Primary and secondary neoplasms of the heart.
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Biomedical subjects
Publications and source records attributed to W C Roberts.
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Cardiac transplantation is performed in some adults having cardiac conditions causing considerable cardiac dysfunction in the absence of an increase in cardiac mass.
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Twelve patients are described who had liver transplantation after coronary artery bypass grafting (CABG). The liver disease in most of the patients was a consequence of hepatitis C resulting from blood transfusions at the time of CABG.
A patient is described in whom severe cardiac dysfunction developed from amyloid deposited entirely in the walls and lumens of intramural coronary arteries, underwent cardiac transplantation, survived another 69 months, died suddenly, and at necropsy had amyloid again limited to the walls and lumens of the intramyocardial coronary arteries in the donor heart. The rather lengthy survival in this patient and the 118-month survival in a similar previously reported patient suggests that cardiac transplantation may be an appropriate procedure for some patients with cardiac amyloidosis.
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Correlation of the structure of the operatively excised aortic valve with various clinical variables has received relatively little attention. This report describes certain observations in 115 patients aged >30 years (mean age 70) who had aortic valve replacement for aortic valve stenosis unassociated with mitral valve dysfunction. The operatively excised aortic valve was congenitally unicuspid in 3 patients (3%), congenitally bicuspid in 54 patients (47%), tricuspid in 57 patients (50%), and of uncertain structure in 1. Of the 87 patients (76%) aged > or =65 years (Medicare population), 36 (41%) had congenitally malformed valves (bicuspid in each), and of the 28 patients (24%) aged <65 years, 21 (75%) had congenitally malformed valves. A higher percentage of patients with congenitally malformed valves had peak systolic pressure gradients across the valve >50 mm Hg than did patients with tricuspid valves (57% vs 43%). Concomitant coronary artery bypass grafting (CABG) was performed in 52 patients (45%) (34 men and 18 women), and they had average peak systolic pressure gradients across the valve significantly lower than patients without coronary bypass (46 vs 64 mm Hg): 39% of the 57 patients with congenitally malformed valves and 53% of the 57 patients with tricuspid valves had concomitant coronary bypass (insignificant difference). Thus, in a relatively older population of 115 patients having aortic valve replacement for isolated aortic valve stenosis, with or without associated aortic regurgitation, one half had congenitally malformed valves (either unicuspid or bicuspid valves) and one half had tricuspid valves. Patients having concomitant CABG had significantly smaller gradients across the stenotic valves than those who had no CABG.
OBJECTIVE: The present study was designed to identify the predictors of cross-sectional area narrowing by neointima (%CSAN-N) after balloon angioplasty (BA) in the cholesterol fed rabbit model. METHODS: Angiographic, histomorphometric, and immunohistochemical data were analyzed from 91 femoral arteries of New Zealand white rabbits. Focal atherosclerosis was induced by air desiccation of the endothelium followed by a 2% cholesterol diet for 28 days. The rabbits received heparin (150 U/kg) at the time of BA (2.5 mm; three, 60-second, 10-atm inflations). Arteries were perfusion-fixed and excised 7 (n = 16), 14 (n = 11), 21 (n = 9), or 28 (n = 20) days after BA. Non-angioplastied arteries were de-endothelialized (cholesterol-fed [n = 12] or normal diet [n = 8]), non-injured but cholesterol-fed (n = 7), or normal (n = 8). RESULTS: Univariate regression across all groups showed that the absolute area of the lumen by histomorphometry (LA) correlated significantly with the area bounded by the external elastic lamina (EEL) (vessel size), but no correlation was found with the absolute area of neointima or media, the percentage disruption of the internal elastic lamina (IEL), or the percentage of neointima and media occupied by foam cells. However, %CSAN-N correlated significantly with the area bounded by the EEL, significantly with the absolute neointimal area, and negatively with the absolute LA (p < 0.0001). Significant correlations were also found between %CSAN-N and the % IEL disrupted, the area of neointima and media occupied by RAM-11 + foam cells, and the loss of alpha-actin positivity in the media (p < 0.0001). CONCLUSIONS: These studies show that neointimal formation contributes significantly to luminal narrowing 1 month after angioplasty in this model, that the degree of vascular injury and the extent of foam cell accumulation in the neointima and media are significant independent predictors of neointimal formation, and that the area of the neointima, and the percent narrowing by neointima, are important predictors of remodeling itself (EEL area). These predictors were not identifiable when the analysis was focused on the determinants of absolute luminal area alone.
