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PubMed1979

Production of coronary arteriosclerosis with sex hormones and human chorionic gonadotropin (HCG) in juvenile steelhead and rainbow trout, Salmon gairdneri.

Coronary arteries were examined for significant changes in myointimal hyperplasia in one-year old juvenile steelhead or rainbow trout treated with estradiol, testosterone or human chorionic gonadotropin (HCG). In one experiment juvenile steelhead trout were injected weekly with 2 microgram/g HCG, 5 microgram/g estradiol cypionate or 5 microgram/g testosterone cypionate for 50 days. Control fish were those killed prior to treatment or injected with fish saline or cottonseed oil. In two experiments juvenile nonanadromous rainbow trout were treated with estrogen and testosterone with the same weekly doses as juvenile steelhead for 42 and 30 days, respectively. In the first experiment juvenile rainbow were injected weekly with 2 microgram/g HCG. Juvenile rainbow treated with estradiol, testosterone and HCG and juvenile steelhead treated with testosterone had larger coronary lesions than untreated or control fish. Coronary hyperplastic nodules resembled morphologically those observed previously in sexually mature steelhead and rainbow trout. These data support the hypothesis that reproductive hormones are causal factors in spontaneously occurring arteriosclerosis in spawning Salmo gairdneri.

Animals↗
PubMed2002

Coronary arteriosclerosis in salmon: growing old or growing fast?

A review is presented of what we know and what we suspect regarding the formation of coronary arteriosclerotic lesions in salmonids. Coronary lesions are a fact of life for both Atlantic and Pacific species of migrating salmon. Severe forms of lesions, usually restricted to the main coronary artery, are typically found in the majority of a salmon population when they are spawning. Vascular injury to the coronary artery, as a result of the bulbus arteriosus being excessively distended, is proposed as an initiating mechanism for coronary lesion formation, possibly explaining why severe lesions are restricted primarily to the main coronary artery. Evidence is presented that coronary arteriosclerosis in salmonids develops in immature fish, well before maturation, and progresses with age. Growth and growth rate are implicated in lesion progression. A faster growth rate could produce a more stressful life style, which in turn initiates more coronary vascular injury. Dietary factors, especially polyunsaturated fatty acids (and their metabolites), can significantly stimulate vascular smooth muscle proliferation in the salmon coronary artery, but a possible linkage to the progression of coronary lesions has yet to be studied. Whether coronary lesions negatively impact blood flow to the salmon heart has not been properly studied. Nevertheless, the coronary blood supply to the heart has functional importance when salmon exercise and the coronary flow reserve may be reached when fish swim under mild hypoxic conditions. If coronary arterial lesions do adversely affect blood flow to the heart, the selective effects would be most prominent in years when upstream migration conditions are particularly severe.

Animals↗
PubMed1998

Fas-mediated apoptosis in accelerated graft arteriosclerosis.

Pathological conditions have been recognized where vessel destruction is a prominent feature of the pathogenic process. One such condition consists of the chronic rejection of blood vessels in transplanted solid organs. Accelerated graft arteriosclerosis (AGA) is a multifactorial process characterized by the concentric proliferation of smooth muscle cells (SMCs) within the intima of the vessel wall of transplanted organs. Proliferation of SMCs within the intima corresponds to a response of these cells to injury. In situations like restenosis post-angioplasty, the mechanism of injury: the mechanical disruption of the tunica media, is evident. However, in the case of AGA, the mechanism of injury has remained elusive. In this report, we provide evidence that injury to SMCs in AGA vessels requires an intact Fas pathway. The resulting damage to the tunica media and internal elastic lamina, in turn, might trigger the proliferation of intimal smooth muscle cells that appear to be less sensitive to Fas mediated killing, particularly when supported by a favorable context of inflammatory cytokines and growth factors, as it is the case in AGA. This pathogenic process results in a absolute loss of functional blood vessels that is not being compensated by an efficient angiogenic response.

Journal Article↗
PubMed1997

Prevention of graft coronary arteriosclerosis by antisense cdk2 kinase oligonucleotide.

