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PubMed2006

Clopidogrel reduces the development of transplant arteriosclerosis.

BACKGROUND: Transplant arteriosclerosis, the hallmark feature of chronic rejection, is still the major limiting factor for the long-term success of heart transplantation. Platelets have been implicated to play a role in the pathogenesis of this disease. Therefore the aim of this study was to investigate whether platelet inhibition alone has a positive effect on the development of transplant arteriosclerosis. METHODS: Fully major histocompatibility complex-mismatched C57BL/6 (H2(b)) donor aortas were transplanted into CBA (H2(k)) recipients, and mice received different doses (1, 10, and 20 mg/kg) of clopidogrel or control saline as a daily intraperitoneal injection for 30 days. Blood was analyzed on days 2, 7, 14, and 30 by using a platelet aggregation test (adenosine diphosphate) for effectiveness of the treatment. Grafts were analyzed by means of histology and morphometry on day 30 after transplantation. RESULTS: When mice were treated daily with 1 mg/kg clopidogrel in the absence of any other immunosuppression, transplant arteriosclerosis was significantly reduced compared with that seen in saline-treated control animals (intimal proliferation of 66% +/- 9% [1 mg/kg clopidogrel] vs 77% +/- 5% [control], n = 7, P < or = .03). Daily application of 10 mg/kg and 20 mg/kg clopidogrel also significantly reduced the development of transplant arteriosclerosis compared with that seen in control animals (intimal proliferation of 61% +/- 11% [10 mg/kg clopidogrel] vs 54% +/- 10% [20 mg/kg clopidogrel] vs 77% +/- 5% [control], n = 8, P < or = .003). There was, however, no additional beneficial effect when compared with mice treated with 1 mg/kg clopidogrel (P = .06). Isografts did not show any signs of vascular lesions on day 30 after transplantation. CONCLUSION: These results demonstrate that monotherapy with clopidogrel can effectively reduce the formation of transplant arteriosclerosis in a murine aortic allograft model.

Animals↗

PubMed1976

[Clinical course of arteriosclerosis of coronary and lower limb arteries (author's transl)].

The clinical course of arteriosclerosis was evaluated in 9 patients with coronary sclerosis and in 25 with peripheral arterial occlusive disease by means of repeat angiographies following primary angiography after 22.5 and 36.6 months, respectively. During the period of observation arteriosclerosis had progressed in all cases except in two patients with peripheral arterial occlusive disease. Despite intensive therapeutic efforts including control of risk factors, dietary care, guided or unguided exercise and the attempt to change unsatisfactory living conditions, progression of arteriosclerosis could not be interrupted. If treatment delayed progression of arteriosclerosis cannot be decided. All vascular areas were affected indiscriminately by progression and no particular localisation was preferred. Intensive exercise does not seem to delay progression of arteriosclerosis.

Angiography↗

PubMed1966

Experimental induction of athero-arteriosclerosis by the synergy of allergic injury to arteries and lipid-rich diet. I. Effect of repeated injections of horse serum in rabbits fed a dietary cholesterol supplement.

In rabbits that received a dietary supplement of cholesterol, 0.5% by weight, and concommittant injections of horse serum (group III) over a period of 80 days, coronary arterial lesions developed that in the main were different in quality and distribution from those in rabbits that received the cholesterol supplement alone (group I), and of different quality from but in distribution similar to those in rabbits that received horse serum alone (group II). Fatty lesions developed in small, rarely in medium, but never in large arteries of rabbits in group I, and these changes do not resemble coronary athero-arteriosclerosis in man. Proliferative lesions without fatty change developed in large, medium, and small arteries of rabbits in group II, and some of these closely resemble human coronary arteriosclerosis without fatty change. The changes that developed in large, medium, and small arteries of rabbits in group III were in very large majority fatty-proliferative lesions. Some of these closely resemble the changes that in some cases constitute coronary athero-arteriosclerosis in man. Nuclei with caterpillarlike chromatin pattern in longitudinal section and owl eye appearance in transverse section were observed to occur in many of the proliferating cells in thickened arterial intima in hearts of rabbits in groups II and III and in some of the lipid rich "foam" cells in arterial intima and subjacent media in hearts of rabbits in group III. Such nuclei have been observed to occur in some reacting smooth muscle cells and normal immature and reacting mature striated muscle cells of the heart. These observations indicate that at least many of the cells, including "foam" cells, in thickened intima in the experimentally induced and in naturally occurring coronary athero-arteriosclerosis are smooth muscle cells that evolved in proliferative reaction to arterial injury. Fatty change developed in aortas of the rabbits in groups I and III, and was significantly greater in group III. Results of this investigation support the hypothesis that the synergy of allergic injury to arteries and lipid-rich diet can lead to athero-arteriosclerosis.

