Biomedical subjects

R Virmani

Publications and source records attributed to R Virmani.

At least 145 records · Page 8Linked to original sources

PubMed1995

Localized vasculitis of the gastrointestinal tract.

We studied the clinical and pathologic findings of 63 patients with localized vasculitis of the gastrointestinal tract, including 35 partial bowel resections, 14 cholecystectomies, five partial pancreatectomies, six appendectomies, one omentectomy, one gastrectomy, and one esophagectomy. Vasculitis was classified histologically as polyarteritis (n = 33), phlebitis (n = 12), Churg-Strauss angiitis (n = 8), small-vessel vasculitis (n = 6), Buerger's disease (n = 2), and giant-cell arteritis (n = 1). Nineteen of 33 cases of polyarteritis affected the small bowel or gallbladder, and nine patients with polyarteritis had elevated serum antinuclear antibodies or rheumatoid factor. Eight of 12 cases of phlebitis affected the right colon; there were giant cells in four of these 12 cases, a history of medication use in seven of eight cases, and no evidence of serum autoantibodies. Short-term follow-up (mean, 5 years) demonstrated that systemic disease developed in six of 23 patients with polyarteritis (four of whom had elevated serum rheumatoid factor or antinuclear antibodies), the patient with giant-cell arteritis, and one of two patients with Buerger's disease. Systemic vasculitis did not develop in patients with other types of vasculitis. We conclude that patients with gastrointestinal phlebitis, polyarteritis without serum autoantibodies, and small-vessel vasculitis have a low short-term risk for the development of systemic disease.

Adult↗

PubMed1995

A modified directional atherectomy catheter for resection of calcified atherosclerotic plaques.

BACKGROUND: The purpose of this study was to determine the feasibility of resecting calcified atherosclerotic plaques in human cadaveric vessels by using a modified directional coronary atherectomy catheter and to correlate these results with bench tests using an in-vitro sea coral model. METHODS: The conventional directional coronary atherectomy catheter was modified by changing the cutter blade to a tungsten carbide material and by increasing the torsional strength of the drive cable. The performance of the modified directional coronary atherectomy (DCA) catheter was compared with the conventional catheter using a sea coral model to simulate calcified material. Then, 10 human ex-vivo arteries (eight with calcification) were treated with both conventional and modified catheters, and the results studied with intravascular ultrasound and confirmed by histologic examination. RESULTS: Using the modified directional coronary atherectomy catheter it was possible to perform effective and consistent longitudinal cutting, and to resect a significantly larger amount of coral (1.0 +/- 0.1 mm2 versus 0.2 +/- 0.1 mm2 with conventional cutter, P < 0.0001). In heavily calcified ex-vivo arteries, the modified catheter was more effective in removing calcified plaques (13 +/- 11 mg versus 3.7 +/- 1.4 mg with conventional cutter, P = 0.07). Intravascular ultrasound confirmed the effective atherectomy (residual area stenosis 28 +/- 16% versus 47 +/- 10% with the conventional device, P < 0.05), and histologic examination showed calcified nodules in the atherectomy samples obtained with the modified cutter (area of calcium 1.43 +/- 0.89 mm2 versus 0.93 +/- 0.83 mm2 with the conventional cutter). CONCLUSIONS: The modified directional coronary atherectomy catheter effectively removed both non-calcified and calcified plaques in the ex-vivo human cadaveric arteries, thus demonstrating the feasibility of directional coronary atherectomy of calcified plaques. This modified device shows promise for treating calcified coronary lesions, especially in larger vessels.

Animals↗

PubMed1995

In vivo adenovirus-mediated gene transfer via the pulmonary artery of rats.