Graft coronary arteriosclerosis, which limits the long-term survival of allograft recipients, is characterized by diffuse intimal thickening composed of proliferative smooth muscle cells. We observed that messenger RNA of the cell cycle regulatory enzyme cyclin-dependent kinase (cdk) 2 kinase, which mediates smooth muscle cell proliferation, was elevated in the thickened intima of coronary arteries of murine heterotopic cardiac allografts. We studied the effects of antisense phosphorothioate oligodeoxynucleotide (ODN) against this enzyme using gene transfer mediated by a hemagglutinating virus of Japan (HVJ)-liposome complex intraluminally delivered to inhibit the intimal hyperplasia. At 30 days after transplantation, antisense cdk2 kinase ODN treatment had dramatically inhibited neointimal formation in the allografts. Expression of vascular cell adhesion molecule-1 was also suppressed by antisense cdk2 kinase. However, these effects were not observed in the sense or scrambled ODN-treated allografts. Thus, an intraluminal administration of antisense ODN directed to a specific cell cycle regulatory gene can inhibit neointimal formation after cardiac transplantation.

Animals↗
PubMed1993

ECAT angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography.

The ECAT Angina Pectoris Study is a European multicentre study investigating the pathogenetic and possibly predictive role of the haemostatic system in the progress of coronary heart disease. In this paper we report the cross-sectional analysis of haemostatic factors in 3043 patients, who underwent coronary angiography due to angina pectoris. Fibrinogen levels were higher in patients with one or more coronary stenoses of at least 50% than in patients without, by an average of 0.16 g.l-1 (P < 0.0001). Depressed fibrinolytic activity due to higher levels of PAI was also associated with the presence of coronary stenoses. There was no association with the extent of coronary arteriosclerosis, as assessed by the number of involved arteries, except that patients who had more vessels with total occlusions had higher fibrinogen levels. Depressed fibrinolytic activity was also clearly associated with diabetes, obesity, higher triglyceride levels, smoking and impaired cardiac pump function as assessed by ejection fraction. Cholesterol levels were particularly correlated with protein C and plasminogen.

Angina Pectoris↗
PubMed1993

Noninvasive visualization of coronary arteriosclerosis by computed tomography.

I report a new, extremely rapid, noninvasive technique for the diagnosis of coronary artery occlusion. An ultrafast x-ray cine-computed tomographic scanner (cine-CT) allows visualization of the coronary arteries without injection of contrast material. The arteries can be seen because of the CT contrast between blood in the arteries and the pericardial fat. This theory is supported by a study of 200 patients followed up for 5 years. This examination is extremely short and noninvasive, so it is a potentially efficient method of mass screening for coronary arteriosclerosis.

Adipose Tissue↗
PubMed1995

Evidence that graft coronary arteriosclerosis begins in the early phase after transplantation and progresses without chronic immunoreaction. Histopathological analysis using a retransplantation model.

The histopathological features of chronic rejection and its initiation were assessed using rat heterotopic heart transplantation and retransplantation models. Fully allogeneic or minor, non-MHC antigen-mismatch heart grafts transplanted into recipient rats treated with a short course of FK506 showed long-term survival but developed graft atherosclerosis after 40 days posttransplantation. Retransplantation of allografts back into the original donor strain did not prevent graft atherosclerosis if the grafts had resided in the primary recipient for up to 5 days; residence in the primary allogeneic recipient for less than 4 days did not result in graft atherosclerosis in the secondary recipient. Short-course administration of FK506 did not affect the production of these changes. Graft coronary arteriosclerosis begins between 3 and 5 days posttransplantation and progresses without continuous allogeneic immunological drive. The present findings will provide a new means by which to approach the analysis of development of chronic allograft rejection.

Animals↗
PubMed1999

Histological evidence of concomitant intramyocardial and epicardial vasculitis in necropsied heart allografts: a possible relationship with graft coronary arteriosclerosis.

