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PubMed1999

Multiglycosidorum tripterygii, a new immunosuppressant, supresses coronary arteriosclerosis after heart transplantation.

BACKGROUND: Graft coronary arteriosclerosis is the major limiting factor for long-term survival after heart transplantation. In this study, we investigate the effect of multiglycosidorum tripterygii on graft coronary arteriosclerosis and platelet-derived growth factor A mRNA expression of transplanted hearts. METHODS: Three groups of Lewis rats (n = 7/Group) underwent heterotopic heart transplantation from Wistar-King donors and were treated with cyclosporine A (10 mg/ kg/day) for 60 days (Group A) or with multiglycosidorum tripterygii (30 mg/kg/day) for 60 days (Group B) or with cyclosporine A for the first 30 days and followed by multiglycosidorum tripterygii for another 30 days (Group C). Histological evaluations of rejection and coronary arteriosclerosis, as well as Northern blot analysis on graft platelet-derived growth factor A mRNA expression were made 60 days after transplantation. RESULTS: Morphometric results indicated no significant difference in rejection among three groups. However, the extent of graft coronary arteriosclerosis in Group B (1.12 +/- 0.21) and Group C (1.41 +/- 0.19) was significantly less than that seen in Group A (1.72 +/- 0.18) (p < 0.01 andp < 0.05, respectively). Furthermore, the incidence of diseased vessels was significantly less in Group B (29.5% +/- 7.8%) and Group C (42% +/- 9.1%) compared with Group A (69.1% +/- 11%) (p < 0.01 and p < 0.05, respectively). The expression of platelet-derived growth factor A mRNA of cardiac allograft was also significantly suppressed in Group B (25.4 +/- 6.2) and Group C (39.8 +/- 9.4), when compared with Group A (62.2 +/- 12.9) (p < 0.01 and p < 0.05, respectively). CONCLUSION: Multiglycosidorum tripterygii is superior to cyclosporine in prevention and attenuation of graft coronary arteriosclerosis and this efficacy is probably associated with the depressed expression of graft platelet-derived growth factor A mRNA in the multiglycosidorum tripterygii-treated groups.

Animals↗

PubMedDate not supplied

Effect of cholesterol lowering and cardiovascular risk factors on the progression of aortoiliac arteriosclerosis: a quantitative cineangiography study.

The post-Coronary Artery Bypass Graft (Post-CABG) trial has shown that aggressive compared to moderate lowering of low-density lipoprotein cholesterol (LDL-C) delayed the progression of obstructive disease in aortocoronary saphenous vein grafts and in the left main coronary artery. Patients had been allocated to high-and low-dose lovastatin therapy for a 4-5 year period. The present study evaluated the effect of LDL-C lowering and the role of cardiovascular risk factors on the progression of arteriosclerosis in the distal abdominal aorta and common iliac arteries. From one of the participating centers of the post-CABG trial, 145 patients who had adequate imaging of the aortoiliac arteries at baseline and follow-up were included. Angiographic outcomes, presumed to reflect progression of arteriosclerosis and obtained from lumen diameter (LD) measurements using quantitative cineangiography, were as follows: significant decrease of the minimum lumen diameter (LD) and increase of the maximum LD, percent lumen stenosis, and percent lumen dilatation. These outcomes were not significantly less frequent in patients randomly allocated to aggressive compared to moderate LDL-C lowering. Of 9 cardiovascular risk factors, only 2 were significantly related to progression of aortoiliac arteriosclerosis. Current smoking predicted both percent lumen stenosis increase and, to a lesser degree, percent lumen dilatation increase (p = 0.010 and p = 0.055, respectively). Abnormally high body mass index (BMI > or = 25 kg/m2) correlated with percent lumen dilatation increase (p = 0.006). Aggressive compared to moderate LDL-C lowering did not prevent or delay the progression of aortoiliac arteriosclerosis. Smoking predicted both lumen narrowing and dilatation presumably caused by arteriosclerosis. Abnormally high BMI, reflecting overweight or obesity, was strongly associated with vessel dilatation.

Aged↗

PubMedDate not supplied

Ultrastructural evidence of cell-mediated endothelial cell injury in cardiac transplant-related accelerated arteriosclerosis.

