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PubMed1997

Inflammatory cytokines cause coronary arteriosclerosis-like changes and alterations in the smooth-muscle phenotypes in pigs.

We recently developed a porcine model in which chronic, local treatment with interleukin-1 beta (IL-1 beta) causes coronary arteriosclerosis-like changes and hyperconstrictive responses. This study was designed to examine whether or not other major inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) might also cause similar coronary responses and whether those responses are associated with alterations in the smooth-muscle phenotypes. A segment of the porcine coronary artery was aseptically wrapped with cotton mesh, absorbing IL-1 beta, TNF-alpha, and IL-1 alpha. Two weeks after the operation, coronary arteriography showed the development of mild stenotic lesions at the cytokine-treated sites, where hyperconstrictive responses were repeatedly induced by intracoronary serotonin or histamine. Histologically mild intimal thickening was noted at those cytokine-treated sites. Immunostaining and immunoblotting demonstrated that all three myosin heavy chain isoforms, SM1, SM2 (smooth-muscle type), and SMemb (nonmuscle type), were noted in the normal coronary segments, whereas in the segments treated with inflammatory cytokines, SM1 and SM2 were markedly reduced, and only SMemb was noted. These results indicate that inflammatory cytokines all have a similar ability to induce coronary arteriosclerosis-like changes and hyperconstrictive responses, which are associated with alterations in smooth-muscle phenotypes toward dedifferentiation.

Animals↗

PubMed1998

Estradiol inhibits allograft-inducible major histocompatibility complex class II antigen expression and transplant arteriosclerosis in the absence of immunosuppression.

BACKGROUND: The etiology of transplant arteriosclerosis is unknown, but current data point to the alloimmune response. Previously, we found that estradiol-17beta (E2) with immunosuppressant cyclosporine abolishes major histocompatibility complex (MHC) class II expression in the allograft. This study determines the effect of E2 on MHC class II antigen expression in the allograft, in the absence of immunosuppression. METHODS: Lewis male rats received orthotopic abdominal aorta allografts from male Brown-Norway rats. The recipients were treated continuously subcutaneously with either 20 microg x kg(-1) x day1 of E2 (n=20) or placebo (n=20), from 2 days before transplantation until death on posttransplant days 1, 3, 7, and 14. The allografts were harvested and processed for morphometry and for immunohistochemical staining of MHC class II antigens, macrophages, CD4 and CD8 T lymphocytes, interferon-gamma (IFN-gamma), and IFN-gamma receptor. RESULTS: With E2 treatment, we observed that inducible MHC class II antigen expression is abolished in the media of the vascular allograft; the expression of IFN-gamma and IFN-gamma receptor is unaffected; and macrophage infiltration of the vascular allograft is inhibited significantly (P<0.01), whereas the CD4 and CD8 T lymphocytes are not significantly (P=0.07) suppressed. The myointimal hyperplasia in the allografts from E2-treated-recipients was 3-4-fold less than that from the placebo-treated recipients. CONCLUSIONS: Without immunosuppression, E2 inhibition of transplant arteriosclerosis is still associated with inhibition of inducible MHC class II antigen expression in the allografts. The estradiol-17beta abolition of inducible MHC class II antigen expression in the aorta allograft occurs in spite of up-regulation of IFN-gamma ligand and receptor protein.

Animals↗

PubMed2001

In vivo gene transfer of dominant-negative rho-kinase induces regression of coronary arteriosclerosis in pigs.

Small GTPase Rho and its target Rho-kinase play an important role in various cellular functions that may be involved in the pathogenesis of arteriosclerosis. Here we show that adenovirus-mediated transfer of dominant-negative Rho-kinase (AdDNRhoK) induces a regression of coronary constrictive remodeling and abolishes coronary vasospastic activity in vivo. Porcine coronary segments were chronically treated with interleukin-1,beta which resulted in the development of constrictive remodeling and vasospastic responses to serotonin in vivo. AdDNRhoK, but not that of beta-galactosidase, into the interleukin-1beta-treated coronary segment caused regression of constrictive remodeling and abolished vasospastic activity in 3 weeks. The unregulated phosphorylation of the target proteins of Rho-kinase at the coronary lesion was significantly suppressed by AdDNRhoK. These results indicate that Rho-kinase is substantially involved in the mechanism of coronary arteriosclerosis, which can be reversed by selective inhibition of the molecule in our porcine model in vivo.

