Healed left-sided infective endocarditis: a clinicopathologic study of 59 patients.
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Biomedical subjects
Publications and source records attributed to W C Roberts.
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Echocardiographic observations are described in 25 opiate addicts with active infective endocarditis involving apparently previously normal valves. Infective endocarditis was isolated to the tricuspid valve in 11 patients, involved both right- (tricuspid valve) and left-sided valves in 7 and was isolated to the left-sided valves in 7 (mitral valve in 6). Twenty patients (80%) had tricuspid valve regurgitation, 12 had mitral regurgitation, 3 had aortic regurgitation and none had pulmonary valve regurgitation. Considering the 75 cardiac valves (excluding the pulmonary) in the 25 patients, echocardiographic abnormalities consistent with active infective endocarditis were detected in 26 (74%) of the 35 clinically incompetent valves but in none of the 40 competent valves. Comparison of the 20 incompetent tricuspid valves with the 12 incompetent mitral valves indicated that (1) the echocardiogram was less sensitive in detecting tricuspid valve lesions, (2) rupture of tricuspid valve chordae tendineae was absent or not detectable, and (3) tricuspid valve vegetations tended to be larger.
Gross and histologic changes are described in 51 Hancock glutaraldehyde-preserved porcine heterograft bioprostheses from 41 patients: 33 valves from 25 patients had been in place for less than 2 months ("early") and 18 valves from 17 patients were examined at later periods up to 75 months ("late") after implantation. The major gross changes were thrombosis (five bioprostheses) and degeneration (three bioprotheses) of the cusps. Major histologic changes observed in 44 bioprostheses (26 early and 18 late) examined histologically were: (1) fibrin deposits on inflow and outflow surfaces of the cusps; (2) inflammatory cell infiltrates; (3) histiocyte deposition; (4) giant cell formation, and (5) focal disruption of the fibrocollagenous structure of the cusps. These observations indicate that porcine bioprostheses are not biologically inert in the human circulation. However, valve failure is rare at the implantation periods studied.
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Clinical and morphologic observations are described in a 46 year old woman with fatal trichinosis. Attention is called to the occurrence of extensive ventricular endocardial damage with superimposed thrombosis; Evidence is presented to indicate that the most likely cause of the endocardial damage is the associated eosinophilia. The mechanism by which eosinophils damage endocardium, however, remains obscure.
Massive medial calcific deposits (Mönckeberg's calcinosis) are described in the peripheral and visceral arteries, and similar but small-sized deposits in the coronary arteries of a 41 year old woman with diabetes mellitus. Although observed by roentgenogram fairly commonly during life in the muscular arteries of the legs in middle-aged men, medial calcinosis infrequently involves the visceral arteries and has never, to our knowledge, been documented in the coronary arteries. Although it may be associated with intimal atherosclerosis, medial calcinosis, per se, does not obstruct the lumens of the arteries and, therefore, does not lead to symptoms or signs of limb or organ ischemia. The cause of medial calcinosis remains a mystery, but it appears to affect people with diabetes more frequently than those without.
Clinical and morphologic features are described in two relatively young adults with aortic regurgitation secondary to chronic aortitis. The regurgitation in each was severe enough to require aortic valve replacement. Both patients had normochromic, normocytic anemia, considerable weight loss despite congestive cardiac failure, and negative serologic tests for syphilis. These systemic manifestations in association with the aortitis suggest that both had Takayasu's arteritis. In addition, one patient had total occlusion at the origin of one subclavian artery (classic pulseless disease). Takayasu's arteritis must be added to the list of causes of severe aortic regurgitation.
Clinical and morphologic observations are described in two patients with severe pulmonary arterial hypertension without pulmonary venous hypertension from fibrosing mediastinitis. In one patient, both main pulmonary arteries and one major pulmonary vein were severely narrowed by dense fibrous tissue; in the second patient, only the right main pulmonary artery was severely narrowed. Both patients had normal intrapulmonary arteries and normal pulmonary parenchyma. Of nine previously described necropsy patients with pulmonary hypertension due to fibrosing mediastinitis, seven had severe narrowing of multiple large pulmonary veins and in six of them the pulmonary hypertension was entirely due to pulmonary venous obstruction. In one other patient, the pulmonary hypertension was due to obstruction of one main pulmonary artery and several large pulmonary veins. Each of these seven previously described patients had severe changes in the small intrapulmonary arteries. Of the other two previously described patients with pulmonary hypertension from fibrosing mediastinitis, one had severe narrowing of only the main right pulmonary artery, and the other, of both main pulmonary arteries. Thus, although pulmonary arterial hypertension in patients with fibrosing mediastinitis is usually due to obstruction of multiple large pulmonary veins and to severe secondary changes in small intrapulmonary arteries, fibrosing mediastinitis can cause severe pulmonary hypertension by obstructing the right or both main pulmonary arteries.
