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Biomedical subjects

V J Ferrans

Publications and source records attributed to V J Ferrans.

At least 379 records · Page 21Linked to original sources
PubMed1976

Spherical microparticles in human myocardium: an ultrastructural study.

Clusters of spherical microparticles (SMP) that averaged 500 A in diameter and were composed of dense cores surrounded by single trilaminar membranes were found in operatively obtained myocardial biopsies from 29 of 70 patients with various types of heart diseases including: left atrial myocardium (14 patients) and right atrial myocardium (four patients) of 14 patients with mitral valvular disease; left ventricular myocardium of three of 16 patients with aortic valvular disease, three of 16 patients with hypertrophic cardiomyopathy, and two of four patients with combined mitral and aortic valvular disease; and crista supraventricularis muscle of seven of 20 patients with congenital heart diseases associated with muscular obstruction to right ventricular outflow. SMP were consistently associated with interstitial fibrosis and with degeneration of the muscle cells. SMP occurred along the outer surfaces on the sides and free ends of muscle cells in areas of fibrosis, in the widened spaces between membranes of partially dissociated intercellular junctions, and within cytoplasmic vesicles considered to be phagocytic. SMP frequently were joined together by minute nexuses that were structurally identical with those forming parts of intercellular junctions of muscle cells. Evidence is presented to show that SMP occur commonly in tissues other than myocardium. It is concluded that SMP form in the heart as part of a process that mediates the remodeling of cellular surfaces, especially those of intercellular junctions undergoing dissociation.

Cardiomegaly↗
PubMed1976

Intracellular collagen fibrils in prolapsed ("floppy") human atrioventricular valves.

Ultrastructural study of prolapsed atrioventricular valves from five patients, one of whom also had the Marfan syndrome, disclosed granular cells that were characterized by numerous membrane-bound, electron-dense inclusions resembling those in the Hurler syndrome. Collagen fibrils were present within some of these inclusions. The intracellular collagen deposits may form as a consequence of abnormal interactions between newly secreted collagen and acid mucopolysaccharides.

Adolescent↗
PubMed1976

Ultrastructural alterations in skeletal muscle of pigs with selenium-vitamin E deficiency.

Light and electron microscopic studies were made of lesions which developed in skeletal muscles of 24 of 38 young growing pigs fed a semisynthetic diet deficient in selenium and vitamin E for 13 to 59 days. The major alterations in injured fibers progressed from hyaline degeneration, with subsequent macrophagic invasion and phagocytosis of disrupted sarcoplasm, to muscle fiber regeneration by myoblastic proliferation, fusion, and differentiation into fibers with mature myofibrils. The earliest electron microscopic alterations were myofibrillar lysis and disruption, with thick filaments persisting longest. Disruption of mitochondria, sarcoplasmic reticulum, and plasma membranes occurred in fibers with myofibrillar alterations. The basal lamina of the sarcolemma remained after destruction of the enclosed sarcoplasm and served as a scaffold for subsequent regeneration. Stages of regeneration included myoblastic proliferation, fusion into cords and myotubes, and, finally, fibrillogenesis to restore contractile material. The sequence of structural alterations in skeletal muscles of these affected pigs was discussed in terms of present theories of the biochemical role of these nutrients in maintaining cellular integrity.

Animals↗
PubMed1976

Ultrastructural changes in skeletal muscle of selenium-vitamin E-deficient chicks.

Chicks fed a semisynthetic basal diet deficient in selenium and vitamin E for 14 to 22 days developed skeletal myodegeneration and exudative diathesis. Chicks fed the basal diet supplemented with either 0.2 ppm of selenium (as selenite) or 100 IU alpha-tocopherol acetate/kg were protected from deficiency disease, but chicks fed the basal diet plus 0.4% L-cystine were not protected. Pectoral muscles of deficient chicks were red and edematous. Light and electron microscopic study of affected muscles revealed fibers with hyaline and granular degeneration. In hyalinized fibers, the initial ultrastructural alterations were increased density of the sarcoplasm and myofibrils, dilatation of sarcoplasmic reticulum, formation of subsarcolemmal vacuoles, and disruption of mitochondrial membranes. In later stages, alterations in these fibers included myofibrillar disruption and lysis, nuclear pyknosis and lysis, disruption of the plasma membrane with persistence of basal lamina and scattered adhering satellite cells, and eventual invasion by macrophages. In fibers with granular degeneration, the ultrastructural observations included decreased density of the sarcoplasm, prominent mitochondrial swelling and distortion, and multiple foci of myofibrillar lysis that eventually coalesced to produce generalized lysis. Prominent vascular lesions associated with exudative diathesis were present in degenerated muscle but were not considered to precede development of fiber alterations. Affected blood vessels had endothelial cells with mitochondrial damage and accumulations of cytoplasmic dense bodies and areas of endothelial disruption with adhering fibrin thrombi.

