precedes the onset of hypertension, PRA and plasma aldosterone were measured before and after treadmill exercise in 129 young adults with relatively high, intermediate, or relatively low blood pressures sustained over 5 yr. PRA and aldosterone responses to exercise were lower (P less than 0.01) in the high blood pressure group. In contrast, plasma renin substrate was lower (P less than 0.01) in the low blood pressure group. Unrelated to blood pressure, PRA, but not aldosterone, was lower in black than in white subjects both before and after exercise. In conclusion, renin suppression precedes the onset of hypertension and may be an appropriate response to higher levels of arterial pressure.
M-mode echocardiographic records of 26 patients with surgically proven complete atrioventricular canal defect were reviewed. Fragmentation of the interventricular septum and anterior displacement of the mitral annulus into the left ventricular outflow tract were noted in all patients. In 25 of 26 a common atrioventricular valve leaflet echo could be identified in the left ventricular outflow tract at the area of the left ventricle demonstrated separate "mitral" and "tricuspid" contributions to atrioventricular valve echoes in all 13 patients with type A defect, and a single common atrioventricular valve leaflet in 10 of 11 patients with type C complete atrioventricular canal. Two patients with type B defect had findings intermediate between these two patterns. M-mode echocardiography presumptively diagnosed complete atrioventricular canal in all 26 patients and diagnosis was definitive in 25 of 26. In addition, echocardiographic atrioventricular valve patterns permitted anatomic classification in the large majority of cases.
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