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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 469 records · Page 26Linked to original sources

M-mode echocardiographic observations during and after healing of active bacterial endocarditis limited to the mitral valve.

Analysis of 99 M-mode echocardiograms recorded during and up to 144 months after healing of active bacterial endocarditis limited to the mitral valve in 27 patients disclosed the following: (1) Little to no change occurred in the echocardiographic size of the vegetations during the first 6 weeks after diagnosis and institution of appropriate antibiotic therapy unless a major systemic embolus occurred. (2) The echocardiographic size of the vegetations did not determine the amount of cardiac damage or dysfunction produced by the valvular infection. (3) The larger the vegetations by echocardiogram, the greater was the likelihood of a clinical event compatible with a systemic embolus. (4) The gravest prognostic sign yielded by the echocardiogram was evidence of rupture of chordae tendineae. (5) Although a useful adjunct to diagnosis before appropriate antibiotic therapy was instituted, once bacteriologic cure was achieved, the echocardiogram was of limited value in delineating an active from a heated vegetation. (6) The echocardiographic appearance of the vegetations was not determined by the type of infecting bacterium.

Acute Disease↗

Quantification of amounts of coronary arterial narrowing in patients with types II and IV hyperlipoproteinemia and in those with known normal lipoprotein patterns.

The amount of cross-sectional area narrowing by atherosclerotic plaques in each 5 mm long sement of the left main, left anterior descending, left circumflex, and right coronary arteries was analyzed at necropsy in 15 patients with type II hyperlipoproteinemia (HLP), in 13 with type IV HLP, and in 10 with known normal lipoprotein patterns. All 38 study patients had clinical evidence of coronary heart disease. Of the 2593 five mm segments examined histologically, narrowing of 76% to 100% in cross-sectional area by aterosclerotic plaques was as follows: type II = 39%, type IV = 67%, and normal lipoprotein pattern = 35% (controls = 4%). Utilizing a scoring system of 1 to 4 for the four categories of narrowing (0% to 25%, 26% to 50%, 51% to 75%, 76% to 100%), the mean score per 5 mm segment for the patients with type IV HLP was significantly higher (3.5) than that for the patients with type II HLP (3.0), normal lipoprotein patterns (3.0), and the controls (2.3). Thus, our patients with type II HLP and those with normal lipoprotein patterns had similar amounts of severe coronary narrowing and significantly less severe coronary narrowing than the patients with type IV HLP.

Adult↗

M-mode echocardiographic observations in active bacterial endocarditis limited to the aortic valve.

Analysis of 37 M-mode echocardiograms recorded during the period of active bacterial endocarditis (ABE) involving the aortic valve (AV) in 17 patients disclosed one or more echocardiographic abnormalities involving the aortic valve cusps or their immediate vicinity in 15 (88%), including "shaggy" echoes indicative of vegetations in 12 (71%). Of the 12 patients with echocardiographic evidence of AV vegetation, 11 developed overt congestive heart failure (CHF) and either died or had AV replacement, and seven had clinical events compatible with systemic emboli; of the five patients without echo-demonstrated vegetations, only one had CHF, none had AV replacement, two died, and one had a systemic embolus. In comparison to our previously reported echocardiographic observations in patients with ABE involving either the mitral (29 patients) or tricuspid valve (23 patients), infection involving the AV was far more liable to produce overt CHF and systemic emboli, to necessitate valve replacement, and to cause death during the period of active infection.

Adult↗

Ebstein's anomaly of the tricuspid valve and prolapse of the mitral valve.

The hearts from 10 necropsy patients with Ebstein's anomaly of the tricuspid valve were examined for abnormalities of the mitral valve. Five patients were under 1 year of age and none had an abnormal mitral valve. The other five patients were ages 18 to 72 years (mean 36 years); all had focal fibrous thickening of the mitral leaflets and three had prolapse of one or both mitral leaflets. Only one of the three patients with mitral valve prolapse had an atrial septal defect (secundum type), indicating that the association of mitral valve prolapse with Ebstein's anomaly is not due to the presence of an atrial septal defect.

Adolescent↗

Occurrence and significance of endothelial cells in implanted porcine bioprosthetic valves.

Histologic and scanning and transmission electron microscopic studies were made to determine the frequency of occurrence of endothelial cells in 49 porcine valve bioprostheses removed from 43 patients 2 days to 113 months (average 35 months) after implantation. Endothelial cells were found in none of 17 bioprostheses in place for less than 1 year, in 5 (23 percent) of 22 in place for 1 to 5 years and in 7 (70 percent) of 10 in place for longer than 5 years. The 12 bioprostheses in which endothelial cells were present had been implanted in the atrioventricular position (7 of 32 in the mitral position and 5 of 6 in the tricuspid position) for 21 to 113 months (average 71). Endothelial cells were not found in any of 11 bioprostheses implanted in the semilunar position (9 in the aortic position and 2 in pulmonary conduits); however, all but one of these bioprostheses had been in place for less than 5 years. Endothelial cells were concentrated along the basal regions of the cusps. These cells did not grow in direct contact with valve collagen, but were attached to fibrin, thrombi or fibroelastic host tissue (fibrous sheath) on the valve surfaces. The growth of endothelial cells and associated fibrous tissue may serve to increase the structural stability of bioprosthetic valve cusps, which may be of functional importance several years after implantation when the porcine connective tissue may have undergone significant deterioration.