BACKGROUND: The significance of medial lymphocytic vasculitis in intramural coronary vessels in heart transplantation is very poorly understood. This study was designed to identify histological evidence of an association between the presence of epicardial coronary lesions and the occurrence of intramyocardial vasculitis and/or myocardial ischemia. METHODS: We analyzed the frequency of medial vasculitis and other myocardial histological alterations in a retrospective study of 24 human cardiac allografts from patients who died of ischemic heart disease and/or myocardial rejection. RESULTS: Medial lymphocytic vasculitis in the myocardium was associated with vasculitis in the vasa vasorum of the epicardial coronary arteries and the presence of microfoci of acute myocardial infarction but was independent of the occurrence of myocardial fiber rejection. Chronic graft epicardial arteriopathy revealed two patterns of lesions. One pattern was similar to that of usual atherosclerosis, compromising mainly the proximal segments of the coronary artery, and was not associated with intramural vasculitis. The other pattern demonstrated diffuse involvement of the epicardial artery associated with vasculitis of its vasa vasorum and lymphocytic vasculitis of the intramural vessels. This second type of epicardial coronary lesion seemed to evolve to fibrotic arteries with thinned walls, frequently demonstrating aneurysmal dilatation with severe fibrosis of the adventitia and poor vasa vasorum. CONCLUSION: Medial vasculitis affecting intramyocardial vessels is associated with adventitial epicardial coronary vasculitis in the transplanted heart. The process of vasculitis may be involved in the development of chronic graft arteriosclerosis and is associated with ischemic myocardial lesions, but seems independent of myocardial fiber rejection.

Acute Disease↗
PubMed2000

Accelerated coronary atherosclerosis and arteriosclerosis in young human-immunodeficiency-virus-positive patients.

OBJECTIVE: To determine the type of lesions observed in young patients infected with human immunodeficiency virus-1 (HIV-1). DESIGN: Examination of coronary networks in corpses of 13 men and two women who had died aged 23-32 years after having been infected with HIV-1 virus, having been seropositive for 2-5 years. Causes of death were infectious complications (five cases), infection with cytomegalovirus leading to gastro-intestinal haemorrhaging (one case), infection with cytomegalovirus and Kaposi's sarcoma (one case), overdoses of drugs (five cases) and sudden death (three cases). METHODS: The pathological analysis was carried out on the proximal and distal coronary networks. In order to characterize the lesions better, the cells and the cytokines involved were characterized by immunohistochemistry. RESULTS: In all 15 cases we observed thickening of intima in the proximal network at least as great as that of the media, caused by a proliferation of secreting cells, phenotypically identified as smooth muscle cells, with exaggerated production of elastic fibres and in association with an increase in the expression of tumor necrosis factor-alpha and interleukin-1 alpha. In nine cases, atherosclerosis had developed from and on the surface of this proliferation and in four cases arteriosclerosis had an unusual appearance, in the form of mamillated vegetations with endoluminal protrusions. A similar proliferation was found in the distal network in four cases, but with a significantly smaller proportion of elastic fibres. CONCLUSIONS: The lesions we examined in these young HIV-1-infected patients presented particular features and were intermediate between the lesions observed during common coronary atherosclerosis and atherosclerosis associated with chronic rejection of cardiac transplants.

Adult↗
PubMed2006

Increased expression of Toll like receptor 4 on peripheral-blood mononuclear cells in patients with coronary arteriosclerosis disease.

The family of Toll-like receptors (TLRs) initiates innate immune responses, and Toll-like receptor 4 (TLR4) was considered to be an important player in the initiation and progression of atherosclerotic disease. The aim of the study was to investigate the expression of TLR4 on peripheral-blood mononuclear cells (PBMCs) in patients with coronary arteriosclerosis disease (CAD). We have examined the expression of TLR4 protein and mRNA by flow cytometry (FCM) and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). In addition, the levels of plasma lipids were determined by automatic biochemistry analyzer. The results showed that the positive rates and the mean mRNA copy number of TLR4 in CAD group were significantly higher than that in controls. But no significant difference was found in the positive rate and the mean mRNA copy number of TLR4 between CAD group with normal level of plasma lipids and the CAD group with abnormal level of plasma lipids. We suggest that expression level of TLR4 on peripheral-blood mononuclear cells is increased in atherosclerotic, but the differential expression of TLR4 has no correlation with the level of plasma lipids.

