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Biomedical subjects

W C Roberts

Publications and source records attributed to W C Roberts.

At least 451 records · Page 25Linked to original sources

Osteogenic sarcoma metastatic to the heart.

Of 20 patients with fatal osteogenic sarcoma who underwent postmortem examination, four had metastases to the heart. One had recurrent ventricular tachycardia, and one had anatomic evidence of aortic regurgitation due to massive periaortic neoplastic infiltration that prevented coaptation of the aortic cusps during ventricular diastole, one had massive invasion of the peri-superior vena caval syndrome, and one had neoplastic obstruction of the inferior vena cava as it entered the thorax. Among patients with either primary or secondary neoplasms to the heart, osteogenic sarcoma is unique because the metastases contain bone and, therefore, may be radiographically visible; they are usually large and often intracavitary.

Adolescent↗

Pathology of active infective endocarditis: a necropsy analysis of 192 patients.

Successful treatment of infective endocarditis often requires cardiac valve replacement during the active infection. This is especially the case with aortic valve infection, and with infection of valve prostheses in either the aortic or mitral position. Valve excision with or without replacement, however, is also sometimes required for tricuspid valve infection (1). This discussion will focus on the morphologic aspects of active infective endocarditis involving both right and left-sided native cardiac valves. It will also examine certain morphologic aspects of mechanical and bioprosthetic valve substitutes. The information is derived from necropsy examination by the authors of 192 patients with active infective valvular endocarditis (Table 1). Of the 192 patients, 129 were described in an earlier publication (2). Patients with infective endocarditis complicating congenital heart disease with a shunt (6 patients), and those with infective endocarditis following valvulotomy (4 patients) are omitted from this analysis.

Adult↗

Hypertrophic cardiomyopathy in infants: clinical features and natural history.

The clinical and morphologic features of hypertrophic cardiomyopathy in 20 patients recognized as having cardiac disease in the first year of life are described. Fourteen of these 20 infants were initially suspected of having heart disease solely because a heart murmur was identified. However, the infants showed a variety of clinical findings, including signs of marked congestive heart failure (in the presence of non-dilated ventricular cavities and normal or increased left ventricular contractility) and substantial cardiac enlargement on chest radiograph. Other findings were markedly different from those usually present in older children and adults with hypertrophic cardiomyopathy (e.g., right ventricular hypertrophy on the ECG and cyanosis). Consequently, in 14 infants, the initial clinical diagnosis was congenital cardiac malformation other than hypertrophic cardiomyopathy. Twelve of the 14 infants who underwent left-heart catheterization showed substantial obstruction to left ventricular outflow (peak systolic pressure gradient greater than or equal to 35 mm Hg). However, unlike older patients with hypertrophic cardiomyopathy, infants with this condition commonly had marked obstruction to right ventricular outflow (35-106 mm Hg) (nine patients); in six patients, the magnitude of obstruction to right ventricular outflow was at least as great as that to left ventricular outflow. Asymmetric hypertrophy of the ventricular septum relative to the left ventricular free wall was present in the 16 patients who had echocardiographic or necropsy examination. Ventricular septal thickening was substantial in patients studied both before and after 6 months of age (mean 16 mm), indicating that in patients with hypertrophic cardiomyopathy, marked left ventricular hypertrophy may be present early in life and is probably congenital. The clinical course was variable in these patients, but the onset of marked congestive heart failure in the first year of life appeared to be an unfavorable prognostic sign; nine of the 11 infants with congestive heart failure died within the first year of life. In infants with hypertrophic cardiomyopathy, unlike older children and adults with this condition, sudden death was less common (two patients) than death due to progressive congestive heart failure.

Angiocardiography↗

Sudden death in hypertrophic cardiomyopathy: a profile of 78 patients.