Accelerated arteriosclerosis secondary to chronic allograft rejection is a major long-term complication of heart transplantation. Accelerated arteriosclerosis has been associated with an endothelialitis, and the majority of the involved inflammatory cells are T lymphocytes and macrophages. Coronary arteries from six heart allograft recipients with transplant-related arteriosclerosis were examined by transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Four hearts were explants from heart transplant recipients with severe accelerated arteriosclerosis who were undergoing retransplantation, and two were obtained from autopsied recipients. The patients ranged in age from 6 to 60 years (mean, 44 years). The graft survival for these six hearts ranged from 1.4 to 5.6 years (mean, 4.3 years). Lymphocytes, macrophages, and smooth muscle cells were identified by TEM in the intimas of all the vessels examined. The lymphocytes were often in contact with macrophages or in close proximity to injured endothelial cells. Areas of endothelial injury were characterized by vacuolization of endothelial cells and partial denudation of the endothelium with fibrin deposition. SEM also revealed endothelial cell injury with disorganization of the endothelium and gaps between endothelial cells. Leukocytes and platelets were often noted in these gaps. These findings suggest that accelerated arteriosclerosis in heart transplant recipients is associated with an accumulation of macrophages, lymphocytes, and smooth muscle cells in the intima as well as with lymphocyte-directed endothelial injury.

Adult↗

PubMed1985

Heart graft arteriosclerosis. An ominous finding on endomyocardial biopsy.

Heart graft arteriosclerosis remains a severe and irreversible complication of allogeneic heart transplantation despite prophylactic therapy. Immunologically mediated endothelial damage has been proposed as a stimulus for the development of graft arteriosclerosis. The vascular lesions may accumulate large amounts of lipid resembling atheromas, or may be purely proliferative, as illustrated in the case of a 42-year-old heart transplant patient who developed slowly progressive graft dysfunction at eight months posttransplantation. Endomyocardial biopsy ten months posttransplantation revealed proliferative arteriolar occlusion, while changes on the coronary angiogram were minimal. Repeat biopsy at eleven months showed ischemic myocardial necrosis. The patient expired shortly thereafter. On postmortem examination, proliferative graft arteriosclerosis affecting both intramural and epicardial vessels was present, along with massive biventricular infarction. Tissue immunofluorescence studies demonstrated extensive vascular deposition of immunoglobulin and complement. We propose that (1) the presence of proliferative arteriolar occlusion on endomyocardial biopsy is predictive of poor heart graft survival; (2) proliferative graft arteriosclerosis may appear as advanced small vessel disease before extensive large vessel involvement is detected by coronary angiogram; and (3) immunofluorescence results support an immune-mediated mechanism of vascular injury in proliferative heart graft arteriosclerosis.

Adult↗

PubMedDate not supplied

Effects of cyclosporine and 15-deoxyspergualin on coronary arteriosclerosis after heart transplantation in the rat.

The development of graft coronary arteriosclerosis remains a serious consequence after heart transplantation and may limit long-term survival. The purpose of this study was to evaluate the effects of 15-Deoxyspergualin on graft coronary arteriosclerosis after heterotopic heart transplantation in a rat model and compare the effects to those of cyclosporine treatment. Two groups of Lewis rats (n = 7 each group) underwent heterotopic heart transplantation from Fischer 344 donors and were treated with either cyclosporine (10 mg/kg/day) or 15-Deoxyspergualin (3 mg/kg/day). Histologic evaluations of rejection (scale: 0 = none, 3 = severe) and graft coronary arteriosclerosis (scale: 0 = normal, 4 = occluded) were made 60 days after transplantation. No significant difference was found between the two groups with respect to the degree of rejection (2.0 +/- 0.7 in the cyclosporine-treated group versus 2.0 +/- 0.5 in the 15-Deoxyspergualin-treated group). However, the extent of graft coronary arteriosclerosis in the 15-Deoxyspergualin-treated group was significantly less than that seen in the cyclosporine-treated group (1.11 +/- 0.34 versus 1.71 +/- 0.24, p < 0.01). Furthermore, the incidence of diseased vessels among all observed vessels was significantly lower in the 15-Deoxyspergualin-treated group compared with the cyclosporine-treated group (63% +/- 12% versus 76% +/- 7%, p < 0.05). Although the protective mechanism of 15-Deoxyspergualin is unknown, it most likely possesses a different immunosuppressive mechanism of action from cyclosporine. We concluded that 15-Deoxyspergualin is superior to cyclosporine in preventing graft coronary arteriosclerosis after heart transplantation.

Abdomen↗

PubMed1977

Relationship between arteriosclerosis and cerebral atrophy in Parkinson's disease.

