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Biomedical subjects

R Virmani

Publications and source records attributed to R Virmani.

At least 109 records · Page 6Linked to original sources
PubMed1997

Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis.

BACKGROUND: Histologic studies of carotid plaques have demonstrated an association between symptomatic disease and plaque rupture. The purpose of this study was to characterize the cellular changes associated with plaque rupture. METHODS: Carotid plaques were obtained from 61 patients undergoing carotid endarterectomy for established indications. Plaques were fixed in formalin, embedded in paraffin, and stained with hematoxylineosin and Movat pentachrome stain to demonstrate plaque structure. Each plaque was examined with light microscopy and classified as containing evidence of plaque rupture (n = 29) or no plaque rupture (n = 32). By using immunohistochemical staining, the fibrous cap was examined for the presence of smooth muscle cells (alpha-actin), macrophages (KP-1), T lymphocytes (UCHL-1), and cell activation (HLA-DR). Data were analyzed with chi-squared analysis. RESULTS: With plaque rupture, macrophages and T lymphocytes were significantly more common than in specimens without evidence of rupture. Similarly, macrophages and T lymphocytes expressing HLA-DR were more often found in sections containing plaque rupture. Furthermore, vascular smooth muscle cells were more common with intact fibrous caps and were diminished with cap thinning. CONCLUSIONS: Rupture of the fibrous cap in carotid artery lesions is associated with increased numbers of macrophages and T lymphocytes, which are in an activated state. The activated inflammatory cells may release cytokines or metalloproteinases, which may be responsible for loss of the fibrous cap. Thus inflammation appears to play a role in the pathogenesis of the neurologic symptoms associated with carotid artery stenosis.

Actins↗
PubMed1997

Causes of sudden death in young and middle-aged competitive athletes.

The incidence of sudden death in athletes is low. Some pathologic conditions may predispose to sudden death during exercise in young athletes. In older individuals, exercise may trigger terminal arrhythmias in patients with severe coronary atherosclerosis. Screening programs with a history and a physical examination are recommended for high school and collegiate sports participants. For older individuals who are likely to have undetected or overt coronary heart disease and are exercising for physical fitness, caution regarding the level of activity and type of symptoms that are frequently associated with coronary disease may help prevent sudden death.

Adolescent↗
PubMed1997

Vascular smooth muscle cell cytotoxicity and sustained inhibition of neointimal formation by fibroblast growth factor 2-saporin fusion protein.

Basic fibroblast growth factor (FGF2) is an important mediator of smooth muscle cell (SMC) proliferation following arterial injury that results in neointimal growth. The present study was designed to explore the effects of recombinant FGF2 linked to the ribosome-inactivating protein saporin-6 (rFGF2-SAP) on vascular SMC cytotoxicity and neointimal formation following arterial injury. Cultured rat aortic SMCs were exposed to various concentrations of rFGF2-SAP, FGF2, and saporin-6 (SAP). Incubation with rFGF2-SAP resulted in a decreased number of SMCs beginning at a concentration of 10(-9) mol/L. Significant cytotoxicity was observed with as little as a 30-minute exposure of SMCs to rFGF2-SAP. To evaluate the ability of rFGF2-SAP in an in vivo model to reduce neointimal formation, Sprague-Dawley rats underwent carotid artery balloon denudation and received an intravenous bolus of vehicle or 5, 10, 15, or 20 micrograms/kg rFGF2-SAP on 0, 3, 6, and 9 days after injury. Rats were euthanized at 14 days, and carotid arteries were analyzed by computerized morphometry. The threshold dose for a significant reduction in neointimal area by rFGF2-SAP was 15 micrograms/kg (47% reduction in neointima). When dosing was extended to include days 16, 19, and 22, the neointima was reduced 33% at 28 days (P = .048). rFGF2-SAP reduced neointima without associated medial thinning or arterial wall dilatation. To determine if rFGF2-SAP directly targets SMCs in vivo, rats underwent carotid injury and received either 15 micrograms/kg rFGF2-SAP or vehicle on day 0 and at 72 hours, with euthanasia at 78 hours after balloon denudation. Medial SMC number was reduced 46% in the rFGF2-SAP group. Tissue sections from arteries 3 days after balloon injury demonstrated rFGF2-SAP binding to medial SMCs and adventitial cells. Staining for fibroblast growth factor receptor 1 revealed a high level of expression in ballooned arteries 3 and 14 days after injury. Taken together, these results provide a molecular and cellular basis for the observed specificity. Prolonged delivery of rFGF2-SAP can affect the natural history of arterial repair after injury.

