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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 163 records · Page 9Linked to original sources
PubMed1991

Composition of atherosclerotic plaques in coronary arteries in women less than 40 years of age with fatal coronary artery disease and implications for plaque reversibility.

This study analyzes the composition of atherosclerotic plaques in the 4 major epicardial coronary arteries in 8 women less than 40 years of age (mean 34) with fatal coronary artery disease (CAD) and compares these data to previous studies of 37 adults greater than 45 years of age (mean 59) with fatal CAD. Histologic sections were taken at 5-mm intervals from the entire lengths of the right, left main, left anterior descending and left circumflex coronary arteries. With the use of a computerized morphometry system, analysis of the 4 major epicardial coronary arteries showed the major component of plaque to be a combination of cellular (mean percent total plaque area = 65%, standard error = 6%) and dense (19%, standard error = 6%) fibrous tissue. Arterial segments narrowed greater than 75% in cross-sectional area from these young women were compared with similarly narrowed arteries from 37 older patients (32 men [86%]) with fatal CAD previously reported by this laboratory, and showed significantly more cellular fibrous tissue and lipid-rich foam cells, and lesser amounts of dense fibrous and heavily calcified tissue. The large amount of lipid-containing foam cells and relative lack of acellular scar tissue in coronary plaques in these young women suggests a greater potential for reversibility of these plaques in this subset of patients with CAD.

Adult↗
PubMed1991

Composition of atherosclerotic plaques in the four major epicardial coronary arteries in patients greater than or equal to 90 years of age.

The composition of atherosclerotic plaques in 733 five-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries of 18 patients greater than or equal to 90 years of age was determined by computerized planimetric analysis. By analysis of all coronary segments of all patients greater than 90, the plaques consisted primarily of fibrous tissue (87 +/- 8%) with calcific deposits (7 +/- 6%), pultaceous debris (5 +/- 4%) and foam cells (1 +/- 1%) occupying a much smaller percentage of plaque area. Analysis of composition according to the 4 degrees of luminal cross-sectional area narrowing revealed marked step-wise increases in pultaceous debris (from 0 +/- 0% at 0 to 25% narrowing to 18 +/- 22% at 76 to 100% narrowing, p = 0.0001) and calcific deposits (from 0 +/- 0 to 10 +/- 15%, p = 0.002), and decreases in fibrous tissue (from 99 +/- 3 to 71 +/- 23%, p = 0.0001) and area occupied by the media (from 35 +/- 8 to 16 +/- 8%, p = 0.0001). When the analysis was restricted to sections narrowed greater than 75%, no significant differences were found in plaque components or medial area between patients with (11 patients) and without (7 patients) myocardial infarcts at necropsy.

Aged↗
PubMed1991

Morphologic comparison of patients with mitral valve prolapse who died suddenly with patients who died from severe valvular dysfunction or other conditions.

Clinical and necropsy findings are described in 56 patients with mitral valve prolapse: 15 patients, aged 16 to 69 years (mean 39), died suddenly and mitral valve prolapse was the only cardiac condition found at necropsy (hereafter called isolated mitral valve prolapse); the remaining 41 patients had other conditions that were capable of being fatal. Of the latter 41 patients, 7, aged 17 to 59 years (mean 45), had associated congenital heart disease, and 34 patients, aged 17 to 70 years (mean 52), had no associated congenital cardiac abnormalities. Compared with the 34 patients without associated congenital heart disease and with nonmitral valve prolapse conditions capable in themselves of being fatal, the 15 patients who died suddenly with isolated mitral valve prolapse were younger (mean age 39 +/- 17 versus 52 +/- 15 years; p = 0.01), more often women (67% versus 26%; p = 0.008) and had a lower frequency of mitral regurgitation (7% versus 38%; p = 0.02). The 15 patients dying suddenly with isolated mitral valve prolapse also were less likely to have evidence of ruptured chordae tendineae (29% versus 67%; p = 0.04). The frequency of increased heart weight (67% versus 59%), a dilated mitral valve anulus (80% versus 81%), a dilated tricuspid valve anulus (17% versus 17%), an elongated anterior mitral leaflet (86% versus 54%), an elongated posterior mitral leaflet (79% versus 77%) and fibrous endocardial plaque under the posterior mitral leaflet (73% versus 63%) was similar between the two groups. The severity of the prolapse (mild 20% versus 11%; moderate 27% versus 58%; severe 53% versus 32%) also was similar between the two groups. Thus, persons with mitral valve prolapse dying suddenly without another recognized condition tend to be relatively young women without mitral regurgitation.

