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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 325 records · Page 18Linked to original sources
PubMed1986

Severe atherosclerotic coronary artery disease, healed myocardial infarction and chronic congestive heart failure: analysis of 81 patients studied at necropsy.

Observations are described in 81 necropsy patients (aged 29 to 91 years [mean 62]; 77 [95%] men) with severe congestive heart failure (CHF) more than 3 months in duration, left ventricular (LV) transmural scar and greater than 75% cross-sectional area narrowing by atherosclerotic plaque of 1 or more of the 4 major epicardial coronary arteries. The duration of symptoms from initial onset of acute myocardial infarction (59 patients) or CHF (18 patients) or angina pectoris (2 patients) to death ranged from 0.5 to 18 years (mean 7.1) (2 unknown). Angina pectoris occurred at some time, however, in 31 patients (38%). Cause of death was CHF in 48 patients (59%), sudden (arrhythmia) in 16 (20%), acute myocardial infarction in 11 (14%), and emboli in 6 (7%). The heart weight ranged from 410 to 800 g (mean 585). Left or right ventricular thrombi or both occurred in 37 patients (46%), only 4 (10%) of whom had systemic emboli; of the 44 patients without intracardiac thrombi, none had any form of emboli. The severity of coronary narrowing was variable. In 24 patients (30%) only 1 artery was narrowed greater than 75% in cross-sectional area; in 22 patients (27%), 2 arteries were so narrowed; in 32 patients (39%), 3 arteries; and in 3 patients (4%), 4 arteries. The size of the LV scar also varied. Of the 81 patients, 58 (72%) had large scars (involving greater than 40% of the LV wall); 10 (12%) had moderate-sized scars (6 to 40% of the LV wall); and 13 (16%) had small scars (less than or equal to 5% of the LV wall).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1986

Severe atherosclerotic coronary arterial narrowing and chronic congestive heart failure without myocardial infarction: analysis of 18 patients studied at necropsy.

Observations are reported on 18 patients (aged 38 to 73 years ([mean 58]; 16 [89%] men) studied at necropsy who had had chronic congestive heart failure (CHF) more than 3 months in duration, greater than 75% cross-sectional area (XSA) narrowing of 1 or more of the 4 major epicardial coronary arteries, and no left ventricular fibrosis or necrosis. Duration of symptoms from onset of CHF to death ranged from 0.3 to 13 years (mean 5.7). Angina pectoris occurred in 2 patients (11%). The mode of death was CHF in 12 (67%), sudden (arrhythmia) in 5 (28%), and emboli in 1 (5%). Heart weight ranged from 410 to 890 g (mean 632). Of 72 major epicardial coronary arteries (right, left main, left anterior descending, left circumflex) in the 18 patients, 30 (42%) were narrowed 76 to 100% in XSA by atherosclerotic plaque (right = 10, left main = 0, left anterior descending = 9 and left circumflex = 11). A mean of 1.7 of 4 major epicardial coronary arteries per patient were narrowed 76 to 100% in XSA by atherosclerotic plaque. In 10 patients, each 5-mm segment of the 4 major coronary arteries was examined histologically (mean 53 per patient): 23 segments (3%) were narrowed 96 to 100% in XSA by atherosclerotic plaque; 58 (11%), 76 to 95; 93 (18%), 51 to 75%; 209 (40%), 26 to 50%, and 146 (28%), 0 to 25%. Left and right ventricular thrombi were found in 9 patients (50%); of the 9 patients, 1 had a systemic embolus; of the 9 patients without intraventricular thrombi, none had systemic emboli.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Diabetes mellitus for 25 years or more. Analysis of cardiovascular findings in seven patients studied at necropsy.

Observations are described in seven patients (four women and three men) aged 38 to 76 years who had had diabetes mellitus for 25 years or more. Five had been treated with insulin, and two had been treated with diet and oral hypoglycemic agents only. Four patients had had bilateral leg amputations, one angina pectoris, and two left-sided congestive heart failure. Two died suddenly, two died of acute myocardial infarction, two died of infection, and one died from trauma. Transmural left ventricular scars were present in five patients and transmural necrosis in three patients. All seven patients had two or more major epicardial coronary arteries narrowed more than 75 percent in cross-sectional area by atherosclerotic plaque. Of 353 segments, each 5 mm, from the four major epicardial coronary arteries from the seven patients (mean 50 per patient), 53 (15 percent) were narrowed up to 25 percent in cross-sectional area, 116 (33 percent) were narrowed 26 to 50 percent, 110 (31 percent) were narrowed 51 to 75 percent, 66 (19 percent) were narrowed 76 to 95 percent, and eight (2 percent) were narrowed 96 to 100 percent. What allowed such long survival in these seven patients is unclear. It is clear that all had severe coronary arterial narrowing by atherosclerosis.

Adult↗
PubMed1986

Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy.