Adult↗

Structure and classification of cuspal tears and perforations in porcine bioprosthetic cardiac valves implanted in patients.

Morphologic studies were made of cuspal tears and perforations in 16 porcine valve bioprostheses that had been implanted in 14 patients (9 male and 5 female) ranging in age from 2 to 65 years. Eleven bioprostheses had been in the mitral position for 30 to 123 months, four in the aortic position for 15 to 40 months and one in a varied pulmonary conduit for 96 months. The cuspal lesions were classified into four types. Type I lesions, which involved the free edges of the cusps, were the most common of all lesions and occurred with equal frequency in mitral and aortic bioprostheses. Regardless of position of implantation, type I lesions were more frequent in the right coronary cusp than in the other cusps. Ultrastructural study showed that these lesions develop as consequences of breakdown of collagen at the free edges of the cusps, usually near the commissures. Type II lesions consisted of linear perforations that extended along the basal regions of the cusps, forming an arc parallel to the sewing ring. These lesions were uncommon an resulted from separation of bundles of collagen. Type III lesions, which were large, round or oval perforations that occupied central regions of the cusps, were more common in aortic than in mitral bioprostheses. They were characterized by marked destruction of cuspal tissue and were most frequently associated with infection. Type IV lesions were small pinhole-like perforations; they usually were multiple, localized in central regions of the cusps and associated with calcific deposits. Type IV lesions were more common in mitral than in aortic bioprostheses. Regardless of position, they were more frequent in the left and noncoronary cusps than in the right coronary cusp (which may be protected by its muscle shelf against this type of perforation). It is concluded that cuspal tears and perforations develop in implanted bioprostheses as consequences of structural failure of connective tissue components.

Adolescent↗

Congenitally bicuspid aortic valve causing severe, pure aortic regurgitation without superimposed infective endocarditis. Analysis of 13 patients requiring aortic valve replacement.

Although stenosis and infective endocarditis are commonly appreciated complications of the congenitally bicuspid aortic valve, pure severe aortic regurgitation complicating this congenital malformation, unassociated with either stenosis or infection, is not well recognized. Among 189 patients who had aortic valve replacement at the National Heart, Lung, and Blood Institute because of isolated pure aortic regurgitation, the congenitally bicuspid aortic valve, never the site of infective endocarditis, was responsible for the aortic regurgitation in 13 (7 percent). This report describes certain clinical and morphologic findings in 13 men, aged 26 to 65 years (mean 43), who required aortic valve replacement because of severe aortic regurgitation secondary to a noninfected, nonstenotic congenitally bicuspid aortic valve. Although not generally recognized, the noninfected congenitally bicuspid aortic valve is an important cause of pure aortic regurgitation severe enough to warrant aortic valve replacement.

Adult↗

Lack of effect of aspirin on myocardial infarct size in the dog.

Pretreatment with platelet-inhibitory doses of aspirin (3 mg/kg body weight) has been shown to augment epicardial collateral flow by more than 50 percent (p less than 0.05) 4 hours after ligation of the left anterior descending coronary artery in dogs. To determine whether this favorable influence of aspirin is sufficient to decrease the amount of infarcted tissue, either intravenous aspirin, 3 mg/kg (n = 17), or saline solution (n = 17) was administered to dogs 10 minutes before occlusion of the left anterior descending coronary artery. Administration of saline solution or aspirin was repeated every 24 hours. By 72 hours, 5 dogs in each treatment group had died. Survivors were killed at 72 hours. The portion of the left ventricle at risk of infarction was delineated by perfusion of the aortic root with Evans blue and simultaneous perfusion of the distal left anterior descending coronary artery with saline solution under equal physiologic pressures. Slices of the stained heart were incubated with triphenyltetrazolium to identify gross infarct (with histologic confirmation). Total mass of left ventricle, myocardium at risk, and infarct size were measured in each dog. A direct relation was found between the mass at risk and the mass infarcted (r = 0.84, p less than 0.001). Aspirin-treated dogs did not differ from control dogs in percent ventricle at risk (mean +/- standard error 37 +/- 2 versus 40 +/- 2), percent infarct weight/left ventricle (29 +/- 3 versus 31 +/- 2) or percent infarct weight/weight of ventricle at risk (78 +/- 4 versus 77 +/- 3). Thus, despite aspirin's ability to inhibit platelet aggregation and to increase epicardial collateral flow by more than 50 percent, aspirin treatment failed to reduce infarct size in this dog model.

Animals↗