Angioplasty, Balloon↗
PubMed1997

Regional variability in the time course of TGF-beta 1 expression, cellular proliferation and extracellular matrix expansion following arterial injury.

Transforming growth factor-beta 1 (TGF-beta 1) has been variably associated with the regulation of cellular proliferation and extracellular matrix expansion after arterial injury. We tested these associations in vivo in the rat carotid injury model. At 0, 3, 7, 14 and 28 days following arterial balloon injury, regional expression of TGF-beta 1 mRNA was assessed using in situ hybridization and the results compared to measures of cellular proliferation and extracellular matrix expansion. Both the TGF-beta 1 concentration measured in culture media of explanted carotid arteries and the quantitative in situ hybridization signal for TGF-beta 1 arterial media and neointima were maximal at 14 days after balloon injury. However, medial cellular proliferation was maximal at 3 days whereas neointimal proliferation was maximal at 14 days and significantly greater than medial proliferation. Neointimal cell density declined significantly between 7 and 14 days, indicating the expansion of extracellular matrix; however, medial cell density was unchanged between 3 and 28 days after balloon injury. Thus, differences in the regional arterial wall relationships between the time course of cellular proliferation, extracellular matrix expansion and the level of TGF-beta 1 expression demonstrate in vivo variability in the response to TGF-beta 1.

Angioplasty, Balloon, Coronary↗
PubMed1997

Experimental Results with the Multi-Linkª Stent in a Porcine Model.

OBJECTIVES: The purpose of this study was to assess the delivery characteristics and the vascular response to placement of the Multi-Linkª stent in normal porcine coronary arteries. BACKGROUND: The Multi-Link stent is a balloon expandable stainless steel stent with an interconnected corrugated ring structure designed to provide a high degree of compressive resistance while preserving longitudinal flexibility. The placement characteristics and vascular response to this stent in normal porcine coronary arteries has not been characterized. METHODS: We tested the delivery characteristics and vascular response to the Multi-Link stent in 19 normolipemic miniature swine. Quantitative coronary angiography was used to define stent performance characteristics such as stent expansion and recoil. Histologic assessment of the stented arteries was used to evaluate the acute and chronic vascular response to stent placement. RESULTS: Thirty-five of thirty-five stents (100%) were successfully implanted in the left anterior descending (n = 14), left circumflex (n = 8) or right (n = 13) coronary arteries of nineteen swine. The baseline angiographic mean lumen diameter of the stented coronary segment was 3.41 +/- 0.32 mm and increased to 3.53 +/- 0.33 mm (p < 0.001) after stent placement. The balloon inflated stent diameter was 3.61 +/- 0.36 mm with minimal recoil to a final minimal lumen diameter of 3.53 +/- 0.33 mm after implant (p = 0.001). Linear regression analysis revealed that the percent stent recoil had a significant positive correlation with the stent to artery ratio or the degree of stent over-sizing (r = 0.67; p < 0.0001). Angiographic and histologic follow-up at 72 hours (n = 9), 14 days (n = 12) and 56 days (n = 12) demonstrated that all stents were patent without evidence of migration, intraluminal filling defect or side-branch occlusion. On histology, there was rare evidence of stent-induced deep arterial wall injury such as rupture of the internal elastic lamina and medial laceration. There was no significant difference in the mean injury score observed on day 3 (0.23 +/- 0.22), 14 (0.35 +/- 0.28) or 56 (0.36 +/- 0.27) after implant (p = 0.27). On day 3, the mean thrombus thickness overlying the stent wires was 70 +/- 98µ. The mean neointimal area was similar at 14 and 56 days after implant (1.63 +/- 1.25 mm2 versus 1.78 +/- 0.68 mm2, p = 0.54). CONCLUSIONS: The MULTI-LINK stent easily tracked the coronary arteries and deployed reliably in this experimental model. The multiple interconnected ring geometry of the stent provides adequate compressive resistance, longitudinal flexibility and uniform coverage of the arterial wall throughout the length of the endoprothesis. The stent has acceptable blood and tissue biocompatibility in normal porcine coronary arteries. Oversizing this stent (>10 percent) may have a theoretical disadvantage resulting in a proportionally higher degree of stent recoil. The results of clinical trials will determine if the design features of the Multi-Link stent favorably impact on procedural outcome or long-term patency.

