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Biomedical subjects

M D Silver

Publications and source records attributed to M D Silver.

At least 37 records · Page 2Linked to original sources
PubMed1992

Morphologic findings and causes of failure in 24 explanted Ionescu-Shiley low-profile pericardial heart valves.

From 1981 to 1987 just over 608 Ionescu-Shiley low-profile bovine pericardial bioprostheses were implanted at the Toronto Hospital. Twenty-four prostheses (11 aortic and 13 mitral) were surgically explanted from 1988 to 1990 from 20 adults (10 men and 10 women). Prosthesis failure was caused by primary tissue failure in 17 valves or by other mechanisms in seven valves. Variable degrees of tissue failure were also seen in four of the seven valves from the latter group. Primary tissue failure was characterized by fluid insudation between collagen bundles, para stent post tears (alignment stitch related, 20 valves), cusp perforation with prolapse, and calcification. The earliest cusp tears occurred at 28 months. Calcification (10 of 24 cases) was minimal in seven of 10 valves (occurring primarily at the margins of the torn cusp), moderate in two, and severe in one. Tissue overgrowth (pannus) was seen in all but three prostheses. Like its predecessor, the Ionescu-Shiley standard pericardial valve, this prosthesis failed at 2 to 5 years largely due to design-related (alignment stitch) causes and tissue degeneration. Calcification was less prominent, while tissue overgrowth (pannus) was more marked.

Adult↗
PubMed1992

Delayed rupture of spontaneous tear of the ascending aorta--report of two fatalities.

A spontaneous tear of the ascending aorta, with or without medial dissection, can cause sudden death from hemorrhage due to aortic rupture. Two representative cases are described. Review of the clinical history and pathological changes showed that the terminal event was delayed allowing healing and reactive changes to occur in the aortic wall. A pathologist confronted with a fatal case of aortic rupture should be aware that death is not always immediate. Recognition of this has medicolegal importance, particularly if medical management is questioned because of a missed clinical diagnosis.

Aortic Rupture↗
PubMed1992

'Hemorrhagic' and microvascular phenomena within the arterial wall.

OBJECTIVE: To study microvasculature and hemorrhage within the arterial wall. DESIGN: Human autopsy specimens of the arch of the aorta, the carotid, brachiocephalic, subclavian and coronary arteries perfused with liquid casting material and maintained at physiological pressure until the material had set. MAIN RESULTS: Evidence of dense microvasculature and other phenomena which have the morphological appearance of 'hemorrhage' within the arterial wall, coupled with calcified matter and other impressions made on the cast by atherosclerotic plaques. CONCLUSIONS: The findings lend support to suggestions in the literature that neovascularization may play a role in the pathogenesis of coronary atherosclerosis and its sequelae, that hemorrhage into the intima may be due to rupture of capillaries which are derived from the coronary lumen, and that an increase in microvasculature occurs in the immediate vicinity of localized atherosclerotic lesions.

Coronary Artery Disease↗
PubMed1992

Altered distribution of desmin filaments in hypertrophic cardiomyopathy: an immunohistochemical study.

Hypertrophic cardiomyopathy (HCM) is characterized by myofiber hypertrophy and disarray. Intermediate filaments play an important role in maintaining of normal cell shape. Desmin filaments have been detected in adult cardiomyocytes, and vimentin and keratin filaments in cardiomyocytes during embryonic development. The pattern of arrangement of intermediate filaments in HCM has not been reported. We examined the distribution of intermediate filaments in formalin-fixed tissue sections of the disarrayed myofibers from 10 hearts with HCM using an immunohistochemical technique and antibodies to desmin, vimentin, and high and low molecular weight keratins. The controls consisted of subaortic tissue from surgically explanted hearts of patients with ischemic heart disease. In the ischemic hearts, desmin was detected in the Z bands and intercalated disks. In all HCM cases, three patterns of staining for desmin were noted: (a) individual myocytes showing a parallel arrangement along Z bands; (b) focal myofibers with decreased or complete loss of labeling of Z bands; and (c) individual myocytes with intense granular cytoplasmic staining especially in disarrayed myofibers. No staining for vimentin or keratins was noted in the cardiomyocytes from either the HCM or ischemic cases. The altered arrangement of desmin filaments in the disarrayed cardiac muscle fibers may play a role in the altered contractility that occurs in patients with HCM.