Gene transfer into the pulmonary vasculature has the potential to be a powerful technique for both investigation of pulmonary pathophysiology and development of genetic therapies for pulmonary vascular disease. To evaluate the potential for in vivo pulmonary arterial gene transfer, we infused adenoviral vectors into the left pulmonary artery of Sprague-Dawley and cotton rats. Access to the left pulmonary artery was obtained by a percutaneous transcatheter approach or through thoracotomy and pulmonary arteriotomy. With the thoracotomy approach, both pulmonary arterial inflow and pulmonary venous outflow were occluded during vector influsion and throughout a subsequent 20-minute dwell period. The success of gene transfer was assessed by staining for evidence of recombinant gene expression in lungs excised at time points ranging from 48 to 72 hours after virus infusion. With the thoracotomy technique, pulmonary gene transfer was successful in 15% of surviving Sprague-Dawley rats and 30% of surviving cotton rats. Percutaneous catheter-based pulmonary gene transfer was not successful. In rats with pulmonary gene transfer, 1% to 8% of total left lung cells expressed the recombinant gene. Recombinant gene expression was found in endothelial cells (0.2% to 18% of total transduced cells), smooth muscle cells (0% to 3%), macrophages (1% to 7%), airway epithelial cells (2% to 50%), and alveolar epithelial cells (38% to 94%). Investigation of the low rate of successful gene transfer in individual animals suggested that insufficient physical contact between the virions and pulmonary cells was the most likely cause. In vivo gene transfer into the rat pulmonary vasculature can be accomplished with adenovirus vectors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoviridae↗

PubMed1995

Endothelium-specific in vivo gene transfer.

Targeted expression of genetic material within the vascular endothelium is potentially a powerful tool for the investigation of endothelial cell (EC) biology. We developed, optimized, and characterized an efficient somatic transgenic model of EC-specific gene transfer. Rat carotid arteries were infused with adenovirus expressing a beta-galactosidase (beta-gal) gene. The level and cell-type specificity of recombinant gene expression were measured by assaying beta-gal activity in vessel extracts and by counting transduced cells in histological sections. Toxicity was evaluated by counting total ECs (3 days) and by measuring neointimal formation (14 days). Effects of transduction on the proliferation of vascular cells were measured with bromodeoxyuridine and [3H]thymidine. Maximum recombinant gene expression resulted from infusion of 1 x 10(10) to 1 x 10(11) plaque-forming units (pfu) per milliliter; approximately 35% of luminal ECs were transduced. A high degree of EC specificity (90% to 98% of total transduced cells) was maintained over this range of virus concentrations. More highly concentrated virus resulted in loss of beta-gal expression and a large decrease in luminal EC number (97% decrease, P < .001). Gene transfer at 4 x 10(10) pfu/mL was efficient, preserved EC integrity, and caused minimal neointimal formation. After gene transfer, there were early (3-day) increases in both EC and smooth muscle cell proliferation. At 14 days, only EC proliferation remained elevated (18% versus 1.4% in vehicle-infused arteries, P = .005). This animal model permits efficient highly EC-specific gene transfer. Vascular toxicity is minimal, although the EC proliferative index is elevated. This model will be useful in experiments that elucidate the biological role of EC gene products and define pathways of EC gene regulation and signal transduction in vivo.

Adenoviridae↗

PubMed1995

Adenovirus-mediated gene transfer into normal rabbit arteries results in prolonged vascular cell activation, inflammation, and neointimal hyperplasia.

Adenovirus vectors are capable of high efficiency in vivo arterial gene transfer, and are currently in use as therapeutic agents in animal models of vascular disease. However, despite substantial data on the ability of viruses to cause vascular inflammation and proliferation, and the presence in current adenovirus vectors of viral open reading frames that are translated in vivo, no study has examined the effect of adenovirus vectors alone on the arterial phenotype. In a rabbit model of gene transfer into a normal artery, we examined potential vascular cell activation, inflammation, and neointimal proliferation resulting from exposure to replication-defective adenovirus. Exposure of normal arteries to adenovirus vectors resulted in: (a) pronounced infiltration of T cells throughout the artery wall; (b) upregulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in arterial smooth muscle cells; (c) neointimal hyperplasia. These findings were present both 10 and 30 d after gene transfer, with no evidence of a decline in severity over time. Adenovirus vectors have pleiotropic effects on the arterial wall and cause significant pathology. Interpretation of experimental protocols that use adenovirus vectors to address either biological or therapeutic issues should take these observations into account. These observations should also prompt the design of more inert gene transfer vectors.