Animals↗

PubMed2000

Intragraft interleukin-4 mRNA expression after short-term CD154 blockade may trigger delayed development of transplant arteriosclerosis in the absence of CD8+ T cells.

BACKGROUND: It has recently been shown that, although anti-CD154 induces CD4+ T-cell tolerance, it is unable to prevent allograft rejection mediated by CD8+ T cells. We have also shown that anti-CD154 monotherapy does not protect the graft from the development of transplant arteriosclerosis even in the absence of CD8+ T cells. This study was designed to investigate and characterize possible mechanisms responsible for the development of transplant arteriosclerosis after CD154 blockade in the absence of CD8+ T cells. METHODS: C57BL/6 (H2b) recipients received a fully MHC-mismatched BALB/c donor aorta (H2d). Animals were either treated with anti-CD154 monoclonal antibody (mAb) in the presence or absence of CD8 T cells. Histology, morphometric measurements, immunohistochemistry, and the production of alloantibodies (IgM, IgG1, IgG2a) were analyzed on days 14, 30, and 50 after transplantation. Cytokine production within the graft was investigated by competitive reverse transcription-polymerase chain reaction on day 14. RESULTS: Combined treatment with anti-CD154 and a depleting CD8 mAb resulted in a delay in the development of transplant arteriosclerosis (intimal proliferation: 33+/-10% vs. 67+/-11% untreated control, day 30) but ultimately did not prevent its progression (intimal proliferation: 55+/-10% vs. 78+/-9% untreated control, day 50). Although there was a significant decrease in the number of CD4+, CD11b+, and CD40+ graft-infiltrating cells and a reduction in the formation of donor-specific IgG1 alloantibodies in recipients treated with anti-CD154 and anti-CD8 mAbs, mRNA for interleukin (IL)-4 was increased, suggesting a shift in the intragraft cytokine profile towards a Th2-like pattern. CONCLUSIONS: Our data provide evidence that short-term CD154 blockade is insufficient to prevent transplant arteriosclerosis, even in combination with CD8+ T-cell depletion. Moreover, the increased expression of the Th2 cytokine interleukin-4 within the graft may be responsible for the development of transplant arteriosclerosis in the long term.

Animals↗

PubMed2003

Novel anti-inflammatory actions of amlodipine in a rat model of arteriosclerosis induced by long-term inhibition of nitric oxide synthesis.

Amlodipine (a new class of calcium channel antagonist) has been shown to limit the progression of arteriosclerosis and decrease the incidence of cardiovascular events. The mechanisms underlying the beneficial effects of amlodipine, however, remain unclear. Therefore, we hypothesized that amlodipine attenuates the development of arteriosclerosis through the inhibition of inflammation in vivo. Long-term inhibition of nitric oxide (NO) by administration of a NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), to rats induces coronary vascular inflammation [monocyte infiltration, monocyte chemoattractant protein-1 (MCP-1) expression, increased activity of angiotensin-converting enzyme (ACE)], and arteriosclerosis. Here, we used the rat model to investigate the anti-inflammatory effects of amlodipine in vivo. Treatment with amlodipine markedly inhibited the L-NAME-induced increase in vascular inflammation, oxidative stress, and local ACE and Rho activity and prevented arteriosclerosis. Interestingly, amlodipine prevented the L-NAME-induced increase in MCP-1 receptor CCR2 expression in circulating monocytes. Amlodipine markedly attenuated the high mortality rate at 8 wk of treatment. These data suggest that amlodipine attenuated arteriosclerosis through inhibiting inflammatory disorders in the rat model of long-term inhibition of NO synthesis. The anti-inflammatory effects of amlodipine seem to be mediated not only by the inhibition of local factors such as MCP-1 but also by the decrease in CCR2 in circulating monocytes. Inhibition of the MCP-1 to CCR2 pathway may represent novel anti-inflammatory actions of amlodipine beyond blood pressure lowering.