Adult↗
PubMed1992

Right ventricular dysplasia: morphological findings in 13 cases.

OBJECTIVE: To characterize the pathological features of right ventricular dysplasia (RVD). DESIGN: Retrospective morphological case study. SETTING: Three referral-based university medical centres. PATIENTS: Thirteen subjects (one female) aged 16 to 55 years including 10 necropsy hearts from sudden deaths out of hospital, one explant heart and two partial right ventricular resections from patients with intractable ventricular tachycardia. MAIN RESULTS: Most hearts showed hypertrophy and localized or generalized dilatation of the right ventricle. Transillumination revealed myocardial thinning of variable configuration usually conforming to regions of dilatation. Common sites of involvement were apex, infundibular region and posterobasal wall. Histologically, focal or extensive segments of right ventricular myocardium were absent or replaced. Three patterns were found: right ventricle markedly thinned, epicardium and endocardium contiguous, virtually no intervening tissue; wall normal thickness or thinned, myocardium almost totally replaced by fat; and wall normal or thin, myocardium largely replaced by fat with scattered residual myocardial cells and fibrous tissue (the predominant pattern). Endocardial fibrosis was present in eight cases and focal mononuclear cell infiltrates in 10. Electron microscopy in two cases showed nonspecific findings. CONCLUSIONS: RVD has gross and microscopic features which permit its recognition. While a majority of cases are likely congenital (genetic or acquired in utero), the possibility of postnatally acquired conditions (inflammatory, toxic, ischemic) inducing RVD must be explored. The incidence and importance of RVD as a cause of sudden death can only be assessed by continued systematic and detailed studies of patients with recurrent ventricular tachycardia and of hearts, especially from sudden death victims. Although uncommon, RVD should be considered in the differential diagnosis of arrhythmia and sudden death by both clinicians and pathologists.

Adolescent↗
PubMed1990

Pulmonary arterial dissections and ruptures: to be considered in patients with pulmonary arterial hypertension presenting with cardiogenic shock or sudden death.

Four unusual cases of sudden death due to pulmonary arterial hypertension complicated by dissection and/or rupture of the main pulmonary artery are reported. The patients, 3 males and 1 female, ranged from 17 to 77 years old. Each had chronic pulmonary arterial hypertension, marked pulmonary arterial dilation and degenerative medial changes of the large elastic pulmonary arteries. The first patient had a partial thickness tear of the main pulmonary artery with local dissection without external rupture and died of shock. The other three patients died after external rupture of the main pulmonary artery, based on a full thickness tear in one case, a small dissection in another and extensive dissection in the third. In the setting of pulmonary arterial hypertension, dissection, rupture, or dissection and rupture of the pulmonary artery should be considered in the differential diagnosis when patients present in cardiogenic shock or with sudden death.

Adolescent↗
PubMed1989

Autonomic and myocardial changes in middle cerebral artery occlusion: stroke models in the rat.

Stroke models in larger animals such as the cat, dog and monkey are becoming increasingly more expensive and less readily available. However, the rat is an excellent model for focal cerebral ischemia. Rats are readily available, inexpensive and their neuroanatomy and brain function have been studied extensively. Increases in plasma catecholamines and myocardial damage have been observed in clinical stroke. We examined autonomic and myocardial changes in two rat stroke models. In one model only the middle cerebral artery was occluded (MCAO) while the other model involved occlusion of both the MCA and the common carotid artery (MCAO/CCAO). Arterial blood pressure and heart rate were monitored continuously in 25 male rats (326-430 g) that underwent one of the following procedures: (1) MCAO only; (2) MCAO/CCAO; (3) CCAO only; and (4) sham occlusions (SHAM). Arterial blood samples (0.5 ml) for radioenzymatic assay of norepinephrine (NE) and epinephrine (E) were taken twice before the occlusions and at 90 and 180 min after the occlusions. The animals were perfused at the end of the experiment and the heart removed and examined histologically. Tetrazolium salts were reacted with oxidative enzymes to delineate the region of inadequate perfusion. The mean blood pressure and pulse pressure of the SHAM, MCAO/CCAO and CCAO groups significantly declined from initial values (from an average of 78 to 53 mm Hg) during the course of the experiment. However, the mean blood pressure and pulse pressure of the MCAO rats did not change during the experiment, so that the final mean blood pressure and pulse pressure were significantly higher than in the other 3 groups. The levels of both NE and E increased significantly (NE, 1443 +/- 285.9 to 4095 +/- 929 pg/ml; E, 2402 +/- 623 to 3741 +/- 1166 pg/ml) following occlusion in the MCAO group only while the other 3 groups did not change. Four of 6 hearts in the MCAO group were abnormal, showing evidence of subendocardial hemorrhage, ischemic damage or subendocardial congestion. MCAO also resulted in a consistent region of the brain with inadequate perfusion including the insular cortex. These autonomic and myocardial changes appear to mimic some of the changes seen clinically in stroke patients and provide the first acute stroke model for studying autonomic dysfunction in the rat.