Adenoviridae↗

PubMed1995

Proliferative activity in coronary atherectomy tissue. Clinical, histopathologic, and immunohistochemical correlates.

STUDY OBJECTIVE: Although cellular proliferation is considered one of the dominant processes leading to restenosis following coronary intervention, controversy exists over the extent of cellular replication in atherosclerotic tissue. Accordingly, we sought to investigate the level and clinicopathologic correlates of proliferative activity in atherosclerotic tissue obtained via directional coronary atherectomy (DCA). DESIGN: Prospective observational study. SETTING: Tertiary care referral hospital. PATIENTS: Specimens retrieved via DCA from 37 lesions (primary, 26; restenosis, 11) were studied using single-label immunohistochemical staining for the proliferating cell nuclear antigen and basic fibroblast growth factor (bFGF). RESULTS: Restenosis tissue was significantly more likely than primary tissue to contain areas of intimal hyperplasia (64 vs 23%; p < 0.03). However, the frequency of positive staining for proliferating cell nuclear antigen (PCNA) was similar in primary and restenosis lesions (25 vs 30%; p = NS), and the mean percentage of positive cells per slide was similar in the two groups. Positive immunostaining for bFGF was present in 20 lesions (61%), and tended to be more frequently seen in restenotic lesions (80 vs 52%; p = 0.25). However, there was no correlation or colocalization between immunostaining for bFGF and proliferating cell nuclear antigen. We found no clinicopathologic correlations with respect to clinical outcome. CONCLUSIONS: Cellular replication, as measured by expression of the PCNA, occurs in a heterogeneous pattern in both primary and restenotic atherosclerotic tissue obtained from patients undergoing coronary intervention.

Atherectomy, Coronary↗

PubMed1995

Problems in forensic cardiovascular pathology.

Do we have a magic yardstick that will establish whether SCD of the patient is definitely caused by the presence of an underlying abnormality? We are afraid that in most cases of cardiac disease the cause of death is at best probable, or even presumed. It has always been that circumstantial evidence has helped us establish that the cause of death is related to the anatomic abnormality. Even the presence of severe coronary artery disease in a patient who dies suddenly, especially in the absence of a thrombus, cannot be stated categorically to be the cause and effect. With the knowledge we have today, establishing cause and effect are difficult in most cases of SCD.

Adolescent↗

PubMed1995

Localization of human immunodeficiency virus 1 RNA in thymic tissues from asymptomatic drug addicts.

Thymic tissue was collected from 11 human immunodeficiency virus 1 (HIV-1)-seropositive drug users who died suddenly of drug intoxication or trauma. None of the 11 individuals had symptoms related to HIV-1 infection or were known to be seropositive for HIV-1 before death. Secondary B-cell follicles were present in every thymus, and Warthin-Finckeldey giant cells were noted in three cases. These follicles were enlarged or fragmented and appeared similar to those in lymph nodes excised from the same individuals. Localization of viral RNA by in situ hybridization demonstrated abundant virus in a follicular center cell distribution within hyperplastic follicles and in scattered medullary lymphocytes. In nine thymus glands from seronegative drug addicts and five thymus glands from seronegative trauma victims who were not drug addicts, secondary follicles were absent and no hybridization signal was present. Other than the presence of germinal centers associated with HIV-1 RNA, there were no histologic differences among the thymus glands of seropositive drug addicts, seronegative drug addicts, and seronegative controls without a history of drug abuse. We conclude that the thymus gland in early stages of infection with HIV-1 is characterized by induction of secondary B-cell follicular hyperplasia in medullary tissues, the germinal centers of which contain abundant viral RNA.

Adult↗

PubMed1995

Studies on the carcinogenic and myocardial effects of 2-amino-3-methylimidazo [4,5-f] quinoline (IQ) in nonhuman primates.