The clinical profile of 78 patients with hypertrophic cardiomyopathy who died suddenly (or experienced cardiac arrest and survived) was analyzed. At the time of cardiac catastrophe, 71% of the patients were younger than 30 years of age, 54% were without functional limitation and 61% were performing sedentary or minimal physical activity. Nineteen of the 78 patients (24%) were taking propranolol in apparently adequate dosages, indicating that this drug does not provide absolute protection against sudden death. No clinical or morphologic variable was particularly reliable in identifying patients at risk for sudden death. Forty-eight of 62 patients (77%) who died suddenly had a markedly increased ventricular septal thickness of 20 mm or more; however, mean septal thickness was similar in patients who died suddenly (25.2 +/- 0.9 mm) and in age- and sex-matched control patients with hypertrophic cardiomyopathy who have survived (23.6 +/- 0.8 mm). An abnormal ECG was present as often in patients who died suddenly as in control patients who have survived, (51 or 53, 96%). In addition, no particular cardiac symptom or hemodynamic variable (such as the magnitude of left ventricular outflow tract obstruction under basal conditions or left ventricular end-diastolic pressure) was characteristic of the patients with hypertrophic cardiomyopathy who died suddenly.

Adolescent↗

Comparison of amount of extent of coronary narrowing by atherosclerotic plaque and of myocardial scarring at necropsy in anterior and posterior healed transmural myocardial infarction.

The amount of cross-sectional area narrowing by atherosclerotic plaque in each 5-mm-long segment from the entire lengths of the right, left main, left anterior descending and left circumflex coronary arteries and the size, predominant location and extent of myocardial scarring were determined in 59 necropsy patients with a healed transmural myocardial infarct (MI). The mean number of the four major epicardial coronary arteries narrowed severely (76-100% in cross-sectional area) was 3.0 in the 37 patients with posterior MI and 2.6 in the 22 patients with anterior MI (p less than .025). The mean percent of severely narrowed 5-mm segments from all four major coronary arteries was similar in the anterior and posterior MI groups, 38% vs 46%. The patients with anterior MI, however, had a higher percentage of severely narrowed 5-mm segments of the left anterior descending than of the left circumflex but not the right coronary artery, 46% vs 25% (p less than 0.001) and 40% (NS). The patients with posterior MI had a higher percentage of severely narrowed segments of the right and left circumflex coronary arteries than of the left anterior descending artery, 55% and 51% vs 32% (p less than 0.05). The anterior MI group had, on the average, larger left ventricular scars than the posterior MI group (20% vs 9%, p greater than 0.002) and more frequent scarring of the ventricular septum, 16 patients (73%) vs six patients (16%) (p less than 0.001).

Adult↗

NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations.

The idiopathic hypereosinophilic syndrome (HES) represents a heterogeneous group of disorders with the common features of prolonged eosinophilia of an undetectable cause and organ system dysfunction. Fifty patients with the idiopathic HES were studied over 11 years of the National Institutes of Health. Multiple organ systems were involved; bone marrow hypereosinophilia was common to all patients, but the most severe clinicopathologic involvement was of the heart and nervous system. Postmortem gross pathologic examination of the hearts of patients with idiopathic and nonidiopathic HES suggested that the common mechanism of cardiac disease is the eosinophilia. Endomyocardial biopsy findings showed that the endothelial cells in the endocardium and of the microvasculature were the primary targets of the tissue damage. This damage initiates thrombosis; endocardial fibrosis and restrictive endomyocardopathy may follow. In-vitro culture of circulating eosinophil colony-forming units showed some normal studies, some studies showing increased progenitor cells committed to eosinophil development, and others showing an excess production of eosinophil colony-stimulating factor. Chemotherapy to lower the eosinophil counts has resulted in marked improvement of HES prognosis, as have agressive medical and surgical approaches to cardiovascular complications.

Cardiomyopathies↗

Intracuspal hematomas in implanted porcine valvular bioprostheses: clinical and experimental studies.