Animals↗

PubMed1978

Coronary artery ectasia--a variant of occlusive coronary arteriosclerosis.

In a study of 1000 consecutive coronary arteriograms, 12 patients (all men) had coronary artery ectasia. Ectasia was found most frequently in the circumflex or right coronary artery. Only 1 patient had ectasia in the left anterior descending coronary artery. In 11 patients, ectasia of one artery was associated with severe stenosis or occlusion of other vessels, typical of arteriosclerosis. Histology from an ectatic segment in one of this group showed changes of severe arteriosclerosis with extensive intimal fibrosis and destruction of the media. One patient had a mixed collagen vascular disease. Measurement of coronary sinus flow in 2 patients with coronary artery ectasia showed flows in the range of patients with non-ectatic coronary artery disease. At cardiac surgery flows down the graft to ectatic arteries were in the same range as in grafts to non-ectatic vessels. Patients with coronary artery ectasia should be anticoagulated.

Adult↗

PubMed1998

Correlations among expression of intercellular adhesion molecule 1, cellular infiltration, and coronary arteriosclerosis during chronic rejection using the rat heart transplantation model.

Immunologic mechanisms contribute to the development of coronary arteriosclerosis. In this study the rat heart transplantation model was used to investigate correlations among the expression of intercellular adhesion molecule 1, cellular infiltrate, and coronary arteriosclerosis during chronic rejection. Lewis rats served as heart donors and F-344 rats as recipients. Heart transplantations were performed heterotopically. The recipients were treated with cyclosporin A (5 mg/kg/day) by daily intramuscular injection for 30 days, beginning on the day of transplantation. Rejection grade and the intimal area were measured. The expression of intercellular adhesion molecule 1 and the numbers of infiltrating CD4- and CD8-positive cells and macrophages were examined immunohistochemically. The area of the intima was significantly increased in the allograft group after transplantation. In the allograft group, the level of expression of intercellular adhesion molecule 1 was considerably increased over the same time period. There was increased cellular infiltration in the 60-day group, and many expressed intercellular adhesion molecule 1. The expression of intercellular adhesion molecule 1 in vascular endothelium, infiltrating cells, and the sarcolemmal membrane of myocytes remained constant up to 120 days in the allograft group. In the allograft group, the number of infiltrating CD4- and CD8-positive cells and macrophages increased significantly between 30 and 60 days, and the infiltration of these cells remained constant. Continuous expression of intercellular adhesion molecule 1 induces the infiltration of T cells and macrophages, and the inflammation caused by such cells and their soluble products contributes to the arteriosclerotic process.

Animals↗

PubMed2000

Contribution of proliferating leukocytes to phenotypic change in smooth muscle cells during the development of coronary arteriosclerosis in transplanted hearts.

