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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 415 records · Page 23Linked to original sources
PubMed1983

Clinical and morphologic cardiac findings after anthracycline chemotherapy. Analysis of 64 patients studied at necropsy.

The relation between clinical evidence of and histologic signs of anthracycline cardiotoxicity was evaluated by reviewing the clinical and morphologic findings in 64 patients studied at necropsy, all of whom had received doxorubicin or daunorubicin chemotherapy during life. Of the 64 patients, 20 (31%) had documented clinical toxicity consisting of impaired left ventricular systolic performance; in 7 (35%) of these 20 patients, histologic signs of toxicity were absent. In the remaining 13 patients with clinical toxicity, histologic signs of toxicity ranged from mild to severe. Of the 44 (69%) patients without clinical signs of drug toxicity, 21 (48%) had no histologic sign of cardiotoxicity; in 23 (52%) of the patients without clinical toxicity, however, morphologic signs of cardiotoxicity were nevertheless present--mild in most patients, but extensive in 4. Signs of extensive histologic toxicity (19 [30%] of 64 patients) were associated with large doses (greater than 450 mg/m2) of the drug, mediastinal irradiation, and age greater than 70 years. This study suggests that attempts to monitor cardiotoxicity by serial evaluation of cardiac histology in patients undergoing anthracycline chemotherapy may be seriously limited by the fact that clinical evidence of toxicity may be present without histologic signs of toxicity; likewise, histologic signs of anthracycline toxicity may be present without clinical evidence of toxicity.

Adolescent↗
PubMed1983

Juxtaductal aortic coarctation. Analysis of 84 patients studied hemodynamically, angiographically, and morphologically after age 1 year.

Although many studies of juxtaductal coarctation of the aorta have been reported, none has correlated clinical, hemodynamic, angiographic, anatomic, and operative findings. Of 84 patients (62 male and 22 female; age range, 1 to 49 years [mean 17]), all had murmurs; 76 had absent, diminished, or delayed femoral pulsations; 50 had cuff systolic blood pressures in the arm greater than 140 mm Hg, and 30 had diastolic pressures greater than 90 mm Hg. The average pressure gradients (mm Hg) by direct measurements above and below the coarctation in 35 patients were peak systolic, 45; mean, 17; and diastolic, 5. Rib notching, visible in chest roentgenograms in 43 patients, correlated directly with age and inversely with the diameter of the coarctation. Moderate or marked cardiomegaly by radiograph was present in only 1 of 48 patients with isolated coarctation and in 17 of 36 with associated cardiovascular malformations. Electrocardiograms were abnormal in more than two thirds of patients with associated anomalies, but were normal in more than three fourths of those with isolated coarctation. In 70 excised, serially sectioned coarctations the aortic lumens were completely occluded in 4 patients, up to 0.5 mm in internal diameter in 22 patients, from 0.6 to 2 mm in 26 patients, from 2.1 to 5 mm in 14, and greater than 5 mm in 4, and correlated directly with lumens measured angiographically. The most significant anatomic factor causing the coarctation was invagination of the media from the posterior aortic wall, but intimal proliferation (jet lesion) at and immediately distal to the invagination contributed to the narrowing. Three (each with associated anomalies) of 70 patients died early after coarctation repair. Systolic or diastolic blood pressures decreased early postoperatively in 58 (87%) of 67 surviving patients, and both pressures decreased in 42 (63%). Late postoperatively (mean follow-up, 4.7 years), the systolic blood pressure remained elevated in 25% of patients.

Adolescent↗
PubMed1983

Subepicardial adipose tissue producing echocardiographic appearance of pericardial effusion. Documentation by computed tomography and necropsy.

An isolated anterior echo-free space is generally regarded as a false-positive echocardiographic finding for pericardial effusion. Even when an anterior echo-free space is accompanied by a posterior echo-free space, the echo-free spaces have been occasionally reported to be falsely positive for pericardial effusion, principally in patients with cardiac neoplasms. The basis for these findings had never been adequately explained. In the present study, evaluation by computed tomographic imaging or necropsy examination of 5 patients in whom there was either an anterior or posterior echo-free space or both demonstrated that subepicardial adipose tissue is the echocardiographic imitator of pericardial effusion.