Amlodipine↗

PubMed1997

Dose-dependent suppression of transplant arteriosclerosis in aorta-allografted, cholesterol-clamped rabbits. Suppression not eliminated by the cholesterol-raising effect of cyclosporine.

Cyclosporine may suppress transplant arteriosclerosis; however, it also raises plasma cholesterol, which could promote the disease. Our aim was to test these hypotheses experimentally. In experiment 1 (n = 34), cholesterol was clamped at a human level of 5 to 7 mmol/L, and rabbits were given either saline or cyclosporine in a low, medium or high dose. In experiment 2 (n = 15), in which dietary cholesterol was fixed at 0.05 g.kg-1.d-1, and experiment 3 (n = 16), in which no dietary cholesterol was added to the chow, rabbits were given either medium-dose cyclosporine, saline, or vehicle. The duration of each experiment was 5 weeks. In experiment 1, cyclosporine attenuated the development of transplant arteriosclerosis dose dependently (trend test: P < .0001). Cyclosporine also suppressed, in a dose-dependent manner, the activation of the immune system (trend test: P < .05) and the presence of T lymphocytes (trend test: P < .0001) and macrophages in the intima (trend test: P < .01). Despite a higher plasma cholesterol level in cyclosporine-treated rabbits compared with saline-treated rabbits in both experiment 2 (4.9 versus 2.9 mmol/L) and experiment 3 (1.6 versus 0.8 mmol/L), transplant arteriosclerosis was significantly reduced by cyclosporine (Mann-Whitney U test; P < .05 and P < .05). These results suggest that cyclosporine suppresses experimental transplant arteriosclerosis dose dependently. Accordingly, in the assessment of the optimal cyclosporine dose to heart-transplanted patients, it should be taken into account that a dose reduction may promote transplant arteriosclerosis.

Animals↗

PubMed2002

Vascular endothelial growth factor is necessary in the development of arteriosclerosis by recruiting/activating monocytes in a rat model of long-term inhibition of nitric oxide synthesis.

BACKGROUND: It remains unclear whether vascular endothelial growth factor (VEGF) is a proarteriosclerotic or an antiarteriosclerotic factor. We recently reported that long-term inhibition of nitric oxide by administering Nomega-nitro-L-arginine methyl ester (L-NAME) induces coronary vascular inflammation and arteriosclerosis. METHODS AND RESULTS: We used this animal model to investigate the role of VEGF in arteriosclerosis. We blocked VEGF activity in vivo by transfecting with plasmid DNA encoding the murine soluble FLT-1 (sFLT-1) gene into thigh muscle. Soluble FLT-1 can suppress VEGF activity both by sequestering VEGF and by functioning as a dominant-negative inhibitor of VEGF receptors. We observed vascular inflammation associated with increased VEGF expression within 3 days of L-NAME administration, which was prevented by pretreatment with ACE inhibitor, angiotensin II receptor antagonist, or neutralizing monocyte chemoattractant protein-1 antibody. The sFLT-1 gene transfer attenuated the early vascular inflammation and prevented late arteriosclerosis. The sFLT-1 gene transfer also inhibited increased expression of monocyte chemoattractant protein-1 and transforming growth factor-beta, indicating creation of a positive feedback loop to cause arteriosclerosis. CONCLUSIONS: VEGF is necessary in the development of arteriosclerosis by mediating monocyte recruitment and activation in this model.

Animals↗

PubMed2003

Effects of lipid abnormalities on arteriosclerosis and hemostatic markers in patients under hemodialysis.

