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Biomedical subjects

A E Becker

Publications and source records attributed to A E Becker.

At least 19 recordsLinked to original sources
PubMed1992

An immunocytochemical analysis of rapidly progressive atherosclerosis in human vein grafts.

Aortocoronary vein grafts are known to develop atherosclerotic plaques usually superimposed on intimal hyperplasia. The cellular characteristics of these lesions have been studied with immune cytochemical techniques and compared with those in native coronary arteries. Fifteen stenosed grafts showed concentric intimal hyperplasia characterized by massive proliferation of smooth muscle cells (HHF-35+). The subendothelial layer contained numerous T lymphocytes (UCHL-1+, MT-1+) and to a lesser extent macrophages (HAM-56+). Eleven grafts had superimposed atherosclerotic plaques characterized by atheroma but otherwise showing the same cellular constituents. The atherosclerotic plaques in the venous grafts resembled those in the coronary arteries, the main difference being the occurrence of multiple atheromas (up to 4 in a single section), the high number of T lymphocytes and macrophages related to these sites and the presence of atheromas bordering directly onto the luminal surface. It thus appears that the development of atherosclerotic plaques in vein grafts is accompanied by a similar immune inflammatory reaction as in native coronary atherosclerosis, presumably in a more aggravated form. The latter phenomenon could relate to the more enhanced and rapidly progressive nature of vein graft atherosclerosis.

Arteriosclerosis↗
PubMed1992

Aortic valve regurgitation and the congenitally bicuspid aortic valve: a clinico-pathological correlation.

OBJECTIVE: To investigate the morphology of congenitally bicuspid aortic valves causing pure valve regurgitation. DESIGN: A case series collected over five years. SETTING: An academic hospital. PATIENTS AND METHODS: One hundred and forty eight excised congenitally bicuspid aortic valves. The morphological findings were correlated with sex, age, clinical history, and data on haemodynamic function before operation. Pure valve regurgitation was defined as grade 3-4/4 with a gradient less than 30 mm Hg. Aortic root dilatation was evaluated angiographically or echocardiographically or both. RESULTS: Three types were recognised: valves that were purely bicuspid (23%), bicuspid valves with a raphe (34%), and valves with an additional indentation of the free edge of the conjoined cusp (43%). In 14 cases pure valve regurgitation was present. Dilatation of the aortic root was present in 47 cases. The relative risk for regurgitation when the aortic root was dilated (compared with no dilatation) was 3.99. The relative risk for valve regurgitation when there was indentation of the conjoined cusp (compared with no indentation) was 4.95. The mean age at operation in patients with pure regurgitation was 56 years, which is significantly younger (p = 0.0008) than that of patients with a congenitally bicuspid valve with combined valve stenosis and regurgitation (64.7 years). CONCLUSIONS: Congenitally bicuspid aortic valves with a central indentation of the free edge of the conjoined cusp seem particularly likely to develop pure aortic valve regurgitation.

Adult↗
PubMed1992

Adhesion molecules on the endothelium and mononuclear cells in human atherosclerotic lesions.

Atherosclerotic lesions show features of a cell-mediated immune inflammatory process. From this viewpoint, the potential role of arterial endothelium in the recruitment of mononuclear cells (T lymphocytes and macrophages) was studied. The endothelium of diffuse intimal thickening (DIT) and atheromatous plaques (AP) in human coronary arteries and abdominal aortas was characterized for the expression of adhesion molecules ELAM-1, ICAM-1, and the major histocompatibility complex (MHC) class II antigens HLA-DR/DP. A marked increase in expression of ICAM-1 and ELAM-1, and to a lesser extent HLA-DR/DP was observed on endothelial cells that were adjacent to subendothelial infiltrates of T lymphocytes (CD3+, CD11a+, HLA-DR/DP+) and macrophages (CD14+, CD11a+, CD11c+, HLA-DR/DP+). This contrasted with a lower or absent expression of these activation markers at sites without prominent inflammatory cell infiltrates. These findings could be demonstrated in DIT as well as in AP. The observations suggest that cytokines produced by the subintimal infiltrates may activate the endothelium in a similar way as is observed in the microvasculature at sites of immune inflammation. The expression of these activation markers in the microvasculature is associated with enhanced leukocyte adhesion, permeability for macromolecules, and procoagulant activity, features known to occur also in early experimental atherosclerosis. The findings therefore support the concept that arterial endothelium plays an active role in the recruitment of mononuclear cells in atherosclerotic lesions.

Adult↗
PubMed1992

Macrophage differentiation in atherosclerosis. An in situ immunohistochemical analysis in humans.