Journal Article↗
PubMed1997

Infectious endocarditis and sudden unexpected death: incidence and morphology of lesions in intravenous addicts and non-drug abusers.

BACKGROUND: Intravenous drug (IVD) use is a wellknown risk factor for infectious endocarditis (IE), but there are few morphologic and epidemiologic data comparing IVD-related and non-IVD-related IE in cases of sudden death. MATERIAL AND RESULTS: Between 1992 and 1994, acute IE was diagnosed in 13 IVD users at the Office of the Chief Medical Examiner in Maryland, indicating a yearly incidence of IE-related sudden unexpected deaths of 12 per 100,000. Eleven (85%) cases of acute IE occurred on apparently previously normal valves, and there was one unicuspid valve and one infected porcine prosthesis. There were three right-sided (tricuspid) lesions (23%), nine left-sided lesions (69%), and one multivalvular lesion (8%). During the same period, there were five cases of healed IE in IVD abusers, three of which involved the tricuspid valve. The prevalence of incidental healed lesions in autopsies of IVD users was 0.2%. The healed tricuspid lesions consisted of smooth-edged defects in the valve leaflet without perforations characteristic of mitral or aortic IE. The mean age of the deceased with healed lesions was 45 +/- 6 years versus 34 +/- 10 years for those with acute endocarditis (p = 0.03). During the same time period, there were six cases of acute IE among non-drug users, indicating a yearly incidence of sudden unexpected death of 0.04 per 100,000. Acute IE occurred on congenitally malformed (n = 5) or prosthetic (n = 1) valves. There were two cases of incidental healed IE (mitral and aortic valves), indicating a prevalence of 0.02%. CONCLUSION: IVD users are 300 times more likely to die suddenly with IE than non-IVD users, and healed lesions are 25 times more common. Healed IE of the tricuspid valve is associated with IVD abuse, and has a characteristic gross appearance that differs from healed left-sided IE.

Adult↗
PubMed1996

Effect of hypertension and cardiac hypertrophy on coronary artery morphology in sudden cardiac death.

BACKGROUND: Epidemiological studies have shown that hypertension and left ventricular hypertrophy (LVH) increase the risk of sudden cardiac death (SCD) in patients with severe coronary artery disease (CAD). However, autopsy studies comparing the morphological substrates for SCD in normotensives and hypertensives are lacking. METHODS AND RESULTS: Heart weight and coronary plaque morphology were prospectively compared in SCD in 36 hypertensive and 63 normotensive individuals. The frequency of CAD was similar in hypertensives (69%, n = 25) and normotensives (73%, n = 46). In 71 hearts with CAD, acute coronary thrombi were present in 76% of normotensives versus 36% of hypertensives (P = .002), LVH was present in 64% of hypertensives versus 33% of normotensives (P = .01) and in 72% of hypertensives with one-vessel disease versus 17% of normotensives with one-vessel disease (P = .0005), and a healed or acute infarct without acute thrombus was present in 36% of hypertensives versus 9% of normotensives (P = .007). Heart weight was higher in all cases of plaque rupture (519 +/- 109 g) than eroded plaque (381 +/- 92 g, P = .0002). In contrast to hypertensives, normotensive hearts with severe CAD showed a stepwise increase in heart weight with one-, two-, and three-vessel disease (P = .01). CONCLUSIONS: Severe CAD is present in most SCD in hypertensive and normotensive individuals, but acute thrombi are more common in normotensives. LVH is an important contributing mechanism of SCD in hypertensives, especially in cases of one-vessel disease. LVH is associated with plaque rupture and extent of disease in SCD in normotensives with severe CAD.

Body Weight↗
PubMed1996

Effects of endovascular radiation from a beta-particle-emitting stent in a porcine coronary restenosis model. A dose-response study.