Aged↗
PubMed2004

Lowering of oxidative stress in hemodialysis patients by dialysate cleaning: in relation to arteriosclerosis.

The objective of this study was to investigate changes in oxidative stress associated with the cleaning of the dialysate. Thirty-six dialysis patients were studied. Changes in soluble CD-14 (sCD-14), malondialdehyde-low-density lipoprotein (MDA-LDL), and oxidized-LDL (Ox-LDL) were monitored for 1 year before and 1 year after dialysate cleaning. The mean endotoxin (ET) level in the dialysate had previously been confirmed to decrease from 39.0 EU/L to an undetectable level after the cleaning. The mean levels of sCD-14, MDA-LDL, and Ox-LDL decreased significantly after the cleaning (sCD-14, P < 0.0001; MDA-LDL, P < 0.001; Ox-LDL, P < 0.001). One year after the cleaning, six cases still showed high levels of MDA-LDL and Ox-LDL. Cardiovascular events occurred in four of those six cases within 2.8 years after the cleaning. These four patients suffered from strong oxidative stress during dialysis, even after the cleaning. We therefore concluded that high levels of MDA-LDL and Ox-LDL are improved in dialysis patients by cleaning of the dialysate. These results indicate that even a dialysate containing 50 EU/L or less ET may stimulate monocytes and cause oxidative stress. They also suggest that even low levels of ET may aggravate arteriosclerosis in dialysis patients. Thus, in order to prevent cardiovascular events in dialysis patients, it is necessary to purify the dialysate.

Adult↗
PubMed2000

Gene therapy for heart transplantation-associated coronary arteriosclerosis.

Cardiac allograft arteriosclerosis, which limits the long-term survival of recipients, cannot be prevented by conventional therapies. The arteriopathy is characterized by diffuse intimal thickening made up of proliferative smooth muscle cells. To test the hypothesis that cell cycle-regulatory genes play crucial roles in the development of this arteriopathy in vivo gene therapy targeting cell division cycle (cdc) 2 kinase was attempted in murine cardiac allografts using hemagglutinating virus of Japan (HVJ)-liposome method. Antisense cdc 2 kinase oligodeoxynucleotide (ODN) was transfected into the allografts by intraluminal injection during the operation and the allografts were harvested at 4 weeks after transplantation. Coronary intimal thickening had developed in sense ODN-treated allografts and ICAM-1 and VCAM-1 were enhanced in these arteries. PDGF mRNA was also detected. Antisense cdc 2 kinase ODN inhibited intimal hyperplasia. These data indicate that antisense cdc 2 kinase modulates gene expression and inhibits smooth muscle cell proliferation of graft arteries.

Animals↗
PubMed1993

Comparison of dietary casein and soybean protein effects on plasma lipid and gastrin levels, hepatic delta 6-desaturase activity and coronary arteriosclerosis in male Sprague-Dawley rats. A 9-month study.

An increased concentration of gastrin was observed in plasma of male Sprague-Dawley strain rats fed on soybean protein diet for a 9-month period, compared with rats fed on casein diet. Both diets contained 0.5% (w/w) cholesterol. Protein-dependent differences were also observed in the fatty acid pattern of hepatic phospholipids, hepatic delta 6-desaturase activity, and plasma cholesterol. No signs of arteriosclerosis were observed in the aortas. Sixty percent of the hearts showed various degrees of lipid staining in coronary arterial branches of different sizes. Despite a large difference in plasma cholesterol level, there was no quantitative or qualitative difference between groups in the occurrence of coronary lipid staining.

Animals↗
PubMed2004

Granulocyte macrophage-colony stimulating factor increases the expression of histamine and histamine receptors in monocytes/macrophages in relation to arteriosclerosis.

