Search PubMed⌕ Search

Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 145 records · Page 8Linked to original sources

Severe mitral or aortic valve regurgitation, or both, requiring valve replacement for infective endocarditis complicating hypertrophic cardiomyopathy.

Certain clinical and morphologic findings are described in 11 patients with hypertrophic cardiomyopathy complicated by infective endocarditis that produced severe mitral or aortic valve regurgitation, or both, necessitating valve replacement. All 11 patients had changes in the operatively excised valve or valves characteristic of healed infective endocarditis. The infection involved only the mitral valve in seven patients, only the aortic valve in three patients and both valves in one patient. Study of the operatively excised mitral valves indicated that the healed vegetations were located most commonly on the left ventricular aspects of the anterior mitral leaflet, indicating that vegetation had formed at contact points of this leaflet with mural endocardium of the left ventricular outflow tract. In all 11 patients, the infective endocarditis either worsened preexisting valve regurgitation or initiated valve regurgitation and led to worsened signs and symptoms of cardiac dysfunction, necessitating valve replacement. Functional class improved in the nine patients who survived 7 to 101 months after valve replacement. Hypertrophic cardiomyopathy appears to be a factor predisposing to infective endocarditis. Patients with hypertrophic cardiomyopathy should receive prophylactic antibiotic therapy during procedures that predispose to infective endocarditis.

Adult↗

The heart in Tangier disease. Severe coronary atherosclerosis with near absence of high-density lipoprotein cholesterol.

Cardiac necropsy findings are described in a 72-year-old man with Tangier disease whose plasma total cholesterol levels averaged 70 mg/dL, low-density lipoprotein cholesterol level was 45 mg/dL, and high-density lipoprotein cholesterol level was 1.4 mg/dL, and who had coronary artery bypass grafting for severe atherosclerotic coronary artery disease. At necropsy, 24 of the 72 (33%) 5-mm segments of the 4 major (right, left main, left anterior descending, and left circumflex) native coronary arteries and 4 of the 27 (15%) 5-mm segments of the saphenous vein aortocoronary bypass conduits were narrowed by more than 75% in cross-sectional area by atherosclerotic plaques. The plaques were composed primarily (91% to 97%) of fibrous tissue. Oil red O staining, polarized light microscopy, and electron microscopy revealed cholesterol deposits in the plaques and in the walls of coronary arteries, saphenous vein grafts, and aorta. Such deposits also were found in foam cells of histiocytic origin, fibroblasts in all four cardiac valves, and in Schwann cells of cardiac nerves.

Aged↗

Diversity of structural mitral valve alterations in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by an asymmetrically hypertrophied left ventricle and is regarded as a disease of cardiac muscle. METHODS AND RESULTS: To assess the possibility that the mitral valve itself may be involved in the disease process, we studied mitral valves from 94 patients with HCM and 45 normal control subjects. The area of the mitral leaflets was increased in patients with HCM compared with control subjects (12.9 +/- 3.7 versus 8.7 +/- 2.0 cm2; p less than 0.001). For the overall group of patients, this increase was largely caused by an increase in anterior leaflet length (2.2 +/- 0.5 cm for HCM versus 1.8 +/- 0.3 cm for control subjects; p less than 0.001), because circumference did not differ between the two groups. Mitral leaflet area was increased (greater than or equal to 12.0 cm2) in 55 (58%) of the 94 valves. In 12 of these 55 valves, both the anterior and posterior leaflets were enlarged; the other 43 valves had asymmetrical or segmental enlargement of either the anterior leaflet (36 patients) or a portion of posterior leaflet (seven patients). In addition, nine patients had a congenital malformation of the mitral apparatus in which one or both papillary muscles inserted directly into anterior mitral leaflet (mitral valve area was normal in seven of the nine). CONCLUSIONS: Sixty-two (66%) of 94 mitral valves had a constellation of structural malformations, including increased leaflet area and elongation of the leaflets or anomalous papillary muscle insertion directly into anterior mitral leaflet. These findings expand the morphological definition of HCM by demonstrating that the disease process is not confined to cardiac muscle but rather many patients also have structural abnormalities of the mitral valve that are unlikely to be acquired or secondary to mechanical factors.

Adult↗

Effect of chronic subcutaneous or intramural administration of heparin on femoral artery restenosis after balloon angioplasty in hypercholesterolemic rabbits. A quantitative angiographic and histopathological study.

BACKGROUND: Heparin is known to have antithrombotic, anticoagulant, and antiproliferative effects. We hypothesized that chronic subcutaneous and/or direct intramural administration of heparin would reduce restenosis and inhibit plaque growth after balloon angioplasty. METHODS AND RESULTS: Focal atherosclerosis was induced bilaterally in the femoral arteries of 59 rabbits by air desiccation intimal injury and a 2% cholesterol diet. After angioplasty, the rabbits were assigned to one of four treatment groups. Control arteries (n = 21) received no additional heparin. A second group of 20 arteries was treated with a porous balloon that delivered heparin (1,500 units) directly into the arterial wall. A third group (n = 29) received subcutaneous heparin (350 units.kg-1.day-1) for 28 days, and a fourth group (n = 23) was treated with subcutaneous and intramural heparin. Quantitative angiography showed a modest reduction in restenosis (defined as the change in minimal luminal diameter from immediately after angioplasty to 28 days) with subcutaneous heparin compared with control arteries (0.32 +/- 0.18 versus 0.58 +/- 0.34 mm, p < 0.01); however, luminal diameter was not improved at 28 days compared with before angioplasty. Intramural delivery of heparin by the porous balloon catheter was confirmed by use of fluoresceinated heparin in one animal. Angiographic restenosis was not reduced in arteries treated with intramural heparin versus controls (0.61 +/- 0.54 versus 0.58 +/- 0.34 mm, p = NS). Blinded planimetric analysis of histological sections showed no differences in luminal cross-sectional area narrowing by atherosclerotic plaque, in plaque area, or in plaque/media ratio at 28 days among the four treatment groups. CONCLUSIONS: Chronic subcutaneous heparin after balloon angioplasty results in a modest reduction in angiographic restenosis in this model; however, the absolute luminal diameter is not improved compared with before angioplasty, and plaque area and percent luminal narrowing by plaque were not different among the four treatment groups. Heparin can be delivered into an atherosclerotic plaque by a porous balloon, but this treatment does not reduce restenosis after angioplasty in this model.

Angioplasty, Balloon↗

Clinical and anatomic observations in patients having mitral valve replacement for mitral stenosis and simultaneous tricuspid valve replacement.

Certain clinical and morphologic findings are described in 67 patients (aged 23 to 76 years [mean 52]; 55 women [82%]) who had mitral valve replacement for mitral stenosis (with or without associated regurgitation), and simultaneous tricuspid valve replacement for pure tricuspid regurgitation (58 patients) or tricuspid stenosis (all with associated regurgitation; 9 patients). Of the 58 patients with pure tricuspid regurgitation, 21 had anatomically normal and 37 had anatomically abnormal (diffusely fibrotic leaflets) tricuspid valves. Among these 58 patients, no clinical or hemodynamic variable was useful before surgery in distinguishing the group without from that with anatomically abnormal tricuspid valves. All 9 patients with stenotic tricuspid valves had anatomically abnormal tricuspid valves. The latter group had a lower average right ventricular systolic pressure (tricuspid valve closing pressure) than those with pure tricuspid regurgitation, and none had severe pulmonary arterial hypertension (present in 20 [30%] of the 58 patients with pure tricuspid regurgitation).

Adult↗

The heart in fatal unstable angina pectoris.

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.

Adult↗