The heterocyclic aromatic amine 2-amino-3-methylimidazo [4,5-f] quinoline (IQ) is one of three heterocyclic amine mutagens currently being evaluated for carcinogenic activity in nonhuman primates, primarily cynomolgus monkeys. IQ was administered by gavage five times a week at doses of 10 or 20 mg/kg. Thus far IQ induced tumors in 50 percent of the monkeys at the 10 mg/kg dose and in 85 percent of the monkeys at the 20 mg/kg dose. Because H and E sections of the myocardium from IQ-treated animals demonstrated inflammatory infiltrate and studies of IQ-DNA adducts in monkeys, by the 32P-postlabeling method, showed high levels of adducts in the heart a systematic study of cardiac pathologic changes associated with chronic administration of IQ was undertaken. Both light and electron microscopic abnormalities were seen. The possibility exists that heterocyclic aromatic amines may be etiologic factors for human cancer and myocardial disease.

Administration, Oral↗

PubMed1994

Long-term histologic patency after percutaneous transluminal coronary angioplasty is predicted by the creation of a greater lumen area.

OBJECTIVES: This study assessed the relation between histologic acute and long-term lumen size after coronary angioplasty. BACKGROUND: Angiographic studies suggest that the creation of a larger acute lumen is associated with a reduced incidence of restenosis. Histologic evaluation of the influence of the acute lumen on late outcome has not been previously reported. METHODS: Detailed histologic examination and planimetry were performed in 28 postmortem coronary arteries subjected to angioplasty at an average of 71 weeks antemortem. The lumen area on each histologic segment was defined as the final lumen area. The lumen area immediately after angioplasty, the acute lumen area, was defined by the sum of the neointimal area plus final lumen. A final lumen area > or = 25% of the arterial area was considered a long-term success; a final lumen area < 25% was considered a long-term failure. RESULTS: Arterial size and neointimal area were similar in long-term successes and failures. In successes, the mean (+/- SD) acute lumen area was greater than in failures (4.1 +/- 1.9 vs. 2.7 +/- 1.4 mm2, respectively, p < 0.001). The acute lumen area as a percent of arterial area was 46 +/- 10% in successes versus 27 +/- 11% in failures (p < 0.0001). The corresponding estimated mean acute lumen diameter stenosis was 24 +/- 8% in successes versus 42 +/- 12% in failures (p < 0.0001). Plaque area was greater in failures (7.1 +/- 3.2 mm2) than in successes (4.8 +/- 2.4 mm2, p < 0.002). CONCLUSIONS: Neointimal proliferation after angioplasty occurs in all dilated coronary arteries, and the amount of neointimal growth is independent of vessel size. The creation of a larger lumen and a larger lumen as a percent of vessel size were associated with an improved long-term histologic patency.

Angioplasty, Balloon, Coronary↗

PubMed1994

Morphologic characteristics of lesion formation and time course of smooth muscle cell proliferation in a porcine proliferative restenosis model.