BACKGROUND: It is well known that coronary arteriosclerosis after heart transplantation is concentric and rich in smooth muscle cells (SMCs); however, the role played by rejection in the intimal thickening caused by SMCs in coronary arteriosclerosis remains unclear. In this study, we examined the process of intimal hyperplasia caused by SMCs and evaluated the relationship between the differentiation state of SMCs and local inflammation caused by rejection. METHODS: Lewis rat hearts were heterotopically transplanted into F344 rats (allotransplantation group) or other Lewis rats (isotransplantation group). Cyclosporin A (5 mg/kg/day) was injected intramuscularly for 20 days after transplantation in both groups. The transplanted hearts were examined immunohistochemically using several monoclonal antibodies; namely, HHF-35, CGA7, vimentin, alpha-actin, HIS36, R73 and proliferating cell nuclear antigen (PCNA). To evaluate the degree of local immunological response caused by rejection, the anti-PCNA antibody was used. To reveal the subtypes of proliferating cells in the thickened intima, HIS36 and R73 antibodies were used. RESULTS: In the allotransplantation group, SMCs in the media began to undergo a phenotypic change toward a poorly differentiated state 30 days after transplantation. Intimal hyperplasia was observed 60 days after transplantation, the thickened intima being composed mainly of dedifferentiated SMCs with abundant PCNA(+), most of which were macrophages and T cells. The state of differentiation of SMCs in the thickened intima 90 days after transplantation varied from a dedifferentiated to a highly differentiated state. These changes were strongly correlated with the expression of PCNA. CONCLUSION: The expression of PCNA was strongly correlated with the differentiation state of SMCs. Thus, local inflammation caused by rejection may play an important role in the initiation of phenotypic change in SMCs.

Animals↗

PubMed2003

Association between insulin resistance and carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance.

OBJECTIVE: We examined the possible association between insulin resistance and carotid arteriosclerosis in subjects who had both normal fasting glucose and normal glucose tolerance after intake of a glucose load. METHODS AND RESULTS: Our subjects were individuals who underwent general health screening at our institute, which included carotid ultrasound and oral glucose tolerance testing. Of the 1238 subjects enrolled in our study, 738 (60%) were classified as normal, defined as a normal fasting glucose level and normal glucose tolerance, and 334 (27%) and 166 (13%) were classified as borderline and diabetic, respectively, according to the criteria of the Japan Diabetes Society. The homeostasis model assessment of insulin resistance (HOMA-IR) was used as the index to measure insulin resistance. In normal-type subjects, univariate analysis showed that insulin resistance, but not insulin secretion, was associated with the presence of carotid plaque. Multivariate analysis showed that HOMA-IR was positively associated with carotid plaque in normal-type subjects, with an odds ratio of 1.19 (95% confidence interval, 1.00 to 1.41; P<0.05). CONCLUSIONS: These data suggest the possibility that the presence of higher insulin resistance could be a risk factor for carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance.

Adult↗

PubMedDate not supplied

Coronary arteriosclerosis in Atlantic salmon. No regression of lesions after spawning.

The incidence and severity of coronary arteriosclerosis were studied in 209 wild and cultured Atlantic salmon (Salmo salar L.) during various stages of recovery of bodily condition after spawning. All recently spawned fish had lesions of moderate to extreme severity. The incidence of lesions for each fish was high (73% to 94% of all arterial cross-sections examined). The incidence and severity of lesions did not decrease during 5 months in a group of wild salmon reconditioned in the laboratory. Wild salmon that were examined in the spring angling fishery in the Miramichi River, New Brunswick, about 5 months after spawning had a high incidence (89%) of severe lesions, not significantly different from recently spawned salmon from the same and another river. A population of cultured salmon sampled at intervals from a sea cage during 9 months after spawning showed no evidence of lesion regression, but rather a continued increase in both incidence and severity during recovery of bodily condition and growth. Thus, in contrast with previous studies with steelhead trout and Atlantic salmon where the possibility of lesion regression has been suggested, our observations on a large number of Atlantic salmon from various sources gave no evidence of lesion regression. Coronary arteriosclerosis in Salmo salar appears to be a progressive condition, which continues during recovery of bodily condition and growth after spawning.

Animals↗

PubMed1989

Carotid arteriosclerosis in identical twins discordant for cigarette smoking.