OBJECTIVE: To study the effect of granulocyte macrophage-colony-stimulating factor (GM-CSF) on histamine metabolism in arteriosclerosis, the expression of histidine decarboxylase (HDC; histamine-producing enzyme), histamine receptors 1 and 2 (HH1R and HH2R), and GM-CSF was investigated in human and mouse arteriosclerotic carotid arteries. Furthermore, the molecular mechanisms of GM-CSF-induced HDC and HH1R expression in monocytic U937 cells were investigated. METHODS AND RESULTS: Immunohistochemistry showed that atherosclerotic human coronary and mouse ligated carotid arteries contained HDC-expressing macrophages. Gene expression of HDC, HH1R, HH2R, and GM-CSF was also detected in the lesions. In U937 cells, GM-CSF enhanced histamine secretion and gene expression of HDC and HH1R. A promoter assay showed that GM-CSF enhanced gene transcription of HDC and HH1R but not HH2R. CONCLUSIONS: The present results indicate that HDC and HHR are expressed in arteriosclerotic lesion, and that GM-CSF induces HDC and HH1R expression in monocytes. Locally produced histamine might participate in atherogenesis by affecting the expression of atherosclerosis-related genes in monocytes and smooth muscle cells. The presence of histamine-producing macrophages and gene expression of histamine receptors and GM-CSF was demonstrated in arteriosclerotic lesions. In monocytic U937 cells, GM-CSF upregulated the expression of histamine and HH1R. Coordinated expression of histamine and its receptors by GM-CSF would participate in atherogenesis by affecting monocytic and SMC gene expression.

Animals↗
PubMed1993

Coronary arteriosclerosis in dogfish (Scyliorhinus canicula). An assessment of some potential risk factors.

Coronary myointimal lesions are described in the dogfish (Scyliorhinus canicula). These lesions are similar to those previously described in salmonids and are characterized by breaks in and disappearance of the inner elastic layer and intimal thickening as a result of inclusions of fibers and smooth muscle cells. Lesions are associated with all the branching points in the main subepicardial conal coronary arteries that supply the heart. Intimal thickenings were rare in other parts of these arteries. However, we found extensive lesions unassociated with branching points in two main intramyocardial ventricular arteries that supply the ventricular spongy myocardium. We carried out a statistical study of the incidence and severity of these intramyocardial lesions in relation to several potential risk factors. Intimal thickenings were present in 90.5% of the fish specimens and 40% of the histological sections. Sex, reproductive stage, plasma triacylglycerol, and cholesterol (total and related to high-density lipoproteins) were not significantly related to either the incidence or severity of lesions. Total fish length was significantly correlated with the lesion severity index (r = 0.33, p < 0.01). We also found significant differences in incidence related to the location of lesions. The middle areas of the intramyocardial branches, very close to the atrioventricular canal, were more affected than the cranial and caudal areas. The dorsal and ventral artery walls were also more affected than the lateral ones. The preferential location of the lesions in areas presumably subjected to mechanical stress because of a bifurcating bloodstream or the pulsatile flow throughout the atrioventricular canal suggests that coronary arteriosclerosis in dogfish is an age-related process, with hemodynamic factors playing a primary or secondary pathogenetic role. This disease seems not to be related to some factors suggested for salmonids, such as reproductive cycle, anadromous migration, river pollution, or plasma lipid concentration.

Animals↗
PubMed2001

Adenovirus-mediated transfer of dominant-negative rho-kinase induces a regression of coronary arteriosclerosis in pigs in vivo.

Small GTPase Rho and its target Rho-kinase/ROK/ROCK play an important role in various cellular functions, including smooth muscle contraction, actin cytoskeleton organization, and cell adhesion and migration, all of which may be involved in the pathogenesis of arteriosclerosis. Here, we show that adenovirus-mediated transfer of dominant-negative Rho-kinase (DNRhoK) induces a marked regression of coronary constrictive remodeling and abolishes coronary vasospastic activity in vivo. Porcine coronary segments were chronically treated with interleukin-1beta, which resulted in the development of constrictive remodeling and vasospastic responses to serotonin, as previously reported. Adenovirus-mediated transfer of DNRhoK, but not that of beta-galactosidase, into the interleukin-1beta-treated coronary segment caused a marked regression of the constrictive remodeling and abolished the vasospastic activity in 3 weeks. Western blot analysis showed that the phosphorylation of adducin and the ezrin/radixin/moesin family, the target proteins of Rho-kinase, were upregulated at the coronary lesions and were significantly suppressed by the transfer of DNRHOK: These results indicate that Rho-kinase is substantially involved in coronary constrictive remodeling and vasospastic responses, both of which can be reversed by the selective inhibition of the molecule in our porcine model in vivo.