Vascular events caused by arteriosclerosis are the major cause of death in patients under hemodialysis (HD). Arteriosclerosis is associated with lipoprotein abnormalities such as increased serum levels of low-density lipoprotein (LDL), especially of modified LDL (M-LDL) and oxidized LDL (Ox-LDL). We examined the relationship between markers of arteriosclerosis, hemostasis, and lipid metabolism in patients with chronic renal failure, hyperlipidemia, and healthy volunteers. In patients under HD, the serum levels of total cholesterol, LDL, and triglyceride (TG) were decreased, but the serum levels of M-LDL were increased compared to HL and healthy volunteers. In patients with CRF, the serum levels of Ox-LDL in patients under HD were lower than in those under continuous ambulatory peritoneal dialysis or conservative therapy. The plasma levels of antithrombin and protein C were significantly lower and the plasma levels of thrombomodulin were significantly higher in patients under HD compared to those under conservative therapy. These data show that patients under HD were more in hypercoagulable state than those under conservative therapy. Among patients under HD, only the plasma levels of von Willebrand factor were significantly increased in patients with more than 30 U/L of Ox-LDL compared to those with less than 30 U/L of Ox-LDL. There was no significant difference in the tests of arteriosclerosis among M-LDL values and Ox-LDL values. These findings suggest that abnormalities of lipid are not the main risk factor for arteriosclerosis disease in patients under HD.

Aged↗

PubMed1992

Coronary artery disease in patients with arteriosclerosis obliterans of the lower extremities or aortic aneurysm.

Routine coronary angiography was performed in order to determine the incidence and clinical condition of coronary artery disease in 37 patients with arteriosclerosis obliterans or aortic aneurysm. Coronary angiography demonstrated significant stenosis in 12 (57%) of 21 patients with arteriosclerosis obliterans and in 7 (44%) of 16 patients with aortic aneurysm. The prevalence of risk factors for arteriosclerosis was similar for patients with arteriosclerosis obliterans and those with aortic aneurysm, and similar for patients with and without coronary artery stenosis. But coronary artery disease is often silent in patients with arteriosclerosis obliterans.

Aged↗

PubMed1998

Cellular and molecular mechanisms in transplant arteriosclerosis (Review).

Although significant progress has been made towards the understanding of cellular and molecular mechanisms underlying the pathogenetic pathways of transplant arteriosclerosis, its knowledge is still not comprehensive. Nevertheless, experimental and clinical studies have enabled us to discover some of the complex processes involved in the progression and evolution of transplant arteriosclerosis. Despite the advances in transplantation immunology and atherosclerosis research, transplant arteriosclerosis still remains a major cause of allograft failure. A curative treatment, in order to inhibit or at least modify the development of transplant arteriosclerosis, is urgently needed. This review article highlights some of the more recent aspects of cellular and molecular pathology of transplant arteriosclerosis that may add to our current and future diagnostic and curative interventions.

Animals↗

PubMed1992

[The effect of arteriosclerosis on the wall elasticity of the human common carotid artery].

The arterial distensibility and the modulus of volume elasticity of more than 100 isolated human carotid arteries was measured and correlated with arteriosclerosis and aging. The loss of arterial distensibility progresses steadily with aging. Arteries with severe arteriosclerosis and arteries with minimal arteriosclerosis show almost similar distensibility. On the other side the differences between distensibility of arteries with moderate arteriosclerosis and arteries with minimal as well as severe arteriosclerosis, especially in the younger and middle ages, are significant.

Aging↗

PubMedDate not supplied

[Clinical significance of arteriosclerosis indices of lipid metabolism and age dependence].

Age, arteriosclerosis indices, HDL-cholesterol, hyperlipoproteinemia, lipoproteins In 193 normal persons, 86 patients with arteriosclerosis obliterans of the lower extremities, 170 HLP patients, 87 adiposity patients and 22 chronic alcoholics were determined the arteriosclerosis indices (formula; see text) The arteriosclerosis indices increase in healthy males from the age of 30 and healthy females from the age of 45. In case of peripheral arterial occlusion HLP and adiposity the arteriosclerosis indices are elevated and give diagnostic and prognostic hints as to increased arteriosclerotic risk for these diseases.

Adolescent↗

PubMed1996

[Arteriosclerosis and osteoporosis].