From a nationwide twin panel, identical twin pairs with highest discordance in cigarette smoking were selected for a study of arteriosclerosis (49 pairs with a mean age of 52 years). Smoking history was obtained in 1975, 1981, and 1986. The mean life-long smoking dose of the smoking cotwins was 20 package-years. The smoking and nonsmoking cotwins had similar systolic and diastolic blood pressures, total plasma cholesterol level, body mass index, and some psychosocial factors; the only difference was found in use of alcohol, which was greater among smoking cotwins. Duplex sonography of carotid arteries was performed. Carotid artery stenoses (narrowing of area of the lumen with 15-60%) were found in nine pairs: in nine smoking twins and in two of their nonsmoking cotwins (p = 0.036). The total area of carotid plaques was 3.2 times larger in smoking cotwins (p less than 0.001). The thickness of the inner layer of carotid arteries was more marked in smoking cotwins (p less than 0.001). The size of plaques and the degree of inner layer thickening correlated with the dose of smoking (NS). The association of smoking with carotid arteriosclerosis was highly significant even after the adjustment for age, total plasma cholesterol level, diastolic blood pressure, and body mass index in multiple logistic regression analyses.

Carotid Arteries↗

PubMed1999

Effects of immunosuppressants on platelet-derived growth factor-A chain mRNA expression and coronary arteriosclerosis in rat cardiac allografts.

Graft coronary arteriosclerosis (GCA) that results in proliferative and obstructive lesions limits the long-term success of cardiac transplantation. Despite extensive study, the pathogenic mechanisms underlying GCA are still unclear and therapeutic strategies for this condition have been inadequate. In this study, we compared the therapeutic effectiveness of cyclosporine A (CsA), 15-deoxyspergualin (DSG), and Multiglycosidorum tripterygii (MT) on GCA. In addition, we studied the correlation between the extent of GCA and the degree of platelet-derived growth facter (PDGF)-A chain mRNA expression in cardiac grafts. Lewis rats receiving heterotropic heart transplants from Wistar King donors were treated with 10 mg kg(-1) day(-1) of CsA (n=7), 5 mg kg(-1) day(-1) of DSG (n=7) or 30 mg kg(-1) day(-1) of MT (n=7) respectively. Histological evaluation of coronary arteriosclerosis and Northern blot analysis of cardiac allograft PDGF-A chain mRNA expression were conducted on day 60 after transplantation. Varying levels of GCA were observed in the 21 transplanted hearts. Significant differences in both the degree of PDGF-A mRNA expression and the extent of GCA were found among the 3 groups. GCA was significantly reduced in allografts treated with MT or DSG in comparison with the level seen in CsA-treated grafts. A significant correlation was found between PDGF-A chain mRNA expression and the grade of arterial intimal thickening (r=0.76, p<0.05) as well as with the incidence of diseased vessels (r=0.82, p<0.01). Our results indicate that both MT and DSG are more effective in the treatment of GCA than CsA. In our cardiac allografts, the degree of PDGF-A chain mRNA expression correlated well with the extent of GCA, suggesting that PDGF-A may play an important role in the development of transplant-related GCA.

Animals↗

PubMed1999

Hyperhomocysteinemia is a risk factor for coronary arteriosclerosis in Japanese patients with type 2 diabetes.

OBJECTIVE: An increased plasma homocysteine level is an important risk factor for vascular disease, including coronary atherosclerosis, in the general population. However, the role of hyperhomocysteinemia in the development of coronary artery disease (CAD) in patients with type 2 diabetes is unknown. Therefore, we have endeavored to determine the relationship between plasma homocysteine levels and the presence of coronary arteriosclerosis in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: The study group consisted of 145 Japanese patients (95 men and 50 women) who underwent routine coronary angiography to assess chest pain or suspected CAD. Plasma total homocysteine level, lipid level, and parameters of fibrinolytic activity were measured. All patients were identified as diabetic or nondiabetic by the new American Diabetes Association (ADA) criteria. The diagnoses of all patients studied were confirmed by coronary angiography. The severity of coronary artery stenosis was quantified using CAD scoring on the basis of prior reports, and subjects were graded as nonstenotic, stenotic single-vessel, stenotic two-vessel, or stenotic three-vessel based on the number of stenotic coronary arteries. Patients were classified into two groups: those with stenotic vessels and those without stenotic vessels. RESULTS: The plasma homocysteine level was significantly higher in patients with than in patients without stenotic vessels (13.8 +/- 3.9 vs. 11.7 +/- 3.9 mumol/l, respectively; P = 0.0009). The number of stenotic coronary arteries, which was used to grade each case as nonstenotic, stenotic single-vessel, stenotic two-vessel, or stenotic three-vessel, was related only to the total homocysteine level in the diabetic (diabetes mellitus [DM]) group, but it was associated with lipoprotein(a) in the nondiabetic (non-diabetes mellitus [non-DM]) group. Spearman's rank correlation test demonstrated that the plasma homocysteine level was strongly correlated with CAD score, both in the entire study group and in the DM group (P = 0.003 for the entire group and P = 0.011 for the DM group). Hyperhomocysteinemia, which was defined as total homocysteine level > 14.0 mumol/l, was seen in 57 (39.3%) of the patients. The CAD score was highest in diabetic patients with hyperhomocysteinemia (P < 0.05). CONCLUSIONS: There seems to be a clear relationship between hyperhomocysteinemia and an increased risk of coronary arteriosclerosis in Japanese patients with type 2 diabetes.