Adolescent↗
PubMed1991

Dissection of the aorta associated with congenital malformation of the aortic valve.

The association of congenital aortic valve malformation and aortic dissection is analyzed. Over a 30 year period, 186 patients with non-iatrogenic aortic dissection were studied at necropsy. The aortic valve was tricuspid in 170 (91.4%), bicuspid in 14 (7.5%) and unicuspid in 2 (1.1%). Among the 16 patients with aortic dissection and a congenitally malformed valve, the age at death ranged from 17 to 82 years (mean 52) and 13 (81%) were men. The entrance tear of the aortic dissection was located in the ascending aorta in all 16 patients with a malformed valve but in only 68% of those with a tricuspid aortic valve. The aortic valve was stenotic in 6 of the 16 patients with a congenitally malformed valve. Fatal rupture of the false channel occurred after acute ascending aortic dissection in each of the 11 patients (none with healed dissection) who did not have operative therapy for the dissection. Two of the 16 patients with a malformed valve compared with no patient with a tricuspid aortic valve had aortic isthmic coarctation. Histologic sections of aorta from 10 patients disclosed severe degeneration of the elastic fibers of the media in 9 patients. Thus, a congenitally malformed aortic valve appears to be present at least 5 times more frequently in adults with than in those without aortic dissection, and in our patients the entrance tear was always in the ascending aorta, which usually had severe loss of elastic fibers in its media.

Adolescent↗
PubMed1991

Combined thoracic aortic dissection and abdominal aortic fusiform aneurysm.

Certain clinical and autopsy findings are described in 13 patients who had both aortic dissection (AD) and fusiform abdominal aortic aneurysm (AAA). All 13 patients had severe and extensive aortic atherosclerosis. The AAA was diagnosed clinically in 9 patients, and 5 had the AAA resected. The AD was diagnosed clinically in 5 patients, and 2 underwent attempted operative repair. Two patients who had the AAA resected because of suspected rupture were found later to have ruptured a more proximal AD. Thus, AD occurs occasionally in patients who have AAA. In older persons with suspected rupture of an AAA, a more proximal rupture of an AD should be ruled out. When both AAA and AD are present in the same patient, the AD is more likely the cause of cardiovascular collapse than is rupture of the AAA.

Acute Disease↗
PubMed1991

Morphologic comparison of frequency and types of acute lesions in the major epicardial coronary arteries in unstable angina pectoris, sudden coronary death and acute myocardial infarction.

The frequency and type of acute lesions in the four major (right, left main, left anterior descending, left circumflex) epicardial coronary arteries were examined at necropsy in 14 patients with unstable angina pectoris, 21 patients with sudden coronary death and 32 patients with a fatal first acute myocardial infarction. None of the 67 patients had a grossly visible left ventricular scar (healed myocardial infarct) and only the group with acute myocardial infarction had left ventricular myocardial necrosis. Although the frequency of intraluminal thrombus was similar in patients with unstable angina (29%) and sudden death (29%) and significantly lower than in those with acute infarction (69%) (p = 0.02), the thrombus in the patients with unstable angina and sudden death consisted almost entirely of platelets and was nonocclusive, whereas the thrombus in the group with acute infarction consisted almost entirely of fibrin and was occlusive. The frequency of plaque rupture was insignificantly different in the groups with unstable angina (36%) and sudden death (19%), and was significantly lower than in the group with acute infarction (75%) (p = 0.02). The frequency of plaque hemorrhage was insignificantly different in the groups with unstable angina (64%) and sudden death (38%) and was significantly lower than in the group with acute infarction (90%) (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina, Unstable↗
PubMed1991

Aortic dissection with the entrance tear in the descending thoracic aorta. Analysis of 40 necropsy patients.