Intracuspal hematomas were found in three of 57 porcine valvular bioprostheses implanted as substitute cardiac valves in 50 patients and in 11 of 29 similar bioprostheses implanted in sheep. The three values implanted in patients had been in the mitral position for 27, 65, and 107 months. Of the valves implanted in sheep, six had been in the mitral position and five in the tricuspid position for periods of time ranging from 20 minutes to 7 months. In each patient and in four of 11 sheep, the hematomas involved more than one cusp. These lesions were localized in the spongiosa, extended from the basal region toward the free edge of the cusp, and formed a plane of dissection which involved the spaces left in the spongiosa by the removal of proteoglycan material during preimplantation commercial processing. In one patient, the hematomas limited the mobility of the cusps and appeared to have been the cause of clinically significant prosthetic mitral stenosis; in the other two patients and in the experimental animals, the hematomas were smaller and of uncertain hemodynamic significance. Intracuspal hematomas may become sites of eventual formation of calcific deposits. The pathogenesis of intracuspal hematomas is related to the entry of blood into the space between the sewing ring and the most basilar region of the bioprosthetic tissue. This space extends throughout the circumference of the bioprosthesis and is continuous with the spongiosa, the layer in which the hematoma develops. The blood penetrates into this space through the suture line between bioprosthetic tissue and sewing ring on the inflow surface of porcine valvular bioprostheses which have been mounted on atrioventricular type stents. Intracuspal hematomas were not found in bioprostheses mounted on aortic type stents, in which these sutures are more protected and more closely spaced, or in pericardial bioprostheses, which do not have a spongiosa.

Adolescent↗

Intracuspal hematomas in bioprosthetic valves: pathologic findings and clinical implications.

The presence of intracuspal hematomas (ICHs) was investigated in 156 valvular bioprostheses, including 57 (all porcine aortic valvular bioprostheses) that had been implanted in patients and 99 (64 porcine aortic valvular bioprostheses, 29 bovine pericardial bioprostheses and six human dura mater bioprostheses) that had been implanted in sheep. ICHs were found in three mitral bioprostheses in patients and in 14 porcine aortic valvular bioprostheses (nine mitral and five tricuspid) in sheep. Hematomas were not found in the dura mater or pericardial bioprostheses. In each patient and in six of the 14 sheep, the hematomas involved more than one cusp and consisted of erythrocyte accumulations in the spongiosa. They extended from the basal region toward the free edge of the cusp and formed a plane of dissection that involved the spaces left in the spongiosa by removal of proteoglycan material during commercial processing. ICHs may become sites of formation of calcific deposits. ICHs result from entry of blood into the space between the sewing ring and the most basilar region of the bioprosthetic tissue. This space extends throughout the circumference of the bioprosthesis and is continuous with the spongiosa, the layer in which the hematoma develops. The blood penetrates this space through the suture line between bioprosthetic tissue and sewing ring on the inflow surface of porcine valvular bioprostheses mounted on atrioventricular-type stents. ICHs were not found in porcine valvular bioprostheses mounted on aortic-type stents, in which the sutures are more protected and more closely spaced, on in bioprostheses constructed of tissues (parietal pericardium and dura mater), which lack a spongiosa.

Adolescent↗

Type III hyperlipoproteinemia: Quantification, distribution, and nature of atherosclerotic coronary arterial narrowing in five necropsy patients.

The amount of cross-sectional area (XSA) narrowing in each 5 mm long segment of each of the four major epicardial coronary arteries was determined in each of five patients with type III hyperlipoproteinemia (HLP) and symptomatic, fatal atherosclerotic coronary disease (CAD). Four had angina pectoris; two had acute myocardial infarcts which healed, and two died suddenly. Of the four major epicardial coronary arteries, all four were narrowed 76% to 100% in XSA by atherosclerotic plaques in two patients, three were narrowed to this degree in two patients, and two were so narrowed in one patient. Three patients had severe narrowing of the left main coronary artery. The percent of 5 mm long segments of coronary artery narrowed to various degrees was as follows: 96% to 100%, 0 to 37 (mean 14); 76% to 95%, 14 to 61 (mean 35); 51% to 75%, 9 to 41 (mean 24); 26% to 50%, 0 to 42 (mean 16), and 0% to 25%, 0 to 27 (mean 11). Utilizing a scoring system of 1 to 4 for the four categories of narrowing (1 = 0% to 25%, 2 = 26% to 50%, 3 = 51% to 75% and 4 = 76% to 100% XSA narrowing), scores per 5 mm segment for each patient ranged from 2.5 to 3.9 (mean 3.1). Thus these five type III HLP patients had severe diffuse coronary narrowing by atherosclerotic plaques.

Aged↗