Computed tomographic examinations of parkinsonian patients revealed a high incidence of cerebral atrophy, in most cases a combination of cortical atrophy and ventricular enlargement. The present study considered the relationship between cerebral atrophy and physical signs indicating or promoting arteriosclerosis such as overweight, electrocardiographic changes, hypertension, calcification of the internal carotid artery and aorta as well as elongation of the aorta. The study is based on 173 treated and untreated parkinsonian patients (89 men, 84 women) aged from 37--84 years (mean 64.6), on whom CT was performed about 5.4 years after the onset of the first symptoms of the illness. The results demonstrate an increase of pathological CT findings as well as of calcification in the carotid siphon with advanced age. No correlation was found between the other items and increasing age. Further analysis of the relationship between cerebral atrophy and signs of arteriosclerosis revealed only a statistically relevant correlation with calcification of the carotid siphon, especially with calcification of the media. Since pathological CT findings and calcification of the internal carotid artery are both related to advanced age, whereas all the other items which may be considered to be indications of arteriosclerosis do not have any clear relationship, it is concluded that the cerebral atrophy in Parkinson's disease is not caused by arteriosclerosis.

Adult↗

PubMed2000

[Arteriosclerosis and media sclerosis. A comparison of 2 calcifying vascular diseases].

PATHOGENESIS: Arteriosclerosis and Mönckeberg's mediasclerosis are vascular diseases associated with calcification of the artery wall. While mediasclerosis in most cases develops in type 2 diabetic patients, arteriosclerosis is the result of a combination of different vascular risk factors. Mönckeberg's mediasclerosis typically involves the tunica media, whereas arteriosclerosis-associated calcifications primarily involve the intima. CLINICS: Isolated mediasclerosis does not cause narrowing of the blood vessel. The disease is usually asymptomatic, specific therapy has not yet been established. The involvement of the intima in arteriosclerosis finally leads to a decreased circulation.

Arteriosclerosis↗

PubMed2003

Attenuation of aortic graft arteriosclerosis by systemic administration of Allotrap peptide RDP58.

There remains no treatment for chronic allograft rejection mainly manifested by progressive arteriosclerosis. We investigated the effect of Allotrap peptide RDP58 therapy on arteriosclerosis in an aortic allotransplant model. RDP58 was administered intraperitoneally at 0.1, 0.5, or 2.5 mg/kg, every other day after transplantation. RDP58 therapy markedly inhibited vascular intimal thickening, media necrosis, and adventitial cellular inflammation. The attenuation of arteriosclerosis was associated with the induction of heme oxygenase (HO)-1 expression, inhibition of TNF-alpha production in aortic allografts, as well as decreased specific complement-dependent cytotoxic antibodies in serum. RDP58 inhibited both smooth muscle cell (SMC) proliferation with an 80% inhibition at 100 microM without evidence of cytotoxicity and TNF-induced apoptosis of SMCs in a dose-dependent fashion. These data suggest that the suppressive effect of RDP58 on allograft arteriosclerosis is due to multiple actions of the peptide, including induction of HO-1, inhibition of TNF-alpha, and a direct effect on SMC proliferation.

Animals↗

PubMed2005

A study of arteriosclerosis in healthy subjects with HBV and HCV infection.

BACKGROUND: It is unclear whether infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) affects arteriosclerosis. We performed a cross-sectional study to clarify the effect of HBV and HCV infection on arteriosclerosis. METHODS: The study subjects were 1806 healthy individuals who visited Shimane Environment and Health Public Corporation for routine medical check-ups. Serum levels of total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, and blood glucose were investigated in all subjects. The degree of arteriosclerosis was assessed using systolic blood pressure, the bilateral ankle brachial index (ABI), the heart-carotid pulse wave velocity (HCPWV), and the heart-ankle PWV (HAPWV). These cardiovascular parameters were compared between control subjects and subjects with HBV and HCV infection, using analysis of covariance to adjust for confounding factors (sex, age, body mass index, and smoking and drinking). RESULTS: Of the 1806 subjects, 39 and 31 were diagnosed as positive for HBV and HCV infection, respectively. The remaining 1736 were considered to be the controls. Adjusted serum lipid levels in the subjects with HBV and those with HCV infection tended to be lower than those in the control subjects. Adjusted arteriosclerotic parameters in the subjects with HBV and HCV infection were similar to those in the control subjects, even after adjusting for serum lipid levels. CONCLUSIONS: Infection with HBV or HCV does not influence the severity of arteriosclerosis in healthy subjects.