Animals↗
PubMed1976

Striated membranous structures in human hearts. An ultrastructural study.

Straited membranous structures (SMS), which consisted of sheets or ribbons of 130 to 220 A in thickness, showed variable patterns of periodic substructure, and resembled SMS described in renal and ocular tissues in various diseases, were found in extracellular locations in a) mitral valve (2 patients) and tricuspid valve (1 patient) of 2 patients with mitral valvular prolapse, b) mitral valve and femoral artery of 1 patient with Marfan's syndrome and prolapsed mitral valve, and c) myocardium (2 patients) and thickened endocardium (3 patients) of 3 patients with congenital heart disease associated with muscular obstruction to right ventricular outflow. Striated membranous structures measured up to several microns in diameter, often were highly folded and convoluted, and sometimes appeared circular in outline. Some SMS measured from 130 to 150 A in thickness and had indistinct edges and poorly defined periodicity. The majority of SMS, however, had greater thicknesses, in the range of 200 A, and a periodicity characterized by alternating light and dark bands with a spacing that varied from 100 to 160 A. The structures were associated with thickened basement membranes, elastic fibers, and membrane-bound bodies of the type thought to be involved in elastogenesis. Evidence available suggests that SMS results from an unusual pattern of arrangement of a component, possibly Type IV collagen, of basement membrane material.

Adolescent↗
PubMed1975

Myocardial ultrastructure in patients with chronic aortic valve disease.

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severly degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.

Adolescent↗
PubMed1975

Morphological methods for evaluation of myocardial protection.

A review is presented of histological, histochemical, and electron microscopical methods considered useful in the morphological evaluation of intraoperative myocardial protection. Transmural samples of myocardium should be studied since the response of the ventricular walls to ischemic injury is not homogeneous. Collection of samples should be continued until the injury reaches a stable end-point. Emphasis is placed on the fact that ischemic injury is modified considerably by reflow phenomena. Ultrastructural studies are indispensable and histological methods are of limited value in the morphological evaluation of early myocardial injury.

Animals↗
PubMed1975

Ultrastructure of crista supraventricularis muscle in patients with congenital heart diseases associated with right ventricular outflow tract obstruction.

Ultrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, or whom 54 had obstruction to right ventricular outflow. Relationships of anatomic diagnosis, age, peripheral arterial oxygen saturation (PAO2), peak right ventricular systolic pressure gradient and right ventricular end-diastolic pressure (RVEDP) to hypertrophic changes, abnormalities of cellular and myofibrillar orientation, and degenerative alterations were determined. Changes directly related to hypertrophy were: cell diameters greater than 20 mu, irregular cell shape, lobulated nuclei, multiple intercalated discs, dilated T tubules, abnormal Z bands, and increased numbers of ribosomes. Abnormalities of cellular or myofibrillar orientation were focal in distribution and occurred in 12 patients, most of whom had elevated RVEDP, decreased PAO2, markedly enlarged cells, and interstitial fibrosis. Interstitial fibrosis was prominent in 19 patients and was associated with cellular hypertrophy, elevation of RVEDP, and increased age of the patients. Degenerative changes (myofibrillar lysis, abnormally small mitochondria, myelin figure formation, and proliferation of sarcoplasmic reticulum in cardiac muscle cells ocurred in six patients and correlated with increased age, decreased PAO2, and elevated RVEDP. Mitochondria containing glycogen deposits were present in 17 patients, most of whom had decreased PAO2. The variability of morphologic manifestations of chronic cardiac hypertrophy and the relationships of hypertrophic changes to orientation abnormalities and degenerative alterations are discussed.

Adolescent↗
PubMed1975

Congenital heart malformations associated with disproportionate ventricular septal thickening.

Asymmetric septal hypertrophy, or ASH, is a genetically determined myocardial disorder that is transmitted as an autosomal dominant trait. ASH is characterized by a disproportionately thickened ventricular septum that contains numerous hypertrophied, bizarrely-shaped and disorganized cardiac muscle cells. Disproportionate hypertrophy of the ventricular septum has also been observed in association with certain congenital cardiac malformations. To determine whether such congenital cardiac malformations are part of the disease spectrum of genetically determined ASH, cardiac pathologic observations were made in eight patients with disproportionate septal thickening (ventricular septal to posterobasal left ventricular free wall thickness ratios of 1.5 to 2.5) and the following three categories of associated lesions: 1) parachute deformity of the mitral valve (occurring either as an isolated lesion or with ventricular septal defect, coarctation of the aorta, supravalvular ring of the left atrium, or double outlet right ventricle); 2) complete interruption of the aortic arch; and 3) ventricular septal defect. The arrangement of cardiac muscle cells in the disproportionately thickened ventricular septum was normal in six of the eight patients; in the other two patients (one with parachute deformity of the mitral valve and one with ventricular septal defect) numerous bundles of hypertrophied cardiac muscle cells were interlaced in a disorganized fashion among more normally arranged bundles of cells. First degree relatives of six of the eight patients were studied by echocardiography and found to have normal ventricular wall thicknesses and septal-free wall ratios. It is concluded that disproportionate ventricular septal thickening may occur in patients with a variety of congenital heart malformations, but that such a finding is not necessarily a manifestation of the disease spectrum of genetically determined ASH.

