Fatal cor pulmonale caused by extensive tumor emboli in the small pulmonary arteries without emboli in the major pulmonary arteries or metastases in the pulmonary parenchyma.
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Biomedical subjects
Publications and source records attributed to W C Roberts.
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Although a number of clinicopathologic studies in patients with active infective endocarditis (IE) have been reported, none have focused on patients studied at necropsy with active IE isolated to the mitral valve. We studied at necropsy 63 patients (aged 12 to 88 years [mean 50], 44 males [70%]) with active IE limited to the native mitral valve: 21 (33%) had preexisting mitral valve disease (rheumatic in 8, prolapse in 3, hypertrophic cardiomyopathy in 1, and mitral annular calcium in 9), and the other 42 patients (67%) had previously normal mitral valves. Of the latter 42 patients, 22 (52%) had recognized predisposing factors to IE: opiate addiction in 14, habitual alcoholism in 6 and/or chronic hemodialysis in 4. Staphylococcus aureus or epidermidis was the responsible organism in 32 patients (51%), and the active IE was associated with an infection elsewhere in the body in 31 patients (50%). The active IE caused rupture of mitral chordae tendineae in 11 patients (18%), perforation of the anterior mitral leaflet in 7 patients (11%), and mitral ring abscess in 10 patients (16%). Grossly visible systemic emboli were found in 44 patients (70%) and 33 (52%) had infarcts in 1 or more body organs. Thus, active IE isolated to the mitral valve in necropsied patients appears to be more common in males than females (2 to 1); the infection more commonly than not involves a preexisting anatomically normal valve rather than a preexisting abnormal one (2 to 1); the vegetations often do not cause or worsen valvular dysfunction; a predisposing factor is commonly present (2 of 3 patients), and the IE commonly is part of a generalized or systemic infection (1 of 2 patients).
No previous studies, either clinical or morphologic, have compared findings in patients with active infective endocarditis (IE) involving a previously stenotic versus a previously nonstenotic aortic valve. Clinical and cardiac necropsy findings were analyzed in 96 patients with active IE involving the aortic valve. Of the 96 patients, 25 (26%) had active IE superimposed on a previously stenotic aortic valve and 71 (74%) on a previously nonstenotic aortic valve. The patients with stenotic aortic valves compared with those with nonstenotic aortic valves had significantly higher mean ages (61 vs 47 years), a higher percentage > 60 years of age (52 vs 24%), a higher percentage of men (92 vs 73%), a higher frequency of an absent or unknown predisposing factor to infection (68 vs 38%), a lower frequency of a precordial murmur of aortic regurgitation (44 vs 79%), a lower percent with a long duration (> 60 days) of signs and symptoms of active IE (4 vs 23%), a larger mean heart weight (594 vs 514 g), a higher percentage with aortic valve calcific deposits (100 vs 24%), and a higher frequency of associated ring abscess (84 vs 52%). Thus, active IE superimposed on a stenotic aortic valve differs in some features compared with active IE on a nonstenotic aortic valve. Because ring abscess is so common when active IE involves a stenotic aortic valve in adults, operative intervention at an early stage may be warranted.
The mechanism by which obstruction to right ventricular (RV) outflow occurs in patients with hypertrophic cardiomyopathy (HC) is not well understood. To clarify this issue, 5 severely symptomatic patients (aged 18 to 55 years, mean 30) with HC and marked subpulmonic obstruction (basal peak systolic pressure gradients 60 to 118 mm Hg) were studied. Four patients also had obstruction to left ventricular outflow (maximal basal or provocable pressure gradient 12 to 110 mm Hg). The RV outflow obstruction in each patient resulted from greatly hypertrophied musculature comprised of crista supraventricularis, moderator band or trabeculae. Operative resection of portions of this muscle resulted in abolition or substantial reduction of the RV outflow gradient (to 0 to 11 mm Hg) in the 3 patients with both pre- and postoperative hemodynamic studies. The left ventricular wall and ventricular septum also were massively thickened (32 to 40 mm) in each patient. These findings support the view that marked RV outflow tract obstruction in patients with HC is due to greatly hypertrophied RV muscle, and that operative resection will relieve the outflow gradients and normalize RV systolic pressure. The muscular RV hypertrophy causing obstruction appeared to constitute a primary and excessive hypertrophic process involving both ventricles.