Alcohol Drinking↗

PubMed1984

Thromboxane B2, 6-keto-PGF1 alpha, PGE2, PGF2 alpha, and PGA1 plasma levels in arteriosclerosis obliterans: relationship to clinical manifestations, risk factors, and arterial pathoanatomy.

Current concepts of atherogenesis based on animal and human investigations indicate prostaglandins as a key factor in atherosclerotic lesions. The plasma profiles of thromboxane B2 (TXB2), 6-keto-PGF1 alpha, PGE2, PGF2 alpha, and PGA1 were investigated by means of a sensitive radioimmunoassay technique in 40 patients with arteriosclerosis obliterans and in 30 healthy control subjects. Abnormally high levels of TXB2 and PGE2 (222.97 +/- 320.86 pg/ml, mean +/- SD, vs 20 +/- 2.1 and 352.66 +/- 235.54 vs 24.4 +/- 3, p less than 0.01) were detected in arteriosclerosis obliterans patients. The ratio between TXB2 and 6-keto-PGF1 alpha was increased from 1.2 in control subjects to 6.0 in patients. In arteriosclerosis obliterans TXB2 increased in relation to clinical manifestations and to the extension of the vascular damage. In addition, TXB2 was positively related to serum triglyceride content (r = 0.562, p less than 0.05) and inversely related to platelet count (r = 0.727, p less than 0.001). The marked imbalance between the stable metabolites of thromboxane and prostacyclin in arteriosclerosis obliterans patients provides biologic evidence which fits well with the thrombogenic theory of atherosclerosis. These results further support the theory that prostaglandins may be heavily involved in atherosclerosis.

6-Ketoprostaglandin F1 alpha↗

PubMed1981

Coarctation of the aorta. A risk factor in children for the development of arteriosclerosis.

Pressure recordings in 120 patients, aged 0-35 years, undergoing operation for coarctation of the aorta, show a slow but steady rise in both systolic and diastolic peak pressures, the highest peak registered being in patients aged 16-18 years. The finding of significant morphological changes in the aorta in this age group is the rule and these arteriosclerotic changes become more severe as the patients get older. In long-standing coarctation, the degree of mineralisation proximally is up to 10 times higher than distally. The microscopic and ultrastructural changes in the proximal segment are essentially arteriosclerotic. In conclusion, the role of coarctation of the aorta in the pathogenesis of arteriosclerosis is essentially that of hypertension, a most important risk factor of arteriosclerosis. Since arteriosclerosis also develops in the region of low blood pressure, other factors are operative. We suppose that the reduced pulse and volume pressures, which in turn diminish the "windkessel" function of the aorta may effect a change in the blood flow patterns to favour the development of arteriosclerosis.

Adolescent↗

PubMed1986

Milk and arteriosclerosis.

Milk consumption is related to arteriosclerosis. Recent landmark studies confirm a previously suspected close correlation between milk intake and arteriosclerotic heart disease. Support is therefore provided for a recently proposed novel hypothesis that arteriosclerosis is a chronic infectious disease caused by blue-green bacteria and that milk is a carrier vehicle for these contaminant organisms. A revisionist view of diet and milk in the causation of arteriosclerosis is developed. Previous hypotheses relating milk consumption to arteriosclerosis and advances in pasteurization techniques are discussed and integrated with this infection theory.

Animals↗

PubMed1987

Arteriosclerosis in East Asians.

Arteriosclerosis is remarkably common in East Asians, both in the greater subcontinent and in their adopted countries after migration. Since arteriosclerosis is an acquired disease, East Asians must possess and preserve a common cultural practice related to the cause of arteriosclerosis and its complications. Therefore, an unusual opportunity is provided to examine East Asian migration and customs, especially diet, searching for a clue to the etiology of this disease. The result of this analysis provides additional support for a new theory proposing arteriosclerosis as an infectious disease caused by Cyanobacteria.

Arteriosclerosis↗

PubMed1995

Virally induced arteriosclerosis: increased life expectancy?