A certain number of elements suggest a link between arteriosclerosis and osteoporosis. Generally, osteoporosis in women is considered to result from altered secretion of sexual hormones after menopause and in elderly subjects from hyperparathyroidism secondary to calcium and vitamin D deficiency. As for the heart, the brain, the kidney or muscle, bone tissue could also be altered by vascular aging and arteriosclerosis. Large epidemiological studies have demonstrated a relationship between bone mineral density, measured by monophotonic absorptiometry and mortality due to cerebral vascular events. Several hypotheses have been proposed to explain this relationship including lower endogenous estrogen levels and arteriosclerosis of the renal vessels favoring perturbed vitamin D metabolism. Arteriosclerosis could also have a direct effect on bone tissue via an ischemic mechanism. The pathophysiolojical mechanisms are not fully understood, but could involve hormone and cytokine-dependent bone remodeling and the complementary actions of bone tissue and the hematopoietic bone marrow functioning as an unit. Further epidemiological studies would be useful to confirm the relationship between arteriosclerosis and osteoporosis. The efficacy of vasodilator drugs on osteoporosis could be tested and histology and immunochemical studies could help in our understanding of the effect of ischemia on bone metabolism.

Animals↗

PubMed1977

[Arteriosclerosis and liver cirrhosis (author's transl)].

The degree of arteriosclerosis in 176 autopsies of liver cirrhosis (patients in the age range of 51 to 70 years) was compared with that of controls (without liver disease). It was found that the "protective influence" of liver cirrhosis of the process of arteriosclerosis is only true for normotonic. Associated with arterial hypertension severe arteriosclerosis is predominant in liver cirrhosis. There is even some evidence that arteriosclerosis in hypertonics with liver cirrhosis is more increased than in controls without liver diseases. The factors influencing arteriosclerosis in liver cirrhosis are discussed.

Aged↗

PubMed1977

Obliterative arteriosclerosis of extremities in patients with coronary heart disease.

In a group of 314 patients after past myocardial infarction or an episode of acute coronary insufficiency, angiological examination, repeated after a one-year interval, was performed. In the first examination, signs of obliterative arteriosclerosis in the lower extremities were found in 18.8% of the patients. It was noteworthy that 34% of patients with peripheral obliterative arteriosclerosis had no complaints connected with an impairment of circulation in the limbs. On the basis of the second examination, performed after a one-year interval, it was found that the annual incidence of obliterative arteriosclerosis in the lower extremities was 7.4%. In 66% of patients showing signs of obliterative arteriosclerosis at the first examination, objective impairment of peripheral circulation was observed after a one-year interval. In none of the patients did the investigators find signs of obliterative arteriosclerosis in the upper extremities.

Adult↗

PubMed1998

[Chlamydia pneumoniae chronic infection in the development of arteriosclerosis].

On the basis of several epidemiological investigations performed simultaneously in the eighties and then in early nineties, a presumption has been put forward that is a relationship between the incidence of arteriosclerosis, especially of the coronary arteries and the presence of antibodies against antigens of Chlamydia pneumoniae in the blood serum. These investigations revealed that an infections by Chlamydia pneumoniae is an independent risk factor in the development of arteriosclerosis as well as hypertension, cigarette smoking and increased level of lipids in the blood serum. The present work is a survey of the current literature on the subject of presumable role of these bacteria in the process of arteriosclerosis. Clinical and epidemiological reports have been presented and two investigations on the animal models using rabbits and mice have been discussed. On the basis of the presented studies, it can be observed that Chlamydia pneumoniae has a specific tendency to accumulate not only in the respiratory system, but also in the arteries affected by arteriosclerosis. However, studies of the relationship between an infections by these bacteria and development of arteriosclerosis are far from final explanation of this problem.

Animals↗

PubMed2003

[Cardiac risk in men with angiographically normal coronary arteries or minimal coronary arteriosclerosis].