Adipose Tissue↗
PubMed1983

Hypertrophic cardiomyopathy: a common cause of sudden death in the young competitive athlete.

The causes of sudden, unexpected death in highly-conditioned competitive athletes are summarized. In the vast majority of young athletes (less than 35 years of age) sudden death is due to underlying structural cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths and may account for about one-half of the sudden deaths in a youthful athletic population. Cardiovascular abnormalities that appear to be less frequent important causes of sudden death include anomalous origin of the left coronary artery from the anterior sinus of Valsalva, ruptured aorta (due to cystic medial necrosis), idiopathic concentric left ventricular hypertrophy and coronary artery atherosclerosis. Other diseases which are probably particularly uncommon causes of sudden death in the young athlete include mitral valve prolapse, aortic valvular stenosis, acute myocarditis, QT interval prolongation syndromes, hypoplasia of the coronary arteries or sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life. In only about 25% of those competitive athletes who die suddenly is underlying disease identified prior to participation and rarely is the correct clinical diagnosis made. In contrast, when sudden death occurs in older competitive or recreational athletes (over 35 years of age) it is usually due to coronary artery disease.

Adolescent↗
PubMed1983

Two-dimensional echocardiographic assessment of the idiopathic hypereosinophilic syndrome. Anatomic basis of mitral regurgitation and peripheral embolization.

Important cardiac manifestations in the idiopathic hypereosinophilic syndrome include mitral regurgitation and peripheral embolization. To determine the anatomic basis of these abnormalities, real-time, wide-angle, two-dimensional echocardiography (2-D echo) was performed in 21 patients with the hypereosinophilic syndrome. Nine patients (43%) had clinical evidence of mitral regurgitation, and each had localized thickening of the posterobasal left ventricular wall behind the posterior mitral leaflet and absent (seven patients) or diminished (two patients) motion of the posterior leaflet. Anatomic observations at operation or necropsy in four patients with mitral regurgitation demonstrated that the echocardiographic abnormalities resulted from posterior mitral leaflet thickening and adherence of the leaflet to the underlying mural endocardium of the posterobasal wall. On 2-D echo, each of the six patients with peripheral emboli had either apical left ventricular echo-dense targets consistent with thrombus or thickening of the posterobasal wall of the left ventricle, and these findings were validated at autopsy or operation in three patients. Hence, in patients with the hypereosinophilic syndrome, 2-D echo is useful in identifying the probable etiology of two important cardiac manifestations. Thickening of the posterobasal wall is usually associated with impairment of posterior mitral leaflet function, resulting in mitral regurgitation. Because the hypereosinophilic syndrome is associated with peripheral embolization, thrombus formation and subsequent endocardial scarring, the noninvasive identification of intracavitary ventricular thrombi may be important.

Adolescent↗
PubMed1983

Systolic anterior motion of the posterior mitral leaflet: a previously unrecognized cause of dynamic subaortic obstruction in patients with hypertrophic cardiomyopathy.

Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.

Adolescent↗
PubMed1983

Cholesteryl ester crystals in a porcine aortic valvular bioprosthesis implanted for eight years.

Masses of crystals, which were largely composed of cholesteryl esters, were found in a porcine aortic valvular bioprosthesis removed eight years after implantation in the mitral position in a patient with rheumatic mitral valvular stenosis. Histologic sections of grossly raised and nonraised yellow lesions in the three cusps of this bioprosthesis revealed large clefts, which on frozen section contained lipid-positive, birefringent crystals. These crystals gave a positive reaction with the Schultz test for cholesterol. Biochemical analyses of isolated nodules revealed a cholesterol content of 40 nmole/mg of wet tissue. Of this cholesterol, 88 percent was esterified, and the remaining 12 percent was free cholesterol. These cholesterol deposits are most likely derived from blood lipids; however, they were not related to hyperlipidemia, since the patient had normal blood levels of cholesterol and triglycerides.

Aged↗
PubMed1982

Severe aortic regurgitation from systemic hypertension (without aortic dissection) requiring aortic valve replacement: analysis of four patients.