The differentiation of macrophages present in diffuse intimal thickening, fatty streaks, and atheromatous plaques, was analyzed with immunohistochemical methods, using segments of aorta, coronary, and carotid arteries obtained at autopsy. Various differentiation antigens were studied with the monoclonal antibodies anti-HLA-DR, EBM-11, Leu M3, OKM1, and OKM5. Adjacent sections were stained for lipids (oil red O) and lysosomal activity (acid phosphatase). Almost all macrophages identified with the pan-macrophage antibody EBM-11, also stained with the anti-HLA-DR antibody. Diffuse intimal thickening showed a predominance of Leu M3+ cells; fatty streaks also showed OKM1+ and OKM5+ macrophages. Classical atheromatous plaques showed a gradual shift in phenotypic expression towards the center of the lesion. Cells in the superficial layers were positive only with Leu M3, deeper localized cells showed double expression of Leu M3 and OKM1 or double expression of OKM1 and OKM5. Cells that were localized adjacent to the atheromatous debris stained only with OKM5. The phenotypic changes occurred in parallel with an increase in both fat uptake and lysosomal activity of the macrophages. This shift in phenotypic expression suggests a process of differentiation and maturation of the macrophages involved. The results indicate that macrophages within the arterial intima are activated and mature towards cells that express receptors for adhesion proteins and complement during the development of atherosclerotic plaques. This may imply that the macrophages involved in lipid metabolism also have a potential to act as effector cells in a chronic inflammatory process, and thus, may contribute to the progression of an atherosclerotic plaque. Functional studies of macrophage subpopulations are needed to verify this hypothesis.

Acid Phosphatase↗
PubMed1991

Chronic non-ischaemic congestive heart disease and endomyocardial biopsies. Worth the extra?

The diagnostic yield of endomyocardial biopsies in patients with chronic congestive heart failure of non-ischaemic aetiology remains questionable and, therefore, the use of endomyocardial biopsies under such circumstances is at stake. The present report documents the correlation between the histologic interpretation of endomyocardial biopsies and the corresponding cardiac explants in 13 patients who underwent cardiac transplantation. The biopsy diagnoses in these patients varied from 'compatible with dilated cardiomyopathy' (n = 6) to 'non-conclusive' (n = 4), 'ischaemia' (n = 2) and 'borderline myocarditis' (n = 1). Correlation with the corresponding cardiac explants revealed hypertrophy of myocytes as the leading histologic feature in the majority of cases. Because of the non-specific histopathology of dilated cardiomyopathy, the discrepancy between biopsy diagnoses and the leading explant diagnosis is mostly a matter of semantics. Ischaemia was present at high incidence, but is considered a result of imparied myocardial perfusion rather than the prime mechanism of heart failure. In four cardiac explants myocarditis was encountered, while the corresponding biopsies showed no cellular inflammation. In two, the cellular infiltrates suggested an early state of repair. One heart contained an active and extensive lymphocytic myocarditis. The fourth case showed an eosinophilic myocarditis, most likely acquired after the biopsy was taken. These discrepancies almost certainly relate to the sampling error and the time interval between biopsy and onset of symptoms. The immediate diagnostic yield of the biopsy, in this particular subset of patients, was minimal, particularly with respect to the diagnosis 'myocarditis'. Nevertheless, biopsy diagnoses such as 'compatible with' and 'non-conclusive' do contribute to the final categorization and management of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

In vitro balloon dilatation of mitral valve stenosis: the importance of subvalvar involvement as a cause of mitral valve insufficiency.

To investigate the mechanism that increases the orifice area of the mitral valve during balloon dilatation 43 surgically excised intact rheumatic mitral valves were studied. The main pathological features were (a) fibrosis of mitral valve leaflets and commissures (10 valves); (b) fibrosis with calcification of one commissure (eight anterolateral, seven posteromedial); (c) fibrosis with calcification of both commissures (seven valves); and (d) predominant involvement of the subvalvar apparatus (11 valves). The valves were assessed by photography and radiography before and after balloon dilatation (balloons up to 38 mm (bifoil 2 x 19 mm) and pressures up to 4 atmospheres). The valve was dilated in stages under direct visual control by balloons of increasing diameter. Splitting of the fused commissures was the most common mode of widening the orifice. However, the mitral valve leaflets were torn in two fibrotic valves and in six valves with extensive involvement of the subvalvar apparatus. In the fibrotic valves (group (a] the tear originated near the valve perimeter, at the thinnest part of the remaining valve leaflet. In the valves with subvalvar involvement splitting started at the apex of spaces between the fused chordal columns and proceeded upward. Where there is extensive involvement of the subvalvar apparatus in rheumatic mitral valve disease the risk of tearing of the valve leaflets by balloon dilatation is increased and this is likely to predispose to the development of acute valvar insufficiency.

Calcinosis↗
PubMed1991

Fibrocellular tissue response after percutaneous transluminal coronary angioplasty. An immunocytochemical analysis of the cellular composition.