Adult↗
PubMed1975

Endocardial papillary elastofibromas. Histologic, histochemical, and electron microscopical findings.

The organization of cellular and extracellular components appeared similar and was distinctive in three endocardial papillary elastofibromas studied. Each tumor papilla contained (1) a dense, central core of collagen and elastic tissue, (2) a peripheral, myxomatous layer with deposits of acid mucopolysaccharides, and (3) an overlying, hyperplastic layer of endothelial cells. Ultrastructural study of one tumor showed that the cells in all three zones had numerous cytoplasmic filaments, 100 Angstroms in diameter, and dilated cisterns of endoplasmic reticulum; endothelial cells also had intercellular junctions and numerous pinocytotic vesicles. The myxomatous stroma varied from amorphous to fibrillar, and the collagenous cores showed focal degeneration. The name "endocardial papillary elastofibroma" is suggested to emphasize those features which are most conspicuous and which serve to differentiate this tumor from myxoma.

Endocardium↗
PubMed1975

Myofibrillar abnormalities following cardiac muscle cell injury.

A review is presented of morphological aspects of myofibrillar alterations which occur in cardiac muscle cells following various types of injury. Emphasis is placed on the association between specific patterns of alterations involving the structure or the orientation of myofibrils and diverse forms of myocardial injury.

Cardiomyopathies↗
PubMed1975

Myocardial injury produced by antineoplastic drugs.

Histologic and ultrastructural studies were performed on the heart of 16 patients with fatal leukemias or solid tumors. Multifocal myocardial degenerative lesions, characterized by alterations in contractile elements, mitochondria, and nuclei, were found in 12 patients treated with high total doses of anthracyclines, but not in 3 patients who did receive such therapy. One patient who received a high dose of cyclophosphamide as well as a high total dose of daunorubicin exhibited extensive hemorrhagic myocardial necrosis and multifocal degenerative lesions. This study documents the cardiotoxic effects of anthracyclines and cyclophosphamide.

Cell Nucleus↗
PubMed1975

Pathologic anatomy of the cardiomyopathies. Idiopathic dilated and hypertrophic types, infiltrative types, and endomyocardial disease with and without eosinophilia.

This presentation summarizes necropsy observations in patients with three types of cardiomyopathy: idiopathic, infiltrative, and endomyocardial disease. The idiopathic variety is subdivided into two types depending on the size of the ventricular cavity. In the dilated ventricular type the left ventricular wall is frequently less than 1.5 cm. thick, intracardiac thrombi are common, the atrioventricular valve rings usually are mildly dilated, and focal myocardial and endocardial scars are common. In the nondilated type (hypertrophic cardiomyopathy), the ventricular septum is usually thicker than the left ventricular free wall, which also is thick (greater than 1.5 cm.). When the septum is similar in thickness to the left ventricular free wall (symmetric), left ventricular outflow obstruction does not occur. When the septum is thicker than the left ventricular free wall (asymmetric), left or right ventricular outflow obstruction may or may not be present. The orientation of myocardial fibers one to another in the ventricular septum in the nondilated (hypertrophic) type is abnormal, whereas it is normal in the dilated ventricular type. Intracardiac thrombi are rare and atrioventricular valve rings are never dilated in the nondilated type of idiopathic cardiomegaly. The infiltrative types of cardiomyopathies include iron, calcium, lipids, mucopolysaccharides, granulomas, amyloid, and neoplasms. The first four usually are located within myocardial cells and the latter three, between myocardial cells. It is probable that all these myocardial infiltrates are capable of producing cardiac dysfunction, primarily on a restrictive basis. Endomyocardial disease may or may not be associated with eosinophilia. When the latter occurs, the eosinophils are structurally normal. Death is related to congestive cardiac failure. This category is actuality also in idiopathic.

Adolescent↗
PubMed1975

Ultrastructural features of degenerated cardiac muscle cells in patients with cardiac hypertrophy.

Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.

Adolescent↗