Aged↗

PubMedDate not supplied

Lymphocytic subsets and histopathologic changes associated with the development of heart transplant arteriosclerosis.

Transplantation of vascularized organ allografts is associated with the development of arteriosclerosis in the vessels of the donor graft. We have recently examined the distribution of lymphocytic/mononuclear inflammatory cell subsets and histopathologic changes seen in the sequential development of transplant arteriosclerosis in cardiac allografts exchanged between inbred rat strain combinations (LEW-to-F344) that differ for weak histocompatibility loci. The donor grafts were harvested at 7, 14, 21, 28, 50 to 65, and 90 days after transplantation, and the vascular lesions were characterized for the immunopathologic changes associated with the chronic rejection of the grafts. The inflammatory cell infiltration of the graft myocardium was present as early as 7 days after transplantation (53.37 +/- 9.06 inflammatory cells/high-power field), and the accumulation of cells increased at 3 and 4 weeks after transplantation (112.12 +/- 16.58 and 130.40 +/- 21.24 cells/high-power field, respectively). The infiltrating inflammatory cells in the grafts at 4 weeks after transplantation were predominantly ED-1+ macrophages (63.39%), with a substantial number of OX19+ T lymphocytes (28%), OX8+ Tc/s cells (25.4%), 3.2.3+ natural killer cells (16.89%), W3/25+ Th cells (20.2%), and a small number of OX33+ B lymphocytes (1.13%) and interleukin-2 receptor+ T lymphocytes (2.6%). Among the T-cell population, most (87.6%) were positive (R73+) for T-cell receptors. The arteriosclerotic lesions present in the cardiac grafts exhibited a gradual increase in severity of the vascular intimal proliferation and a similar pattern of increased intensity of cellular infiltration. The lesions were infiltrated with inflammatory cells beginning in the first week and increasing for the first month after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

[Short-term effect of paclitaxel-eluting stent in the treatment of coronary heart disease due to coronary arteriosclerosis].

OBJECTIVE: To evaluate the short-term safety and efficacy of paclitaxel-eluting stent (TAXUS stent, Boston Scientific) in the treatment of coronary heart disease (CHD) due to coronary arteriosclerosis. METHODS: From July 2003 to November 2004, 300 consecutive patients with CHD due to coronary arteriosclerosis were admitted for selective percutaneous coronary intervention (PCI) and paclitaxel-eluting stent implantation in the coronary arteries. The immediate effects after PCI and follow-up results were investigated. RESULTS: Altogether 350 lesions were treated and 355 paclitaxel-eluting stents implanted in the 300 cases. Of these lesions, 248 (70.9%) was complicated lesions of B2 type or worse, 94 (26.5%) small-caliber stents (2.50-2.75 mm) and 130 (36.6%) long stents (>20 mm) were implanted, without occurrence of severe intra-operative complications. Follow-up study of 250 cases (83.3%) lasting for 1 to 15 months was conducted, and chest pain was reported in 8 cases, 2 of which underwent coronary artery angiography and no in-stent restenosis was found. One patient developed myocardial infarction 5 months after PCI, and 2 died for non-cardiogenic factors. CONCLUSION: Paclitaxel-eluting stent implantation in patients undergoing PCI is safe approach with good short-term efficacy.