Clinical and necropsy findings are described in 40 patients who had aortic dissection with the entrance tear in the descending thoracic aorta. Their ages at death ranged from 39 to 91 years (mean, 66 years); 24 (60%) were men and 16 (40%) were women. Systemic hypertension was present by history in 33 patients (83%) and the hearts were of increased weight in 78%. Of the 40 patients, 31 (78%) had no operative intervention, while 9 (22%) underwent operation for aortic dissection. Of the 31 patients without operative therapy, the diagnosis of aortic dissection was established in life in 9 patients (29%) and at necropsy in 22 (71%). The interval from aortic dissection to death was 30 days or less in 13 patients (42%); rupture of the false channel was the cause of death in 9 patients (69%), renal failure in 2 (15%), and the cause was unclear in 2 (15%). The interval from aortic dissection to death was more than 30 days in 18 (58%) of the 31 patients without operative therapy. The cause of death in these 18 patients was related to the dissection in 11 (61%) (rupture of the false channel in 5; renal failure from dissection in 3, and rupture of the false channel of a second acute dissection in 3), but in the other 7 patients (39%) death was unrelated to the dissection but a nonfatal complication, specifically stenosis of the true channel from compression by a thrombus-filled false channel, occurred in 4 of these 7 patients. Thus only 3 (10%) of the 31 patients without operative therapy had no complications of aortic dissection. All nine patients who underwent operation had had an aortic dissection within 30 days, and the operation was performed because of a major complication of the dissection. Four patients survived 8 to 84 months after the operation. Thus early operative intervention (before the appearance of complications) appears justified in patients with aortic dissection with the entrance tear in the descending thoracic aorta to prevent rupture of the false channel acutely or after initial healing; to prevent renal failure from compression of renal arteries by an aneurysmal false channel; to prevent true channel stenosis from compression by a thrombus-filled false channel; and possibly to prevent the recurrence of acute dissection.

Adult↗
PubMed1991

Effectiveness of recombinant desulphatohirudin in reducing restenosis after balloon angioplasty of atherosclerotic femoral arteries in rabbits.

BACKGROUND: The effectiveness of balloon angioplasty is limited by a restenosis rate of approximately 30%. Recombinant desulphatohirudin (r-hirudin [CGP 39393]) has been found to be highly effective in preventing acute platelet-rich thrombosis after deep arterial injury as compared with heparin. METHODS AND RESULTS: This study evaluated the effect of intravenous r-hirudin, a selective inhibitor of thrombin, on restenosis after balloon angioplasty in 29 rabbits. Focal femoral atherosclerosis was induced by air desiccation endothelial injury followed by a 2% cholesterol diet for 1 month. At angioplasty (2.5-mm balloon with three 60-second, 10-atm inflations 60 seconds apart), the rabbits received heparin (150 units/kg bolus, n = 16) or r-hirudin (1 mg/kg bolus followed by infusions of 1 mg/kg for the first hour and 0.5 mg/kg for the second hour, n = 13). Angiograms performed before and after angioplasty and before death were analyzed quantitatively by a blinded observer. Rabbits were killed 2 hours (n = 14) or 28 days (n = 15) after angioplasty. Femoral arteries were fixed in situ by perfusion of 10% formaldehyde at 100 mm Hg. The mean luminal diameter of the arteries with successful angioplasty (greater than or equal to 20% increase in luminal diameter) in rabbits treated with heparin (n = 8 arteries) increased from 1.18 +/- 0.29 mm before angioplasty to 1.86 +/- 0.24 mm immediately after angioplasty (p less than 0.001) and decreased to 0.94 +/- 0.69 mm (p = 0.0004) at 28 days after angioplasty. In rabbits treated with r-hirudin (n = 11 arteries), the mean luminal diameter increased from 1.14 +/- 0.17 mm before angioplasty to 1.68 +/- 0.20 mm immediately after angioplasty (p less than 0.001) and decreased to 1.37 +/- 0.47 mm (p = 0.01) at 28 days after angioplasty. The mean reduction in luminal diameter by angiography was less in the r-hirudin-treated group than in the heparin-treated group (0.30 +/- 0.33 versus 0.92 +/- 0.61 mm, p = 0.01). Blinded planimetric analysis of stained histological sections of the femoral arteries also showed less cross-sectional area narrowing by plaque in rabbits treated with r-hirudin compared with those treated with heparin (22 +/- 16% verus 48 +/- 29%, p = 0.01). Both groups had similar numbers of arteries with histological evidence of balloon-induced plaque tear (12 of 13 versus 13 of 15). CONCLUSIONS: Rabbits receiving r-hirudin at the time of experimental balloon angioplasty had significantly less restenosis by angiography and by quantitative histopathology than rabbits receiving heparin.