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We investigated at autopsy or at retransplantation the frequency and characteristics of coronary thrombosis in 76 cardiac allografts: 37 in place for < or = 2 months (early) and 39 in place >2 to 99 months (late). The 76 allografts were inserted in 69 patients: a single 1 in 56 patients and 2 allografts in 13 patients, 7 of whom subsequently died and had an autopsy. An average of 140 sections from 70 5-mm-long segments of 8 epicardial coronary arteries were examined from each of the 76 allografts with both hematoxylin-eosin and Movat pentachrome stains. Thrombus was found in only 1 coronary artery (3%) (the right one) of the 37 early allografts, and in 24 of 39 late allografts (61%). Of the latter 39 grafts, 29 (79%) had allograft vascular disease (AVD) and 24 (83%) of them had coronary thrombosis. Of the 312 epicardial coronary arteries (4 major and 4 minor) examined in the 39 late cases, 66 arteries (21%) contained thrombus. Of the 24 late cases with thrombus in at least 1 artery, thrombus was present in 66 (34%) of the 192 epicardial coronary arteries examined: in 6 of the 8 arteries in 3 patients; in 5 arteries in 2 patients; in 4 arteries in 1 patient; in 3 arteries in 5 patients; in 2 arteries in 6 patients, and in a single artery in 7 patients. In all 66 arteries with thrombus (24 patients) the thrombus was longer than 5 mm. The thrombus in the late cases was entirely nonocclusive (mural) in 51 (77%) of the 66 epicardial coronary arteries containing thrombus and entirely occlusive in 10 arteries (15%). It consisted exclusively of multiluminal channels in 6 arteries (9%) and combinations in 1 artery (2%). Acute myocardial infarcts were present in 3 patients, all of whom had occlusive thrombi. In all 10 arteries with occlusive thrombi, the thrombus was larger than the underlying plaque and no occlusive thrombi were located over ulcerated plaques. These observations demonstrate that thrombus is common in epicardial coronary arteries >2 months after cardiac transplantation.
Conclusions from this review, based primarily on study of 39 cardiac allografts in place for >2 months, but also on a study of 37 grafts in place for </=2 months, might include the following: (1) allograft vascular disease affects all layers of the epicardial coronary arteries and usually the intramural coronary arteries in the outer one-half of the left ventricular wall; (2) the resulting intimal lesion is relatively uniform, consisting mainly of cellular and acellular fibrous tissue; it is diffuse, affecting all segments of the major and minor epicardial coronary arteries; (3) the degree of resulting luminal narrowing is similar in most 5-mm coronary segments, making coronary angiography hazardous in reliably predicting accurately the degree of luminal narrowing; (4) the extensive adventitial fibrosis and the extensive fibrous tissue infiltration of the subepicardial tissues probably inhibit dilation and remodeling of the epicardial coronary arteries and indeed may constrict them; (5) luminal narrowing of the epicardial coronary arteries after transplantation may be the consequence of both intraluminal lesions and exterior compression from the surrounding fibrous tissue; (6) intraluminal and intralesion thrombus is commonly observed as are multiluminal channels in coronary plaques, suggesting that organization of thrombi plays some role in the progression of post-transplant epicardial coronary disease; (7) the coronary lesions developing after cardiac transplantation are morphologically quite different in composition than those occurring in natural (nontransplantation) atherosclerosis; and (8) inflammatory cellular infiltrates are often extensive in the subepicardial tissues and the infiltrates in this area may be extensive even when interstitial myocardial inflammatory infiltrates are minimal or absent.
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OBJECTIVE: To develop clinical, demographic, and pathological profiles of young competitive athletes who died suddenly. DESIGN: Systematic evaluation of clinical information and circumstances associated with sudden deaths; interviews with family members, witnesses, and coaches; and analyses of postmortem anatomic, microscopic, and toxicologic data. PARTICIPANTS AND SETTING: A total of 158 sudden deaths that occurred in trained athletes throughout the United States from 1985 through 1995 were analyzed. MAIN OUTCOME MEASURES--Characteristics and probable cause of death. RESULTS: Of 158 sudden deaths among athletes, 24 (15%) were explained by noncardiovascular causes. Among the 134 athletes who had cardiovascular causes of sudden death, the median age was 17 years (range, 12-40 years), 120 (90%) were male, 70 (52%) were white, and 59 (44%) were black. The most common competitive sports involved were basketball (47 cases) and football (45 cases), together accounting for 68% of sudden deaths. A total of 121 athletes (90%) collapsed during or immediately after a training session (78 cases) or a formal athletic contest (43 cases), with 80 deaths (63%) occurring between 3 PM and 9 PM. The most common structural cardiovascular diseases identified at autopsy as the primary cause of death were hypertrophic cardiomyopathy (48 athletes [36%]), which was disproportionately prevalent in black athletes compared with white athletes (48% vs 26% of deaths; P = .01), and malformations involving anomalous coronary artery origin (17 athletes [13%]). Of 115 athletes who had a standard preparticipation medical evaluation, only 4 (3%) were suspected of having cardiovascular disease, and the cardiovascular abnormality responsible for sudden death was correctly identified in only 1 athlete (0.9%). CONCLUSIONS: Sudden death in young competitive athletes usually is precipitated by physical activity and may be due to a heterogeneous spectrum of cardiovascular disease, most commonly hypertrophic cardiomyopathy. Preparticipation screening appeared to be of limited value in identification of underlying cardiovascular abnormalities.
In summary, 3 patients with HC and LV apical diverticula of various sizes are described. All 3 had morphologic evidence of severe midventricular obstruction, including 2 with documentation of greatly elevated LV systolic pressure and marked LV outflow pressure gradients.