Aged↗

PubMedDate not supplied

Effects of fish oil on graft arteriosclerosis and MHC class II antigen expression in rat heterotopic cardiac allografts.

The effect of fish oil on accelerated graft coronary arteriosclerosis was assessed in Lewis to Brown-Norway rat heterotopic cardiac allografts. Twelve Brown-Norway rats were supplemented with 2 ml/kg/day of fish oil (68.3 mg eicosopentaenoic acid and 47.5 mg decosahexaenoic acid per milliliter). Eleven additional animals, receiving an isocaloric amount of safflower oil, served as control. All diets began 1 week before operation. Immunosuppression was obtained with low-dose cyclosporine (2 mg/kg/d). When killed (100 days), there were no significant differences in percentage weight gain, graft function, or histologic rejection score. Although lipid profiles were comparable, total cholesterol:high-density lipoprotein ratio was marginally higher in animals treated with fish oil (p = 0.069). Mean percentage luminal occlusion (before and after correcting for differences in size between coronary vessels analyzed) and average intimal thickness were similar between animals treated with fish oil and safflower oil as assessed by computer-assisted digitized, morphometric planimetry. In all allografts, donor interstitial dendritic cells were repopulated with recipient dendritic cells. The major histocompatibility complex class II cell density in the fish oil group did not differ significantly from rats supplemented with safflower oil (1.48 +/- 0.68 vs 1.48 +/- 0.65 cells per mm2, p = 0.995). In conclusion, fish oil did not exert any beneficial effect over safflower oil in terms of graft coronary arteriosclerosis, histologic rejection, or plasma lipids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

[Report on cholesterol levels of Spanish children and adolescents. Group of Experts of Spanish Societies of Arteriosclerosis, Cardiology, Pediatrics, Nutrition and Preventive Medicine].

The epidemiological association between blood cholesterol levels and the development of clinical complications of arteriosclerosis, particularly coronary heart disease, is presently well established. The importance of measuring blood cholesterol levels in children and adolescents is supported by numerous evidences: beginning of arteriosclerosis in infancy, relationship between the extent of fatty streaks as determined by post mortem examination of accidentally dead children and previous blood lipid levels, aggregation in children (as in adults) of elevated blood cholesterol levels with other cardiovascular risk factors, tracking of high cholesterol levels (and of other risk factors) from childhood to adolescence and early adulthood, and association of risk factors in children with a parental history of cardiovascular disease. The few epidemiological studies of blood cholesterol in children published in Spain have demonstrated relatively high mean values of blood cholesterol at all ages, which are similar or even higher than those obtained by the LRC Program in the United States during the 1970's. The present report constitutes a metaanalysis of data provided by the authors of 21 Spanish studies, both published and unpublished, carried out during the 1980's on the blood lipid levels of children and adolescents (0-18 years-old) including a total of 19,630 subjects (10,834 males, 8,102 females, and 694 newborns). All data were obtained in cross-sectional studies of normal populations employing different biochemical and statistical methods, thus limiting the value of the conclusions on the true values of blood cholesterol in Spanish children and its changes during recent years. Weighted means were calculated for the means of the different studies taking into account the number of cases in each population, and the distribution in percentiles by age and sex of total cholesterol, triglycerides, LDLc, and HDLc were estimated. For the overall study population, the mean blood cholesterol level and the moderate risk percentile (75) and high risk percentile (95) for both sexes were 173 mg/dl (4.5 mmol/l), 200 mg/dl (5.2 mmol/l), and 225 mg/dl (5.8 mmol/l), respectively. Such levels are between 10 and 15 mg/dl (0.3 and 0.4 mmol/l) higher than those of the LRC Program, and a clear rise was observed from the early to the late 1980's. The present levels of blood cholesterol in children and adolescents have a great potential impact for Public Health policy in Spain. As it occurs in adults, the distributions of blood cholesterol levels in children of different populations reflect their coronary heart disease mortality rates.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMedDate not supplied

Role of smooth-muscle cells and macrophages in cardiac allograft arteriosclerosis in rabbits.