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Clinical and morphologic observations are described in two women with primary sarcoma of the pulmonary trunk, and observations in 35 previously described patients with primary sarcoma involving a major extrapulmonary pulmonary artery are summarized. The neoplasm produces symptoms by causing obstruction to right ventricular outflow or by dislodging tumor fragments to the smaller intrapulmonary pulmonary arteries with or without pulmonary infarction. The sarcoma nearly always arises from the pulmonary trunk to which it is firmly attached. Although it grows to a large size within the lumen, it infrequently, despite its highly malignant histologic pattern, extends through the wall of the pulmonary trunk or metastasizes outside the pulmonary circulation. It may mimic a variety of more common disorders. Diagnosis can be achieved by angiography and treatment starts with total excision.
This report reviews morphologic aspects of pericardial heart disease. A morphologic classification for this condition is presented. An ideal classification of pericardial heart disease obviously would take into account clinical, etiologic and morphologic features of this condition but a single classification combining these 3 components is lacking. Pericardial heart disease is relatively uncommon clinically and when present at necropsy it usually had not been recognized during life. The term "pericarditis" is inaccurate because most pericardial diseases are noninflammatory in nature. Morphologically chronic pericardial heart disease may present clinically as an acut eillness. Even when clinical symptoms are present, however, fewpatients develop evidence of cardiac dysfunction (constriction). When pericardial "constriction" occurs, it is the result of increased pericardial fluid or increased pericardial tissue or both. Increased fluid is treated by drainage; increased tissue is treated by excision. In most patients with chronic constrictive "pericarditis," the etiology is not apparent even after histologic examination of pericardia.
This report describes morphologic changes in saphenous veins used as aortocoronary bypass conduits, and discusses the relative contribution of various factors to these changes. The three primary changes are: (1) medial fibrous replacement, (2) adventitial fibrous proliferation, and (3) intimal fibrous proliferation. Medial fibrous replacement is caused by vein wall ischemia with loss of smooth muscle cells; adventitial fibrous proliferation is the result of organization of fibrin deposits and repair of ischemic injury; and intimal fibrous proliferation results from some stimulus, probably fibrin deposition on injured intima, which causes stimulation of smooth muscle cells to become fibroblasts or "myointimal cells". Although all grafts show some changes, the degree and severity of these three changes is variable along the length of the grafts and among separate grafts in the same patient.
Clinical and morphologic features are described in a 13 week old male infant with ventricular inversion without associated transposition of the great arteries but with concomitant atresia of the left-sided (tricuspid) atrioventricular valve. Isolated ventricular inversion without situs inversus or visceral heterotaxy has previously been reported in English in only three patients, none with tricuspid atresia.
In several patients with asymmetric septal hypertrophy (ASH) diagnosed by echocardiography (septal-free wall thickness ratios greater than or equal to 1.3), we have discovered marked discrepancies between the echocardiographic and necropsy measurements of wall thicknesses that led to uncertainty regarding the actual cardiac diagnosis. To resolve these apparent incongruities, the echocardiograms and hearts of 17 patients with cardiac disease were studied. Six of nine patients with abnormal septal-free wall ratios greater than or equal to 1.3 during life had septal-free wall ratios that were not diagnostic of disproportionate septal thickening at necropsy. Such discrepancies may be explained as follows: 1) echocardiographic measurements during life were made in diastole (as per convention), but measurements at necropsy were made in hearts that appeared to have been in the systolic phase of the cardiac cycle; 2) the left ventricular free wall thickens considerably more than the ventricular septum in systole, as determined by echocardiography. This latter phenomenon resulted in septal-free wall ratios in systole that were consistently smaller than those in diastole. Furthermore, septal-free wall ratios obtained at necropsy corresponded most closely to those obtained by echocardiography in systole.