OBJECTIVES: This study was performed to define the evolution of lesion morphology and its relation to thrombus formation and smooth muscle cell proliferation after experimental coronary stent placement. BACKGROUND: Restenosis after percutaneous revascularization may develop because of thrombus accumulation and smooth muscle cell proliferation. In animal models of restenosis, thrombus may assume a significant role in neointimal formation by providing an absorbable matrix into which smooth muscle cells proliferate. METHODS: Twenty-eight oversized stents were placed in the coronary arteries of 23 juvenile domestic pigs. The histologic degree of vessel injury, lesion morphometry and smooth muscle cell proliferation measured by immunolocalization with a monoclonal antibody to proliferating cell nuclear antigen (PCNA) were assessed at 24 h and 7, 14 and 28 days after stent placement. RESULTS: The area of thrombus was minimal at 24 h ([mean +/- SE] 0.44 +/- 0.12 mm2). Neointimal area at 7 days (0.72 +/- 0.20 mm2) was similar to the area of thrombus, followed by a significant increase at 14 days (3.15 +/- 0.39 mm2) and 28 days (3.30 +/- 0.28 mm2) (p < 0.0036, 24 h and 7 days vs. 14 and 28 days). At 14 and 28 days, neointimal thickness correlated with the histologic degree of vessel injury (p < 0.003). In arteries with severe injury, the increase in neointimal thickness is accounted for by replacement of the damaged media. The smooth muscle cell proliferation index was 18.6 +/- 3.5% at 7 days compared with 9.6 +/- 1.3% by 14 days (p = 0.0247) and declined to 1.1 +/- 0.97% by 28 days (p < 0.008, 7 and 14 days vs. 28 days). CONCLUSIONS: Early thrombus formation is minimal, and thrombus accounts for a small portion of subsequent neointimal formation. Smooth muscle cell proliferation and matrix formation are the major factors relating to neointimal formation in this proliferative model of restenosis. The evolution of neointimal formation after coronary stenting shows maximal smooth muscle cell proliferation at 7 days, with a decline to low levels by 28 days. Therefore, these data may be useful for developing effective therapies for restenosis.

Animals↗

PubMed1994

Coronary artery lumen volume measurement using three-dimensional intravascular ultrasound: validation of a new technique.

OBJECTIVE: To validate an automated algorithm for the measurement of lumen volumes of coronary arteries. BACKGROUND: Current intravascular ultrasound systems use absolute measurements of and changes in areas and diameters for the assessment of coronary artery disease. However, the coronary artery is a three-dimensional structure of complex geometry and volume. METHODS: We used a comprehensive imaging system designed to reconstruct planar intravascular ultrasound images in three dimensions. This system consisted of a 25 MHz transducer-tipped rigid probe (for in vitro studies) or a 25 MHz transducer-tipped catheter within a 3.9F monorail imaging sheath (for in vivo studies), a motorized catheter pullback device that withdrew the transducer at 0.5 mm/sec, and an image processing computer that stacked 15 image slices/mm of vessel axial length and then performed threshold-based three-dimensional image rendering and lumen volume measurement. We imaged 13 human coronary vessels (6 RCA, 6 LAD, 1 LCX) in vitro and 16 vessels (8 LAD, 6 RCA, 2 SVG) in vivo. RESULTS IN VITRO STUDIES: Lumen volumes derived by three-dimensional intravascular ultrasound were 171 +/- 121 mm3 and compared very well with those derived by histology (160 +/- 109 mm3, r = 0.97, SEE = 29 mm3, P < 0.001) and with those derived by manual planimetry of planar intravascular ultrasound images (150 +/- 106 mm3, r = 0.97, SEE = 30 mm3, P < 0.001). In vivo studies: Lumen volumes derived by three-dimensional intravascular ultrasound were 74 +/- 35 mm3 and compared well with those derived by quantitative angiography (52 +/- 20 mm3, r = 0.71, SEE = 25 mm3, P < 0.002). CONCLUSIONS: Three-dimensional intravascular ultrasound is a new technique that can accurately measure coronary artery lumen volumes. Further technical improvements may help to establish this technique as the new standard for lumen volume measurement.

Adult↗

PubMed1994

Cardiotoxicity of heterocyclic amine food mutagens in cultured myocytes and in rats.

Cooked meat contains a number of mutagenic/carcinogenic heterocyclic amines, including 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP). We recently observed that monkeys treated with IQ showed myocyte degeneration and mitochondrial changes. Thus, it was of interest to develop models to investigate heterocyclic amine cardiotoxicity. Primary cultures of fetal rat myocytes were exposed to the activated forms of the carcinogens (N-OH-IQ and N-OH-PhIP). LDH leakage increased in proportion to the carcinogen dose but was significantly greater in cells exposed to N-OH-IQ than that in cells exposed to N-OH-PhIP. Electron microscopy revealed that treated cells had swollen and irregular mitochondria and fewer organelles. However, DNA adducts, assessed using the 32P-postlabeling method, were significantly higher in myocytes exposed to N-OH-PhIP than in cells exposed to N-OH-IQ. The toxic effects of heterocyclic amines were also evaluated in rats given IQ or PhIP (100 mg/kg, po 10 doses over 2 weeks). Light microscopic and ultrastructural cardiac abnormalities were present in seven of eight rats exposed to IQ or PhIP. Whereas control animals had a normal cardiac morphology, carcinogen-treated animals had foci of chronic inflammation with myocyte necrosis, myofibrillar dissolution and disarray, and dilation of T-tubules. These results suggest that, in addition to being carcinogenic, food mutagens may play a role in cardiac degeneration.