BACKGROUND: Neointimal formation causes restenosis after intracoronary stent placement. Endovascular radiation delivered via a stent has been shown to reduce neointimal formation after placement in porcine and rabbit iliac arteries. The objective of this study was to evaluate the dose-related effects of a beta-particle-emitting radioactive stent in a porcine coronary restenosis model. METHODS AND RESULTS: Thirty-seven swine underwent placement of 35 nonradioactive and 39 beta-particle-emitting stents with activity levels of 23.0, 14.0, 6.0, 3.0, 1.0, 0.5, and 0.15 microCi of 32P. Treatment effect was assessed by histological analysis 28 days after stent placement. Neointimal and medial smooth muscle cell density were inversely related to increasing stent activity. The neointima of the high-activity (3.0- to 23.0-microCi) stents consisted of fibrin, erythrocytes, occasional inflammatory cells, and smooth muscle cells with partial endothelialization of the luminal surface. In the 1.0-microCi stents, the neointima was expanded and consisted of smooth muscle cells and a proteoglycan-rich matrix. The neointima of the low-activity (0.15- and 0.5-microCi) stents was composed of smooth muscle cells and matrix with complete endothelialization of the luminal surface. At low and high stent activities, there was a reduction in neointimal area (low, 1.63 +/- 0.67 mm2 and high, 1.73 +/- 0.97 mm2 versus control, 2.40 +/- 0.87 mm2) and percent area stenosis (low, 26 +/- 7% and high, 26 +/- 12%) compared with control stents (37 +/- 12%, P < or = .01). The 1.0-microCi stents, however, had greater neointimal formation (4.67 +/- 1.50 mm2) and more luminal narrowing (64 +/- 16%) than the control stents (P < .0001). CONCLUSIONS: The differential response to the doses of continuous beta-particle irradiation used in this experimental model suggests a complex biological interaction of endovascular radiation and vascular repair after stent placement. Further study is required to determine the clinical potential for this therapy to prevent stent restenosis.

Animals↗
PubMed1996

Apoptosis in myocytes in end-stage heart failure.

BACKGROUND: Heart failure can result from a variety of causes, including ischemic, hypertensive, toxic, and inflammatory heart disease. However, the cellular mechanisms responsible for the progressive deterioration of myocardial function observed in heart failure remain unclear and may result from apoptosis (programmed cell death). METHODS: We examined seven explanted hearts obtained during cardiac transplantation for evidence of apoptosis. All seven patients had severe chronic heart failure: four had idiopathic dilated cardiomyopathy, and three had ischemic cardiomyopathy. DNA fragmentation (an indicator of apoptosis) was identified histochemically by in situ end-labeling as well as by agarose-gel electrophoresis of end-labeled DNA. Myocardial tissues obtained from four patients who had had a myocardial infarction one to two days previously were used as positive controls, and heart tissues obtained from four persons who died in motor vehicle accidents were used as negative controls for the end-labeling studies. RESULTS: Hearts from all four patients with idiopathic dilated cardiomyopathy and from one of the three patients with ischemic cardiomyopathy had histochemical evidence of DNA fragmentation. All four myocardial samples from patients with dilated cardiomyopathy also demonstrated DNA laddering, a characteristic of apoptosis, whereas this was not seen in any of the samples from patients with ischemic cardiomyopathy. Histological evidence of apoptosis was also observed in the central necrotic zone of acute myocardial infarcts, but not in myocardium remote from the infarcted zone. Rare isolated apoptotic myocytes were seen in the myocardium from the four persons who died in motor vehicle accidents. CONCLUSIONS: Loss of myocytes due to apoptosis occurs in patients with end-stage cardiomyopathy and may contribute to progressive myocardial dysfunction.

Accidents, Traffic↗
PubMed1996

Paired comparison of vascular wall reactions to Palmaz stents, Strecker tantalum stents, and Wallstents in canine iliac and femoral arteries.