Clinical and morphologic observations are described in four patients who had severe aortic regurgitation from severe systemic hypertension unassociated with aortic dissection; each patient underwent aortic valve replacement. Although aortic regurgitation of minimal or mild degree is well recognized to occur in patients with systemic hypertension, severe degrees of aortic regurgitation are rare in such patients; aortic valve replacement in such patients has not previously been reported. Why these four patient had such severe aortic regurgitation was not determined. Although systemic hypertension is rarely a cause, it nevertheless must be added to the list of causes of severe pure aortic regurgitation.

Adult↗
PubMed1982

Left ventricular incision midway between the mitral anulus and the stumps of the papillary muscles during mitral valve excision with or without rupture or aneurysmal formation: analysis of 10 necropsy patients.

Certain clinical and morphologic observations are described in 10 patients who had mitral valve replacement (MVR) and lacerations of the left ventricular (LV) free wall midway between the anulus of the mitral valve and the stumps of the LV papillary muscles. In five patients the lacerations led to LV free wall rupture, with immediate hemopericardium in two and delayed (2 to 4 days) rupture in the other three. Of the other five patients, three developed aneurysm of the LV free wall, the mouth of which was located midway between mitral anulus and papillary muscle stumps, the sites of the lacerations observed in the other seven patients. The remaining two patients had midway lacerations which produced neither rupture nor aneurysmal formation. The midway LV lacerations are considered the result of LV incisions made at the time of mitral valve excision, generally in a setting where the left-sided cardiac chambers were only mildly dilated or normal and the tips of the blades of the scissors may have been inadequately visualized during mitral excision. This complication can be prevented by leaving the posterior mitral leaflet and its attached chordae intact or by applying exquisite care during the mitral excision procedure, or both. LV midway rupture may be most common cause of death early after MVR and operatively induced LV lacerations may lead to LV aneurysm late postoperatively.

Adult↗
PubMed1982

Relation of healed transmural myocardial infarct size to length of survival after acute myocardial infarction, age at death, and amount and extent of coronary arterial narrowing by atherosclerotic plaques: analysis of 70 necropsy patients.

The percent of left ventricular wall (including ventricular septum) replaced by scar was determined in 70 necropsy patients with a healed transmural myocardial infarct (MI). The MI involved from 1% to 55% (mean 13%) of the left ventricular wall. The ages at death of the patients ranged from 25 to 82 years (mean 62) and did not significantly correlate with MI size (r = -0.12). Of the 70 patients, 41 (59%) had unequivocal histories of an acute MI: the interval from the MI to death in them ranged from 2 to 276 months (mean 50) and correlated negatively with MI size (r = -0.32, p less than 0.05), and the age at the MI ranged from 26 to 79 years (mean 58) and did not correlate with MI size (r = -0.05). The four major epicardial coronary arteries were examined quantitatively in 56 patients; the number of coronary arteries with severe narrowing ranged from one to four (mean 2.9) and did not correlate with MI size (r = -0.24). The mean MI size in the 12 patients with and in the 44 without severe narrowing of the left main coronary artery was identical (each 13%). The entire lengths of the right, left anterior descending, and left circumflex coronary arteries in the 56 patients were divided into 5 mm long segments and the amounts of cross-sectional area narrowing in each of the resulting 2489 segments were determined by histologic examination. The percent of 5 mm segments with severe (cross-sectional area narrowing 76% to 100%) narrowing by atherosclerotic plaques in each patient ranged from 3% to 93% (mean 44% and did not correlate with MI size (r = -0.20). When the 28 patients with an MI involving greater than 10% of the left ventricular wall were compared to those with an MI involving less than or equal to 10%, a similar overall percentage of 5 mm segments of coronary artery was severely narrowed (43% vs 42%). In addition, a similar percentage of segments was narrowed severely in each of the three major epicardial coronary arteries. Thus in our necropsy patients with a healed transmural MI, the MI size correlated with length of survival after an acute MI (in patients with definite histories of an acute MI) but not with age at death or with the amount, location, or extent of coronary arterial narrowing by atherosclerotic plaques.

Adult↗