Animals↗

PubMed1994

Coronary angioplasty from the perspective of atherosclerotic plaque: morphologic predictors of immediate success and restenosis.

High restenosis rates continue to plague the overall efficacy of percutaneous transluminal coronary balloon angioplasty (PTCA). It is not surprising that predictions of long-term success or failure of PTCA based on coronary angiography are of limited value because these images provide only a circumscribed view of the arterial lumen and offer little insight into underlying plaque morphologic characteristics. Coronary atherosclerotic lesions are quite diverse with respect to plaque characteristics (eccentricity, concentricity, and extent of fibrosis, necrosis, and calcification) and cardiac ischemic syndromes (stable angina, unstable angina, myocardial infarction, and sudden cardiac death). It could thus be expected that dissimilar plaques will respond differently to balloon dilatation, and that plaque morphologic features may play an important role in the immediate and long-term outcome after PTCA. Histologic evaluation of de novo atherosclerotic plaques underscores the heterogeneity of coronary atherosclerosis. From pathologic examination of human coronary arteries subjected to PTCA during life, expansion of the arterial circumference via medial damage is required for an effective increase in lumen size. Eccentric plaques and plaques with a large necrotic core are more likely to be successfully dilated compared to concentric, fibrotic lesions. Intravascular ultrasound studies of PTCA have supported histologic findings. Restenosis involves the complex interaction of growth factors and cytokines, cellular elements (endothelial cells, smooth muscle cells, platelets, and inflammatory cells), and the extent of arterial injury. The effects of underlying plaque morphologic features on the vascular biology of restenosis requires further clarification.

Angioplasty, Balloon, Coronary↗

PubMed1994

Infantile histiocytoid cardiomyopathy: three cases and literature review.

A review is presented of the clinical and cardiac morphologic findings in 50 previously reported and 3 new patients with histiocytoid cardiomyopathy. This disorder occurs in infants and small children and is characterized clinically by severe and often fatal arrhythmias and morphologically by focal collections of altered myocytes that are roundshaped and resemble histiocytes. Sixteen patients had yellowish nodules on the endocardium, epicardium, and/or valves; the other 37 had foci of abnormal myocytes throughout the myocardium. These cells were remarkably similar in all patients and had poorly developed or absent intercellular junctions, few or no contractile elements, and markedly increased numbers of mitochondria, which imparted a granular or vacuolated appearance to the cytoplasm. There was a high prevalence of anomalies involving the nervous system and eyes and of oncocytic cells in various glands. Evidence is presented to exclude the possibilities that the disorder represents a developmental anomaly of the atrioventricular conduction system, a multifocal tumor of Purkinje cells, a developmental arrest of cardiac myocytes, and a diffuse type of mitochondrial cardiomyopathy. Histiocytoid cardiomyopathy is considered to be the result of hamartoma-like aggregations of cardiac myocytes with features similar to those of oncocytes. This syndrome is likely caused by prenatal myocardial or systemic (viral?) injury. Surgical excision of nodules of histiocytoid cells can result in clinical remission.

Cardiomyopathies↗

PubMed1994

Reperfusion enhances the local release of endothelin after regional myocardial ischemia.