Angioplasty, Balloon↗
PubMed1991

Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy. Significance in producing left ventricular outflow obstruction.

BACKGROUND: Obstruction to left ventricular outflow in hypertrophic cardiomyopathy (HCM) is usually due to systolic anterior motion of the mitral valve. Occurrence of structural mitral valve abnormalities in HCM and their significance in producing outflow obstruction (even in the absence of typical systolic anterior motion) has not been fully appreciated. METHODS AND RESULTS: Analysis of 78 mitral valves excised from patients with obstructive HCM showed that 10 (13%) had anomalous insertion of one or both left ventricular papillary muscles directly into the anterior mitral leaflet. This malformation was identified by echocardiography, which demonstrated direct continuity between the hypertrophied papillary muscle and mitral leaflet, resulting in a long rigid area of midcavity narrowing that appeared to be solely or largely responsible for outflow obstruction. Basal subaortic pressure gradients were large (70-150 mm Hg). Mitral valve replacement reduced the outflow gradient substantially to 0-15 mm Hg in four patients with postoperative cardiac catheterization. However, two other patients who underwent septal myotomy/myectomy had persistent symptoms and incomplete relief of obstruction (gradients 60 and 70 mm Hg) because of continued midcavity apposition of papillary muscle and ventricular septum. CONCLUSIONS: Anomalous papillary muscle insertion into anterior mitral leaflet represents a mechanism of obstruction to left ventricular outflow in patients with HCM and differs considerably from typical dynamic obstruction caused by mitral valve systolic anterior motion that occurs in many other patients with HCM. Recognition of this malformation emphasizes the diverse morphological expression of HCM and also has important clinical implications for patients requiring operation because the gradient is likely to persist even after adequate myotomy/myectomy; consequently, mitral valve replacement would appear to be the operation of choice in most such patients.

Adult↗
PubMed1990

Sudden death behind the wheel from natural disease in drivers of four-wheeled motorized vehicles.

The heart was studied in 30 persons who died suddenly from natural causes in the driver's seat of an automobile, truck or bus. Twenty had cardiac arrest while driving and the other 10 while sitting in the driver's seat of a parked vehicle. Of the 20 drivers, 16 died from atherosclerotic coronary artery disease (CAD): 12 (75%) had minor collisions and 4 did not. Of the 16 with fatal CAD, an average of 2.3 +/- 0.8 of the 4 major coronary arteries were narrowed greater than 75% in cross-sectional area (CSA) by plaque; of 668 five-mm segments of the 4 major (right, left main, left anterior descending, left circumflex) coronary arteries in 13 of these 16 cases, 27 (4%) were narrowed 96 to 100% and 127 (19%) were narrowed 76 to 95% in CSA by plaque. The remaining 4 drivers died from noncoronary conditions: aortic rupture associated with the Marfan syndrome in 1; cardiac sarcoidosis in 1; thoracic aortic dissection in 1; and severe mitral regurgitation from infective endocarditis, which had healed in 1. The other 10 persons were found dead in the driver's seat of a parked vehicle and 8 of them had fatal CAD. Of the 8 CAD victims, an average of 2.5 +/- 1.2 of the 4 major coronary arteries was narrowed greater than 75% by plaque; of the 283 five-mm segments of coronary arteries in 7 of the 8 cases, 44 (16%) were narrowed 96 to 100% and 69 (24%) were narrowed 76 to 95% in CSA by plaque.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Traffic↗