BACKGROUND: Palmaz stents, Strecker stents, and Wallstents, all used clinically, differ substantially in their physical characteristics, yet how differently the vascular wall reacts to them has not been demonstrated conclusively. We therefore undertook a side-by-side comparison. METHODS AND RESULTS: One stent was implanted into each canine external iliac and/or the flexing portion of the proximal femoral artery. In 9 dogs, Palmaz stents were placed vis-à-vis Strecker stents, with follow-up of 2 and 4 months. In 7 dogs, Palmaz stents were placed vis-à-vis Wallstents, with 4 months of follow-up. Angiographic midstent luminal diameters immediately after placement and at follow-up as well as midstent cross-sectional areas of neointima were compared for significant differences. In addition, neointimal maturation, medial atrophy, and stent-related trauma were assessed. Angiographically, all arteries remained open. The degree of luminal narrowing by recoil and neointima never reached 50% and was modest for Palmaz stents and Wallstents (P = .33) but significantly higher for Strecker stents (P < .0001 compared with Palmaz stents). This corresponded histologically to a significantly thicker neointima (P = .003) over Strecker than over Palmaz stents but not between Palmaz stents and Wallstents (P = .18). Neointimal buildup was generally more pronounced in the femoral artery segments than in the iliac segments. Maturation of the neointima over Palmaz stents was much further advanced than over Strecker stents and slightly more advanced than over Wallstents. Pressure-related atrophy of the tunica media was least for Strecker stents and more pronounced but similar for Wallstents and Palmaz stents. Wallstent wire ends caused some wall trauma; several femoral Palmaz stent struts protruded through the media. CONCLUSIONS: The lower-hoop-strength, higher-profile tantalum Strecker stent is affected by vascular wall recoil and evokes a greater degree of neointima formation than the lower-profile, higher-hoop-strength Palmaz stent and Wallstent. Medial atrophy is pronounced outside the latter two stents. The rigid Palmaz stent can penetrate through the vascular wall in flexing arteries.

Animals↗
PubMed1996

Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death.

BACKGROUND: Coronary thrombosis has been reported to occur most frequently in lipid-rich plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of extracellular lipid. However, the frequency of coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown. In this study, we compared the incidence and morphological characteristics of coronary thrombosis associated with plaque rupture versus thrombosis in eroded plaques without rupture. METHODS AND RESULTS: Fifty consecutive cases of sudden death due to coronary artery thrombosis were studied by histology and immunohistochemistry. Plaque rupture of a fibrous cap with communication of the thrombus with a lipid pool was identified in 28 cases. Thrombi without rupture were present in 22 cases, all of which had superficial erosion of a proteoglycan-rich plaque. The mean age at death was 53 +/- 10 years in plaque rupture cases versus 44 +/- 7 years in eroded plaques without rupture (P < .02). In the plaque-rupture group, 5 of 28 (18%) were women versus 11 of 22 (50%) with eroded plaques (P = .03). The mean percent luminal area stenosis was 78 +/- 12% in plaque rupture and 70 +/- 11% in superficial erosion (P < .03). Plaque calcification was present in 69% of ruptures versus 23% of erosions (P < .002). In plaque ruptures, the fibrous cap was infiltrated by macrophages in 100% and T cells in 75% of cases compared with 50% (P < .0001) and 32% (P < .004), respectively, in superficial erosions. Clusters of smooth muscle cells adjacent to the thrombi were present in 95% of erosions versus 33% of ruptures (P < .0001). HLA-DR expression was more often seen in macrophages and T cells in ruptures (25 of 28 cases) compared with expression in macrophages in superficial erosion arteries (8 of 22 cases, P = .0002). CONCLUSIONS: Erosion of proteoglycan-rich and smooth muscle cell-rich plaques lacking a superficial lipid core or plaque rupture is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the present study. These lesions are more often seen in younger individuals and women, have less luminal narrowing and less calcification, and less often have foci of macrophages and T cells compared with plaque ruptures.

Adult↗
PubMed1996

Seeding of vascular grafts with genetically modified endothelial cells. Secretion of recombinant TPA results in decreased seeded cell retention in vitro and in vivo.

BACKGROUND: Seeding of small-diameter vascular grafts with endothelial cells (ECs) genetically engineered to secrete fibrinolytic or antithrombotic proteins offers the potential to improve graft patency rates. METHODS AND RESULTS: Sheep venous ECs were transduced with a retroviral vector encoding human tissue plasminogen activator (TPA). The ECs were seeded onto 4-mm-ID synthetic (Dacron) grafts. Retention of the seeded ECs was measured 2 hours after placement of the seeded grafts both in vitro in a nonpulsatile flow system and in vivo (in sheep) as femoral and carotid interposition grafts. On exposure to flow in vitro, ECs transduced with TPA were retained at a significantly lower rate (median, 67%) than either untransduced ECs (81%) or ECs transduced with a control retroviral vector producing beta-galactosidase (beta-Gal) (80%) (P < .05 for TPA versus either control). On implantation in vivo, ECs transduced with TPA were retained at a very low rate (median, 0%), significantly less than the retention of ECs transduced with the beta-Gal vector (32%; P < .00001). Decreased in vivo retention of ECs transduced with TPA correlated modestly with increased in vitro cellular passage level (r2 = .48; P < .0001) but not with in vivo blood flow rate (P = .45). Addition of the protease inhibitor aprotinin to the cell culture and graft perfusion media resulted in a significant (P < .05) increase in in vitro retention of ECs transduced with TPA. CONCLUSIONS: Increased TPA expression significantly decreases seeded EC adherence in vitro and in vivo. Gene therapy strategies for decreasing graft thrombosis may require expression of antithrombotic molecules that lack proteolytic activity.