BACKGROUND: Restenosis after initial, successful percutaneous transluminal coronary angioplasty (PTCA) is due to fibrocellular proliferation. METHODS AND RESULTS: The present study focused on the nature of fibrocellular tissue in humans by use of immunocytochemical techniques. Four hearts (five coronary arteries) were investigated; time lapse between PTCA and death varied between 20 days (two arteries) and 1 year 7 months. Proliferating cells stained positive with smooth muscle cell-specific monoclonal antibodies. Cells from early proliferative lesions (20 days) have a phenotypic expression different from cells in "old" lesions. Proliferating cells stained positive with vimentin but were negative with desmin, irrespective of the lesion's age. CONCLUSIONS: The findings indicate a change in actin isoform expression of smooth muscle cells while adapting to a pathological state.

Actins↗
PubMed1991

The early phenomena of restenosis following percutaneous transluminal coronary angioplasty.

In man the early onset of fibrocellular tissue reaction, which leads to restenosis following an initial successful percutaneous transluminal coronary angioplasty, has been poorly documented because of limited opportunities to study this phenomenon. The present study focused on early changes in seven patients who died within 20 days of a percutaneous transluminal coronary angioplasty procedure. Differences in the mode of laceration were noted between concentric and eccentric plaques. In the former, tears occur at the thinnest site of the plaque or within an already attenuated fibrous cap. The injury usually remains limited to the plaque. In eccentric lesions lacerations tend to occur in the non-atherosclerotic wall segment, affecting the musculoelastic layers and the media. A further site of predilection is the border zone between the non-affected wall and the plaque. Early tissue response is characterized by fibrin-platelet depositions, and a proliferation of macrophages and spindle-shaped cells. The latter express the immunocytochemical characteristics of smooth muscle cells. However, differences occur according to the type of tissue injured. Laceration of the musculoelastic layers or media causes a rapid and extensive cellular response. Injury to an atheroma, on the other hand, mainly causes plaque fissures with either mural thrombosis and total luminal obstruction, extensive plaque haemorrhage or a 'wash-out' of the atheromatous debris. In the latter case the lining of the 'crater' shows an accumulation of macrophages and, once more, a proliferation of spindle-shaped cells. The present observations support the concept that the early response is due to an interaction of platelet-fibrin thrombus and smooth muscle cells, with a possible role for macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Morphology of pulmonary atresia with intact ventricular septum in patients dying after operation.

In 1976, we adopted staged surgical management of pulmonary atresia with intact ventricular septum: stage 1 = establishment of a systemic to pulmonary artery shunt; stage 2 = open reconstruction of the right ventricular outflow tract and pulmonary valve; and stage 3 = closure of the shunt and interatrial communication. The morphological features of nine specimens obtained from 10 patients who died were reviewed. Special attention was given to features that might have influenced the poor surgical outcome in these patients. Survival after stage 1 depends on adequate systemic to pulmonary artery blood flow, initially as a combination of ductus arteriosus and shunt flow, with subsequent modification if the ductus closes. After stage 2, survival is influenced by left ventricular function and mitral valve function. The success of final correction (stage 3) depends largely on the morphology of both ventricles and their atrioventricular valves. It appears that the behavior of the ductus arteriosus and the size of the shunt are of vital importance for the survival of the infant. In 3 of the specimens, no right ventricular outflow tract was present, and in 2 others, short chordal attachments of the mitral valve were observed. Staged surgical correction appears to be a satisfactory approach if these considerations are taken into account.

Aorta, Thoracic↗
PubMed1990

Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers.

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

Cardiac Pacing, Artificial↗
PubMed1990

Renal angiomyolipomas: could the histology serve as a marker for tuberous sclerosis?

The histological features of 43 renal angiomyolipomas were studied in an attempt to evaluate whether the isolated forms and those that present as part of the tuberous sclerosis complex can be distinguished. In two patients the mass was classified as an angioleiomyoma, because no adipose tissue was present. All renal angiomyolipomas showed the same basic histological picture. The combined forms, however, showed additional features such as extension into pre-existent renal parenchyma, scattered foci of hamartomatous lesions, calcified spicules and tubular inclusions. The findings suggest that these features, in an otherwise classical angiomyolipoma, should alert the pathologist to the possibility of tuberous sclerosis.

Biomarkers↗
PubMed1990

Congenitally corrected transposition with normally positioned atria, straddling mitral valve, and isolated posterior atrioventricular node and bundle.

A heart is described with congenitally corrected transposition of the great arteries, normally positioned atria, and a straddling mitral valve. Instead of an anteriorly positioned atrioventricular node, a regularly positioned posterior node and bundle were observed. This observation has important clinical and surgical implications and underlines that close inspection of the alignment of atrial and ventricular septa during operations is mandatory.

Atrioventricular Node↗