Among 481 patients undergoing various mitral valve operations, Aschoff bodies were found in 40 (21%) of 191 operatively excised left atrial appendages, in four (2%) of 273 operatively excised left ventricular papillary muscles (1 per patient), and in one (6%) of 17 patients with both left atrial appendage and papillary muscle operatively excised. Of the total of 45 patients with Aschoff bodies, 44 preoperatively had mitral stenosis, and only one, a 10-year-old boy, had pure mitral regurgitation. Sinus rhythm was present in 38 (84%), and atrial fibrillation in seven (16%). Perioperatively, only one of the 45 patients with Aschoff bodies had clinical or laboratory stigmata compatible with acute rhematic fever, and 58% had an illness compatible with acute rheumatic fever at any time.
The status of the native coronary arteries at necropsy in the vicinity of the coronary anastomoses of saphenous vein aortocoronary bypass grafts in 20 patients with severe coronary heart disease is presented. Of the 37 graft systems (graft plus coronary artery into which graft inserted) analyzed, the lumina of 44% of the native coronary arteries within the first 2 cm distal to the anastomoses were greater than 75% narrowed in cross-sectional area by atherosclerotic plaques, and the native coronary artery at the site of the anastomosis was greater than 50% narrowed in cross-sectional area already by atheroclerotic plaque in 25% of the graft systems. The mean coronary arterial size distal to the site of the coronary graft anastomosis, even after correction for heart weight, was greater in the 13 men than in the seven women. The residual luminal areas squared per gram of heart weight, however, were similar in both men and women. These results suggest that 1) relative coronary vessel size is greater in men than women; 2) the luminal area squared per gram myocardial mass (a relative estimation of flow) is the same in the two groups of patients; and 3) less atherosclerotic plaque is necessary in women then in men to produce similar limitation to coronary flow. Thus, vessel size alone cannot account for the higher reported frequency of unsuccessful aortocoronary bypass procedures in women.
To evaluate cellular and protein components in the lower respiratory tract of patients with idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis (CHP), limited broncho-alveolar lavage was done in 58 patients (19 IPF, 7 CHP, and 32 controls). Analysis of the cells and protein in the lavage fluids from patients with IPF revealed an inflammatory and eosinophilic response and a significant elevation of IgG in the lungs. With corticosteroid therapy, inflammation diminished but eosinophils remained. Lavage fluid from patients with CHP also had eosinophils and elevated levels of IgG. However, in contrast to IPF, lavage fluid from CHP patients contained IgM, fewer inflammatory cells, and a strikingly increased number (38-74%) of lymphocytes. Identification of lavage lymphocytes in CHP showed that T lymphocytes were significantly elevated and B lymphocytes were decreased compared to peripheral blood. These studies suggest nthat the lung in IPF and CHP may function as a relatively independent immune organ, and that analysis of cells and proteins in broncho-alveolar lavage fluid may be of diagnostic, therapeutic, and investigative value in evaluating patients with fibrotic lung disease.
18 patients with idiopathic pulmonary fibrosis were studied to determine if they had morphologic evidence of small airways disease and if physiologic testing could predict morphologic findings. In the presence of normal airway function by standard physiologic studies (forced expiratory volume in 1 s/forced vital capacity and airway resistance by plethysmography), dynamic compliance, maximum expiratory flow-volume curves, and maximum flowstatic recoil curves were measured to detect physiologic alterations consistent with small airways abnormalities. These physiologic data were then compared with estimates of small airways diameter made in lung biopsy specimens.94% (17 of 18) of the patients had peribronchiolar fibrosis or peribronchiolar inflammation or bronchiolitis. 67% (12 of 18) had an overall estimate of small airways diameter of "narrowed," whereas 33% (6 of 18) had airways that overall were "not narrowed." 59% (10 of 17) had frequency-dependent dynamic compliance, 50% (9 of 18) had abnormal maximum expiratory flow-volume curves, and 39% (7 of 18) had abnormal maximum flow-static recoil curves. Comparisons between morphologic and physiologic data revealed a significant correlation between the results of dynamic compliance and the overall estimate of small airways diameter (P = 0.001), and the results of maximum flow-volume curves and the overall estimate of small airways diameter (P = 0.009); there was no significant correlation between the results of maximum flow-static recoil curves and the overall estimate of small airways diameter (P = 0.1). THE RESULTS OF THIS STUDY SUGGEST THAT: (a) idiopathic pulmonary fibrosis is a disease of small airways as well as alveoli; (b) dynamic compliance and the maximum expiratory flow-volume curve can predict the overall status of small airways diameter in idiopathic pulmonary fibrosis; and (c) whereas the maximum flowstatic recoil curve predicts the overall estimate of small airways diameter in most patients with this disease, it is the least sensitive of these three monitors of small airways.