It is accepted that the assessment of the global cardiac risk for the occurrence of a coronary event is basically for preventive strategies. In a retrospective study, we have estimated the initial 10-year risk in 54 consecutive men (mean age 53.1 years) without clinically coronary artery disease (CAD) by using the PROCAM Score Scheme and the FRAMINGHAM Scoring System. All individuals underwent coronary angiography for diagnostic reasons. Inclusion criteria were angiographically normal coronary arteries or coronary vessels with minimal arteriosclerosis (luminal diameter reduction <35%). The extent of initial coronary arteriosclerosis was estimated semiquantitatively by the number of wall changed vessel segments S (proximal, medial, distal) of the 3 large epicardial coronary arteries. Individuals were divided into 3 risk categories with a 10-year risk/PROCAM <5% (gr. I), 5-20% (gr. II) and >20% (gr. III). The mean 10-year risk/PROCAM and FRAMINGHAM of the entire group was 14.0 and 14.1%, respectively. The number of vessel segments with minimal arteriosclerosis averaged S=2.6. There was a significant linear relation between the number of arteriosclerotic segments, grouped by S=0, 1-2, 3-4, >4 and the mean corresponding 10-year risk/PROCAM (r=0.97; p<0.025). The mean 10-year risk/PROCAM and FRAMINGHAM in gr. I was 2.1+/-1.1 and 5.1+/-3.5%, in gr. II 11.1+/-4.4 and 14.5+/-7.1% and in gr. III 25.4+/-3.3 and 20.4+/-6.2%, respectively (gr. I vs II vs III: p<0.005). In gr. I an average of S=0.8+/-1.4 segments, in gr. II of S=2.4+/-1.8 and in gr. III of S 4.1+/-1.8 vessel segments revealed initial coronary arteriosclerosis (gr. I vs II vs III: p<0.01 <0.0025, respectively). In 42 of the 54 men (78%) there were 10-year follow-up data regarding sudden cardiac death, fatal and non-fatal myocardial infarction available. Thirty-two men of the follow-up group (78%) showed no cardiac event (gr. A, mean age 53.3+/-8.3 years). In 10 men (23.8%, 95% CI 19.7-32.5%) a fatal or non-fatal event occurred (gr. B, mean age 55.6+/-7.5 years). At the beginning of the study, the 10-year risk/PROCAM and FRAMINGHAM in gr. A was 12.0+/-9.3 and 14.1+/-8.0%, respectively. In gr. B the estimated 10-year risk was 18.7+/-8.0% (gr. A vs B: p<0.025) and 17.6+/-7.6%, respectively (gr. A vs B: p=ns). No cardiac event occurred in the low risk group <5% (mean 2.4+/-1.2%). In 23.8% (95% CI 19.2-36.8%) of the group with mild or moderate risk (5-20%, mean 10.4+/-4.1%) and in 38.5% (95% CI 29.5-53.1%) of the high risk group (>20%, mean 25.6+/-3.3%) a fatal or non-fatal event occurred. The total cardiac mortality was 7.1% (95% CI 6.6-15.1%). Our study indicates that men mean aged 53 years without clinical CAD and with a high 10-year risk (>20%), judged by the PROCAM Score Scheme, have a high probability of subclinical coronary arteriosclerosis and for the occurrence of a cardiac event. Thus, a strict distinction between primary and secondary prevention does not seem to be justified any more.

Adult↗

PubMed1998

Chlamydia pneumoniae infection is frequent but not associated with coronary arteriosclerosis in cardiac transplant recipients.

We sought to explore the relation between Chlamydia pneumoniae, cytomegalovirus (CMV), and cardiac transplant-associated arteriosclerosis. Serologic evidence of past Chlamydia pneumoniae infection was investigated in 3 patient groups at the time of cardiac catheterization: cardiac transplant recipients (n=49), patients having coronary artery bypass grafting (CABG) (n=39), and a control group free of angiographic coronary artery disease (n=21). High Chlamydia pneumoniae immunoglobulin G titers (> or =1:160) were more frequently observed in cardiac transplant recipients (odds ratio[OR] 13.7; 95% confidence intervals [CI] 1.6 to 117.4, p <0.05) and CABG patients (OR 21.7; 95% CI 1.6 to 287.0, p <0.05) than in controls. However, high Chlamydia pneumoniae titers did not distinguish between cardiac transplant recipients with or without angiographic transplant-associated arteriosclerosis or CABG patients with or without bypass vein graft disease. Furthermore, there was no significant relation between elevated Chlamydia pneumoniae titers and the presence or progression of transplant-associated arteriosclerosis in the subgroup of patients who were also CMV positive. Yet, analysis of the same angiograms demonstrated an association between CMV infection and the recent progression of transplant-associated arteriosclerosis. Thus, patients with cardiac transplantation have evidence of past Chlamydia pneumoniae and CMV infection but Chlamydia pneumoniae does not appear to have an independent role or synergistic relation to CMV in the development of transplant-associated arteriosclerosis.

Adult↗