To assess the effect of left ventricular dilatation on mitral valve size, this study compared the dimensions of the mitral valve in patients with aortic valve disease and hypertrophic cardiomyopathy (HC). A total of 216 valves, removed at operation or necropsy, was analyzed by quantitative morphometric methods from: (1) 2 patient groups with dilated left ventricular cavities (i.e., 17 patients with dilated valvular aortic stenosis [AS] and 31 with pure aortic regurgitation), (2) 2 patient groups without dilated left ventricular cavities (i.e., 29 patients with nondilated AS and 94 with HC), and (3) 45 control subjects without heart disease. Mean mitral leaflet areas in patients with AS with dilated left ventricular cavities (13.1 +/- 3.0 cm2) and aortic regurgitation (12.0 +/- 3.6 cm2) were significantly greater than in control subjects (8.7 +/- 2.0 cm2; p < 0.001). Mean mitral leaflet areas in patients with AS without dilated left ventricular cavities (9.8 +/- 2.0 cm2) were similar to those of normal valves (p = NS). However, mean mitral leaflet area in patients with HC, in whom left ventricular cavities were also nondilated, was significantly greater (12.8 +/- 3.7 cm2) than in those with nondilated AS and in normal subjects (p < 0.001). Therefore, increased mitral leaflet area: (1) is often present in patients with aortic valve disease with dilated left ventricles in whom it appears to be secondary to left ventricular chamber dilatation; and (2) cannot be attributed to left ventricular cavity dilatation in patients with HC, since their cavities were of normal or small size.(ABSTRACT TRUNCATED AT 250 WORDS)
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OBJECTIVES: The aim of this study was to analyze the relation between anomalies of the heart and aortic arch arteries in near-term rat fetuses exposed to the chemical bis-diamine. BACKGROUND: Bis-diamine is known to induce cardiovascular anomalies. METHODS: Bis-diamine was given orally to normal pregnant rats, and the 65 fetuses were examined under a dissecting microscope after formalin fixation. RESULTS: There were 26 rat fetuses (40%) with a ventricular septal defect in the perimembranous portion, of which 14 (22%) had tetralogy of Fallot, 4 (6%) had truncus arteriosus and 8 (12%) had a relatively small defect with no other major anomalies. In 44 fetuses (68%) the middle latitudinal muscle bundle of the ventricular septum was continuous with the right ventricular free wall. There were, isolated or in association, a double- or right aortic arch in 6 fetuses (9%), aberrant subclavian arteries in 9 (14%), right ductus arteriosus in 12 (18%) and agenetic ductus in 4 (6%). The cross-sectional area of the ductus, as corrected by that of the aortic isthmus, was abnormally small in 47 rats (72%). The rat fetuses with a septal defect or abnormal myocardial architecture, or both, usually had a small ductus; it was very small or absent in those fetuses with tetralogy of Fallot. Of the four fetuses with truncus arteriosus, two had a vestigial vasculature on the truncus root and three had a rudimentary infundibulum. CONCLUSIONS: The cardinal defect may be the anomalous and reduced development of the sixth arch arteries, which by imposing pressure overload on the fetal right ventricle, may have led to either or both the persistence of ventricular septal defect as a vent or the formation of myocardial architecture favorable for the generation of pressure in the right ventricle.
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Very little is known about the structural composition of the restenotic plaque in evolution. The responses of atherosclerotic femoral arteries of rabbits to balloon angioplasty (BA), thallium/holmium/chromium: YAG infrared laser angioplasty (LA), combined LA and BA, or no angioplasty were compared by blinded quantitative histomorphometry and angiography. The endothelium was injured by nitrogen/air desiccation, and the animals were fed a 2% cholesterol diet for 1 month prior to the angioplasty procedure. Animals were sacrificed 2 hr or 28 days after angioplasty by pressure perfusion with 10% formaldehyde (100 mm Hg), and arterial segments (4-5 cm) were excised bilaterally. The frequency of thrombus was greatest in arteries with LA. Arteries with combined LA and BA had the greatest initial gain in luminal diameter by angiography, but they also had the greatest reduction in luminal diameter from 2 hr to 28 days and the greatest cross-sectional area narrowing by plaque at 28 days. The principal component of the intimal plaques in all groups was fibrous tissue (approximately 90%), with the remainder consisting primarily of "foam cells." By multiple regression analysis, the strongest predictors of cross-sectional area narrowing were contiguity of foam cells between the intima and media, depth of the tear, percentage of foam cells in the plaque, and the intervention of LA followed by BA. The principal predictors of foam cells in the plaque, irrespective of treatment, were also cross-sectional area narrowing, contiguity of foam cells between plaque and media, and the depth of tear. It is suggested that a large proportion of the foam cells of the intima may be derived from foam cells of the media and adventitia rather than from the lumen. These observations may be of particular importance regarding angioplasty in young people where foam cells occupy a significantly greater proportion of the atherosclerotic plaque.
Subepicardial myocardial lesions are rarely seen at necropsy, and a description of them and their causes has not been reported. Over the last 13 years we have studied 22 patients with subepicardial myocardial lesions. They ranged in age from 14 to 73 years (mean 47), and 20 were men. The lesions were associated with atherosclerotic coronary artery disease in six patients, sarcoidosis in five, idiopathic dilated cardiomyopathy in four, lymphocytic myocarditis in two, and hypoplastic right and left circumflex coronary arteries in one. In four patients the cause was unclear. In the patients with atherosclerotic coronary artery disease, the subepicardial myocardial lesions were small, few in number, and located in the left ventricular posterior wall. In patients with sarcoidosis or myocarditis, the subepicardial lesions were extensive and commonly associated with transmural left and right ventricular lesions. The right ventricular half of the ventricular septum also was frequently affected. In the remaining nine patients, the subepicardial lesions were small and unassociated with transmural left ventricular lesions. Thus subepicardial myocardial lesions occur in a variety of cardiac diseases.
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To assess the effects of reperfusion therapy on acute right ventricular myocardial infarction, we studied at necropsy the hearts from 51 patients who died after receiving intravenous recombinant tissue plasminogen activator for acute left ventricular myocardial infarction as part of the Thrombolysis in Myocardial Infarction (TIMI) study. Right ventricular infarction occurred in none of 29 patients with infarction of the anterior wall of the left ventricle and in 8 of 22 patients (36%) with infarction of the posterior (inferior) wall of the left ventricle. Of the 22 patients with posterior wall infarction, the 8 patients with right ventricular infarction were compared to the 14 patients without right ventricular infarction. The patients with right ventricular infarction had a longer mean interval from tissue plasminogen activator infusion to peak creatine phosphokinase level (19 vs. 11 h, P < 0.03), a lower frequency of hemorrhagic necrosis (2 of 8 vs. 10 of 14, P < 0.04) and higher frequency of luminal thrombus in the infarct-related coronary artery (6 of 8 vs. 3 of 14, P = 0.054). Each of these findings is associated with the absence of coronary reperfusion. Thus, successful reperfusion following acute left ventricular myocardial infarction appears to be associated with a decreased frequency of concomitant right ventricular myocardial infarction.