Animals↗
PubMed1996

Inhibition of neointimal proliferation with low-dose irradiation from a beta-particle-emitting stent.

BACKGROUND: Restenosis after successful percutaneous transluminal coronary angioplasty is the major factor limiting the long-term effectiveness of this procedure. Neointimal proliferation in response to arterial injury is an important contributor to restenosis. The use of radiation for the treatment of malignant and benign proliferative conditions has been well established. External beam irradiation and endovascular irradiation by use of an after-loading technique have been shown to inhibit neointimal proliferation in experimental models of restenosis. The objective of this study was to investigate whether low-dose irradiation from a beta-particle-emitting stent would inhibit neointimal proliferation after placement in porcine iliac arteries. METHODS AND RESULTS: Fourteen titanium-mesh stents were implanted in the iliac arteries of nine NIH miniature swine. There were seven beta-particle-emitting radioisotope stents (32P, activity level 0.14 microCi) and seven control stents (31P, nonradioactive). Treatment effect was assessed by angiography and histomorphological examination of the stented iliac segments 28 days after implantation. There was a significant reduction in neointimal area (1.76 +/- 0.37 mm2 versus 2.81 +/- 1.22 mm2, P = .05) and percent area stenosis (24.6 +/- 2.9% versus 36.0 +/- 10.7%, P = .02) within the beta-particle-emitting stents compared with the control stents. Neointimal thickness, which was assessed at each wire site, was also significantly less within the treatment stents (0.26 +/- 0.04 mm versus 0.38 +/- 0.10 mm, P = .012). Scanning electron microscopy was performed on sections from four stents. This demonstrated endothelialization of both the treatment and control stents. There was no excess inflammatory reaction or fibrosis in the media, adventitia, or perivascular space of vessels treated with the beta-particle-emitting stent compared with control vessels. At 28 days, there was no difference in smooth muscle cell proliferation as measured by the proliferating cell nuclear antigen index. CONCLUSIONS: A local, continuous source of low-dose endovascular irradiation via a beta-particle-emitting stent inhibits neointimal formation in porcine arteries. This low dose of local irradiation did not prevent endothelialization of the stents. This novel technique offers promise for the prevention of restenosis and warrants further investigation.

Animals↗
PubMed1996

Effect of age, race, body surface area, heart weight and atherosclerosis on coronary artery dimensions in young males.

Compensatory arterial enlargement in response to atherosclerosis has been demonstrated for the left main coronary artery. Only limited data is available on the interaction of patient characteristics and atherosclerosis with coronary artery dimensions. The purpose of the present study was to evaluate the influence of age, race, body habitus, heart weight and atherosclerosis on coronary artery dimensions of young males. Hearts from 137 young men (age 32 +/- 8 years; 78 black, 59 white) with unnatural deaths (homicide, suicide, accident, drug overdose) were perfusion-fixed, and histologic sections were obtained from the left main, proximal left anterior descending and left circumflex coronary arteries. Computerized planimetry was performed on Movat stained sections. Multiple regression analysis was used to evaluate the relative contribution of plaque size, age, race, heart weight and body surface area on coronary dimensions and compensatory enlargement in response to atherosclerosis. In the left anterior descending and left main coronary arteries, black race, body surface area and age were independent predictors of increased lumen area. In the left circumflex, age was a predictor of lumen area. Plaque area, black race and body surface area independently predicted increased area enclosed by the internal elastic lamina area. There was compensatory enlargement of internal elastic lamina with increasing plaque size in both races in the three arteries, but the percent luminal stenosis was greater in whites due to smaller artery size. Luminal narrowing did not develop until plaques occupied 30% of internal elastic lamina area. Among a population of young men with non-cardiac deaths, blacks have larger lumen and area enclosed by internal elastic lamina than whites. Age and body surface area are major determinants of lumen areas, and compensatory arterial enlargement was seen in all examined arteries in the present study.

Adolescent↗