Accelerated coronary arteriosclerosis is one of the major complications in allogeneic cardiac transplantation, despite the significant improvement in immunosuppressive therapy. In this study we sought to clarify the cellular components in cardiac allograft arteriosclerotic lesions with monoclonal antibodies specific to either the muscle cell (HHF-35) or the macrophage (RAM-11). Four kinds of heterotopic transplantations were performed in the rabbit: (1) low cholesterol-fed (n = 5), (2) 1% cholesterol-fed (n = 5), (3) low cholesterol-fed and immunosuppressed (n = 6), and (4) 1% cholesterol-fed and immunosuppressed (n = 6). The donor hearts were removed after cardiac arrest in groups 1 and 2, and at 5 weeks after transplantation in groups 3 and 4. In groups 1 and 2 acute rejection was associated with slightly thickened intimal lesions composed of abundant infiltrating mononuclear cells and sparsely intermingled smooth-muscle cells. In group 3 the arterial intima were moderately thickened with the predominant proliferation of smooth-muscle cells. In group 4 coronary lumina were almost completely occupied with the intimal foam cells, which were derived mostly from macrophages and some from smooth-muscle cells. These data suggest that the proliferation of smooth-muscle cells might be a major factor contributing to arteriosclerosis in chronic cardiac rejection and that long-term exposure to hypercholesterolemia could induce the accumulation of smooth-muscle cells or macrophage-derived foam cells.

Animals↗

PubMedDate not supplied

[Sex hormones in men with coronary arteriosclerosis].

Testosterone and estradiol levels were determined in 85 male patients aged between 23 and 52 years with: coronographically diagnosed coronary arteriosclerosis (20 with the instable and 37 with stable coronary disease), and in 28 healthy volunteers serving as a control group. Testosterone concentrations in the instable coronary disease (13.6 +/- 1.7 nM/l) were significantly lower than in the stable form of the disease (18.56 +/- 1.1 nM/l) and in healthy volunteers 20.9 +/- 1.0 nM/l, p less than 0.02 and p less than 0.001 respectively. Estradiol concentrations in male patients with instable coronary disease (228.3 +/- 22.8 pM/l) and with stable form of the disease (157.0 +/- 12.6 pM/l) were significantly higher than in healthy volunteers, p less than 0.02 and p less than 0.001 respectively. The obtained results indicate gonadal disorders in male patients with coronary arteriosclerosis.

Adult↗

PubMedDate not supplied

Dyslipoproteinemias after heart and heart-lung transplantation: potential relation to accelerated graft arteriosclerosis.

Plasma lipid, lipoprotein lipid, and low-density lipoprotein (LDL) apolipoprotein B (Apo B) levels were measured in 34 patients who had undergone heart transplantation and in two patients who had undergone heart-lung transplantation. In contrast to initial reports, atherogenic dyslipoproteinemias were common, with 14% of patients having increased LDL cholesterol levels, 16.7% increased triglyceride levels, 8.3% decreased high-density lipoprotein (HDL) cholesterol levels, and 22.2% increased LDL Apo B levels. Of interest, 14% of patients had an HDL cholesterol level greater than the 95th percentile of the general population. In four patients coronary arteriosclerosis developed after transplantation. All had an atherogenic dyslipoproteinemia. One had type II hypercholesterolemia, and one had isolated low HDL cholesterol levels. Two had hyperapobetalipoproteinemia, one of whom also had low HDL cholesterol levels. The results establish that atherogenic dyslipoproteinemias are frequent in patients after heart transplantation and suggest that these dyslipoproteinemias, along with rejection, may play a role in the pathogenesis of arteriosclerosis after transplantation.

Adult↗