Adenoviridae↗
PubMedDate not supplied

Arteriosclerosis in Atlantic salmon. Effects of dietary cholesterol and maturation.

Coronary arteriosclerosis was examined in cultured Atlantic salmon (Salmo salar L.) maintained on normal and cholesterol-enriched diets in both freshwater and saltwater during the period when they normally mature (June to December). The incidence of lesions was high (48% or greater) in all experimental subgroups (assigned according to diet, salinity, sex, and maturation status). The primary factor in the development of arteriosclerotic lesions was not established, but the high frequency of lesions in immature fish suggests that it was not maturation. However, maturation was associated with a significant increase in the incidence of lesions and was, therefore, an important secondary factor in the etiology of the disease. Furthermore, diet had a secondary influence on the development of lesions since the cholesterol supplement was also associated with an increase in the incidence of lesions. The cholesterol supplement significantly increased the total plasma cholesterol level in all subgroups; the low density lipoprotein fraction (total cholesterol minus the high density lipoprotein fraction) was also elevated in seven of eight paired subgroups. Plasma free fatty acids and triglycerides were unaffected by the cholesterol supplement. The elevated total cholesterol and low density lipoprotein levels resulting from the cholesterol-enriched diet and the associated increase in the incidence of lesions was most prominent in mature males and females held in freshwater. Salinity had no demonstrable effect on lesion incidence, but the severity of lesions tended to be greater in freshwater fish.

Animals↗
PubMed1997

Adhesion molecule P-selectin and vascular cell adhesion molecule-1 in enhanced heart allograft arteriosclerosis in the rat.

BACKGROUND: The increase of P-selectin on endothelial cells (EC) overlying human atherosclerotic plaques in classic atherosclerosis was recently established. We have previously shown that vascular cell adhesion molecule-1 (VCAM-1) is extensively expressed on EC of occluded arteries during accelerated transplant arteriosclerosis. In the present study, with the use of rat heart allografts under different doses of cyclosporine A (CsA), we investigated whether the expression of P-selectin is increased during chronic rejection and possibly coexpressed with VCAM-1 on EC. METHODS AND RESULTS: Rat cardiac allografts from DA donors to WF recipients were used. Without immunosuppression, these allografts show an irreversible rejection 7 days after transplantation. In the acute rejection model, syngeneic and allogeneic grafts were harvested 5 days after transplantation. In the chronic rejection model, allograft recipients received triple-drug immunosuppression, including azathioprine, methylprednisolone, and CsA in different doses. The grafts were removed 3 months after transplantation. During acute rejection, a significant expression of P-selectin (P < .01) and VCAM-1 (P < .05) on microvascular endothelia, but not on arteries, was noticed. During intense chronic rejection (5 mg/kg CsA), arterial EC expressed P-selectin (P < .01) and VCAM-1 (P < .05) extensively. The expression of tumor necrosis factor-alpha, a cytokine inducing both P-selectin and VCAM-1 expression, was upregulated in vascular medial cells (P < .05), in intimal cells (P < .01), and in interstitial mononuclear cells (P < .05). Linear regression analysis revealed a significant correlation between arterial P-selectin (P < .01) and VCAM-1 (P < .01) expression and the intensity of intimal thickening. Also, a significant correlation and coexpression of P-selectin and VCAM-1 in epicardial arteries was demonstrated (P < .05). CONCLUSIONS: The early expression of P-selectin on microvascular EC during acute rejection may be the basis of cell adhesion and infiltration into the site of inflammation. During chronic rejection, the intensity of arterial intimal thickening was significantly correlated with the intensity of P-selectin expression on EC, in addition to that of previously reported VCAM-1 expression. Thus, P-selectin may have a crucial role in the pathogenesis of chronic rejection in the vascular wall, augmenting the immune-mediated injury against the allograft.

Acute Disease↗