Many patients with hypertrophic cardiomyopathy have signs and symptoms of myocardial ischemia and dysfunction. Although hypertrophy and increased left ventricular pressure can account for such abnormalities, altered small intramural coronary arteries have also been described in such patients. To determine the prevalence and extent as well as the clinical relevance of abnormal intramural coronary arteries, a histologic analysis of left ventricular myocardium obtained at necropsy was performed in 48 patients with hypertrophic cardiomyopathy (but without atherosclerosis of the extramural coronary arteries) and in 68 control patients with either a normal heart or acquired heart disease. In hypertrophic cardiomyopathy, abnormal intramural coronary arteries were characterized by thickening of the vessel wall and a decrease in luminal size. The wall thickening was due to proliferation of medial or intimal components, or both, particularly smooth muscle cells and collagen. Of the 48 patients with hypertrophic cardiomyopathy, 40 (83%) had abnormalities of intramural coronary arteries located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (9 patients); an average of 3.0 +/- 0.7 abnormal arteries were identified per tissue section. Altered intramural coronary arteries were also significantly more common in tissue sections having considerable myocardial fibrosis (31 [74%] of 42) than in those with no or mild fibrosis (31 [30%] of 102; p less than 0.001). Abnormal intramural coronary arteries were also identified in three of eight infants who died of hypertrophic cardiomyopathy before 1 year of age. In contrast, only rare altered intramural coronary arteries were identified in 6 (9%) of the 68 control patients (0.1 +/- 0.05 abnormal arteries per section; p less than 0.001) and those arteries showed only mild thickening of the wall and minimal luminal narrowing. Moreover, of those patients with abnormal intramural coronary arteries, such vessels were about 20 times more frequent in patients with hypertrophic cardiomyopathy (0.9 +/- 0.2/cm2 myocardium) than in control patients (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal intramural coronary arteries with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with hypertrophic cardiomyopathy studied at necropsy and may represent a congenital component of the underlying cardiomyopathic process.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1986

Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients.

Certain clinical and cardiac morphologic findings are described in 22 patients, aged 45 to 80 years (mean 64) (15 men [68%]), in whom rupture of a papillary muscle occurred during acute myocardial infarction. In most, the acute infarction associated with papillary muscle rupture was a first coronary event (only 18% had a myocardial scar consistent with prior infarction and 29% had angina pectoris). The posteromedial papillary muscle, presumably because of its more tenuous blood supply, ruptured almost three times more frequently than the anterolateral one (73 and 27%, respectively). Quantitative examination of the amounts of narrowing by atherosclerotic plaque in each of the four major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) disclosed less narrowing in the patients with rupture than in the patients with fatal acute myocardial infarction unassociated with rupture. Of the 519 five mm sections of coronary artery examined (11 patients), only 68 sections (13%) were narrowed greater than 75% in cross-sectional area compared with 34% of 1,403 sections from 27 patients with fatal myocardial infarction without rupture.

Adipose Tissue↗
PubMed1986

Causes of sudden death in competitive athletes.

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.

Adolescent↗
PubMed1986

Left main coronary artery originating from the right sinus of Valsalva and coursing between the aorta and pulmonary trunk.

Findings are described in five patients who at necropsy were found to have origin of the left main coronary artery from the right sinus of Valsalva and coursing of the anomalously arising artery between aorta and pulmonary trunk to reach the left side of the heart. Three of the five patients were boys and died suddenly at ages 13, 14 and 19 years, respectively: two of them had had one or more episodes of syncope and the third had an abnormal electrocardiogram. The fourth patient, a 64 year old woman, died of chronic congestive heart failure 1 year after an acute myocardial infarction. She had insignificant coronary atherosclerosis. The fifth patient, an 81 year old man, died of chronic alcoholism, having been free of symptoms of cardiac dysfunction during life. Additionally, clinical and necropsy findings are summarized in 38 previously reported necropsy patients with the coronary anomaly. Of these 38 (34 male [89%]), 23 (61%) died suddenly in the first two decades of life; death in 6 others (16%) appears to have been related to coronary atherosclerosis and 9 patients (24%) died from noncoronary causes. Thus, this anomaly is life-threatening. Why it frequently causes fatal cardiac arrest in some young individuals and allows a normal life span in others remains unclear.

Adolescent↗
PubMed1986

Morphologic findings in sudden coronary death: a comparison of those with and those without previous symptoms of myocardial ischemia.

In this article, the amount and distribution of coronary arterial narrowing by atherosclerotic plaque at necropsy are described in 70 victims of sudden coronary death. Of 3484 5-mm segments examined from the four major coronary arteries, 950 (27 per cent) were narrowed 76 to 100 per cent in cross-sectional area by atherosclerotic plaque; 1127 (32 per cent) were narrowed 51 to 75 per cent; 689 (20 per cent) were narrowed 26 to 50 per cent; and 718 (21 per cent) were narrowed 0 to 25 per cent. More extensive severe narrowing occurred in the proximal halves compared with the distal halves of the left anterior descending and left circumflex coronary arteries. Comparison between the 31 previously symptomatic victims (either angina pectoris and/or a clinical acute myocardial infarction) and the 39 victims who had previously been asymptomatic disclosed a significantly higher mean percentage of severely narrowed 5-mm segments and a lower mean percentage of minimally narrowed segments in the symptomatic group.

Adult↗
PubMed1985

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