The role of endothelin, a potent long-acting vasoconstrictor peptide, in the pathogenesis of the "no-reflow" phenomenon was investigated in nine closed-chest mongrel dogs undergoing 90 minutes of proximal left anterior descending artery occlusion and 3.5 hours of reperfusion. Endothelin levels were measured serially from the coronary sinus (CS) and aorta (Ao) by radioimmunoassay and correlated with regional myocardial blood perfusion. Prolonged anesthesia, surgery, and vascular instrumentation did not change endothelin levels in four sham animals. A progressive and parallel increase in CS and Ao endothelin levels occurred during coronary occlusion. A further increase in CS levels was observed during the reperfusion period, resulting in significantly higher values of the peptide at 30 and 60 minutes (30 minutes: CS 22.1 +/- 3.5 vs Ao 15.1 +/- 5.1 pg/ml; 60 minutes: CS 21.1 +/- 4.5 vs Ao 15.0 +/- 3.6 pg/ml; p < 0.05 by analysis of variance). Microvascular perfusion determined semiquantitatively with fluorescent beads was significantly reduced in the central ischemic zone (CIZ) compared with that in the nonischemic zone (NIZ) (CIZ endocardium 1.14 +/- 0.4 beads/m2, CIZ midmyocardium 1.19 +/- 0.3 beads/m2, NIZ 3.8 +/- 0.6 beads/m2; p < 0.05). A significant correlation was noted between mean reperfusion levels of endothelin in the CS and endocardial flow in the CIZ (r = -0.88; p = 0.009). This study demonstrates that reperfusion per se enhanced the spillover of endothelin from the cardiac interstitium. Local release of endothelin may contribute to the progressive decrease in microvascular flow in the reperfused bed.

Animals↗

PubMed1994

Systemic lymphadenopathic histology in human immunodeficiency virus-1-seropositive drug addicts without apparent acquired immunodeficiency syndrome.

We examined lymph nodes from multiple sites in 50 individuals infected with human immunodeficiency virus (HIV-1) who died accidentally of drug overdoses and in whom there was no evidence of opportunistic infection. The size, histologic pattern, presence of Warthin-Finkeldey-type giant cells, and estimation of CD4 cell count of these lymph nodes were compared with those of 13 seronegative drug addicts (controls). Lymph nodes from seropositive individuals were slightly but significantly larger than those of controls. Lymph nodes from seropositive cases were much more likely to contain secondary follicles (90%) than were those from controls (20%). Unlike follicles in control nodes, most secondary follicles in the seropositive cases were in various stages of fragmentation and involution. As follicular changes progressed, there was a decrease in CD4 cells and an increase in intrafollicular and paracortical plasma cells. Plasmacytosis was much more prevalent in lymph nodes from seropositive individuals than in controls. Warthin-Finkeldey-type giant cells were present in at least one node in 29 of 50 seropositive cases, were most numerous in those showing follicular hyperplasia with fragmentation (45% of cases), and were especially numerous in Peyer's patches (61% of cases). There was generally good concordance of HIV-1-associated follicular morphology among diverse lymph node groups. There is prolonged generalized, mild hyperplastic lymphadenopathy with frequent syncytial cells in intravenous drug addicts with asymptomatic HIV-1 infection.

AIDS-Related Complex↗

PubMed1994

The association of mast cells and atherosclerosis: a morphologic study of early atherosclerotic lesions in young people.

Mast cell products, such as histamine, may contribute to the initiation and progression of the atherosclerotic plaque. To determine the relationship that may exist between early atherosclerotic plaques and mast cells we studied the aortas and coronary arteries of 115 young subjects aged 15 to 34 years who had traumatic deaths. Lesions were classified as normal intima, fatty streaks, fibro-fatty plaques, and fibrous plaques. Aortic and coronary artery segments with raised lesions had significantly greater numbers of mast cells in the adventitia (and occasionally intima and outer media) compared with those with a normal intima. In the aortic segments greater numbers of mast cells were located in the dorsal portion (lesion "prone") compared with the ventral half (lesion "resistant") (P < .05). These data support the concept that increased numbers of mast cells are associated with atherosclerosis and suggest a role for mast cell products in the evolution of the atherosclerotic plaque.

Adolescent↗