Animals↗
PubMed1989

An improved method for detecting and quantifying cardiac muscle disarray in hypertrophic cardiomyopathy.

The presence of muscle disarray in hypertrophic cardiomyopathy (HC), although well established, has only been semiquantitatively assessed. A quantitative method that uses polarized light microscopy is described. Hematoxylin and eosin-stained sections of ventricular septa from six HC patients and six normal hearts were examined. Cell orientations were measured in five regions from each section using a polarizing microscope with a rotating stage. Histograms of cell orientation angles were plotted and the mean and angular deviation of each sample were calculated. In normal hearts, cells were predominantly aligned parallel to each other. Orientation distributions were sharply peaked, with angular deviations ranging from 4 to 13 degrees. For HC, the sharp peak was lacking and angular deviations varied from 7 to 37 degrees; some distributions were bimodal. Areas in HC septa that appeared normal by gross inspection had abnormal orientation distributions. Polarized light microscopy provides an improved method of detecting and quantifying cellular disorganization in HC.

Cardiomyopathy, Hypertrophic↗
PubMed1988

Pathology of prosthetic cardiac valves.

Heart valve prostheses (HVPs) have been inserted for more than 25 years. That period has witnessed a remarkable evolution and growing sophistication in the diagnosis of valvular heart disease--in anesthetic, perfusion, and operative techniques and in the management of the postoperative patient. As a result, operative mortality related to single valve replacement is in the 3-5% range. Also, the quarter century has seen prosthesis design improve and the introduction of new materials used in their manufacture. The net result is that an individual needing a heart valve replacement now has a better chance both of surviving and of enjoying a prolonged life relatively free of complications related to the prosthesis.

Heart Rupture↗
PubMed1988

Correlation of morphological variables in the coronary atherosclerotic plaque with clinical patterns of ischemic heart disease.

The frequency and severity of "morphological" variables (fibrosis, proteoglycan accumulation, atheroma, intimal vascularization, calcification, acute intimal hemorrhage, and both adventitial and intimal lymphoplasmacellular infiltrates) in atherosclerotic plaques were related to plaque type, percentage of lumen reduction, plaque length, and intimal and medial thickness in 3,640 coronary artery sections sampled at the site of maximal lumen reduction in 8 selected segments from 100 cases of acute myocardial infarct, 50 of chronic angina, 208 of unexpected sudden coronary death with or without prodromata, and from 97 normal subjects dying accidentally. Morphological variables were occasionally observed in 1,519 sections with no lumen reduction. They were found only in sections from ischemic patients. With increasing luminal stenosis and intimal thickness, progression of the coronary plaque seemed to start as a fibrous change followed by proteoglycan accumulation in the deeper portion of the fibrous intima. Proteoglycan deposits appeared as a recurrent phenomenon. In them, atheroma or calcification develop. Intimal hemorrhage was a less frequent variable. It was found mainly in a vessel supplying an infarcted area. Lymphoplasmacellular inflammation correlated mainly with proteoglycan accumulation and atheroma, both showing a parallel increase with increasing intimal thickness and lumen reduction. No correlation was found between plaque variables and sex, age, heart weight, and infarct size. Significant variations in the distribution of plaque variables were observed among hearts of patients in the ischemic groups and between them and controls. In particular, inflammatory reaction was significantly more frequent and severe in ischemic groups than in controls, independent of the degree of coronary stenosis. Coagulative myocytolysis (contraction band necrosis), found in the majority of ischemic patients, correlated with the inflammatory reaction in supplying vessels. A peculiar tropism of mononuclear cell infiltrates for adventitial nerve structures was found. As a result, we question whether this inflammation may trigger coronary spasm and/or coagulative myocytolysis ("active" plaque vs "inactive" plaque).

Arteries↗