The average human life expectancy has been increasing constantly since first observed in Roman Times (particularly during our century). This is usually believed to be related to such 'environmental' factors as sanitation and housing and to medical intervention. Data obtained from Vital Statistics of the United States supported the idea that these explanations are insufficient. Studies on persons who had died from conditions associated with advanced stages of arteriosclerosis (ischemic heart disease, cerebrospinal disease) showed the highest life expectancy. The inflammatory nature of arteriosclerosis and studies (by others) indicating 'protective' effects suggested that the developmental stages of arteriosclerosis (in contrast to the final stages) promote increased life expectancy. Inasmuch as certain viruses (especially the human herpes virus) are involved in the development of arteriosclerosis and because nearly everybody gets infected during childhood, this virus may be a factor in the increase of life expectancy. The work on symbiosis and on hormesis has established the fact that small amounts of parasites are often associated with beneficial effects for both the host and the parasites. All of this is in line with evolutionary expectations.

Animals↗

PubMed2003

Pravastatin decreases cold ischemia--but not alloantigen-dependent transplant arteriosclerosis.

BACKGROUND: Alloantigen mismatch and cold ischemia have been shown to induce transplant arteriosclerosis. Pravastatin (PR) decreases arteriosclerosis probably related to an immunosuppressive effect. Statins possess other nonimmune properties that may be beneficial to transplantation. We studied the effect of PR on cold ischemia and alloantigen-induced transplant arteriosclerosis in syngeneic (SYN) and allogeneic (ALLO) aortic transplantation models. METHODS: Lewis rats served as the donors and recipients for SYN transplants and Brown Norway rats were donors for ALLO transplants. Aortic segments that had been preserved at 4 degrees C in Euro-Collins solution for 0 or 24 hours were transplanted to the infrarenal aorta of the recipients PR (10 mg/kg/d) was administered for 12 weeks prior to morphometric studies. Areas of intimal thickness and its relation to total vessel area were calculated. Lipid levels were measured at 12 weeks. RESULTS: Aorta rings preserved for 24 hours showed marked intimal thickening compared to controls (SYN, CI 0 hours = 21.5% +/- 16.5% vs SYN, CI 24 hours = 50.7 +/- 9.5%, P <.05). PR significantly decreased thickening (SYN, CI 24 hours + PR = 41.7 +/- 12.2 (P <.05) vs SYN, CI 0 hours on SYN, CI 24 hours). There was a nonsignificant decrease in thickening among ALLO transplants treated with PR (ALLO = 31.4 +/- 15.9 vs ALLO + PR = 23.8 +/- 18.8; P >.05). PR had no effect on lipid levels. PR decreases cold ischemia induced transplant arteriosclerosis in this syngeneic aortic transplant model, but does not affect an alloantigen-mediated process. The beneficial effect of PR is not related to its lipid-lowering properties but probably to a nonimmune effect.

Animals↗

PubMed1995

Effect of the antioxidant probucol on transplant arteriosclerosis in aorta-allografted rabbits.

The attenuation of atherogenesis by oral probucol treatment, demonstrated in several animal studies, has been attributed to the antioxidative property of probucol. It is thought that probucol, by inhibiting oxidation of low density lipoproteins (LDL) decreases the uptake of LDL into monocytes, and thereby reduces the development of foam cells and fatty streaks. Also, the neointimal proliferation seen after balloon injury has been attenuated by treatment with probucol. Since foam cells and neointimal proliferation are both important elements of transplant arteriosclerosis, we have investigated whether probucol might also retard the development of experimental transplant arteriosclerosis. The thoracic aorta from one rabbit was transplanted as a bypass graft onto the abdominal aorta of another rabbit. Nine rabbits were treated with 1 g probucol per day and seven animals were treated with vehicle. After a recovery period of 2 weeks, all rabbits were clamped at a human level of plasma cholesterol (6 to 7 mmol/l) for a period of 3 weeks. The amount of dietary cholesterol necessary for this clamping tended to be higher in probucol treated than in vehicle-treated rabbits. The distribution of plasma cholesterol between lipoprotein classes was similar in the two groups, except for the concentration of high density lipoproteins (HDL), which was significantly lowered by probucol. Probucol markedly decreased the susceptibility of LDL and intermediate density lipoprotein plus very low density lipoprotein (IDL + VLDL) particles to oxidation, as measured by the production of conjugated dienes when adding Cu2+. Despite this, the development of transplant arteriosclerosis as well as the number of macrophages in the neointima were not significantly different in the aortic allografts from the two groups. These results suggest that antioxidative agents do not retard the development of experimental transplant arteriosclerosis.

Animals↗

PubMed1999

D-dimers in relation to the severity of arteriosclerosis in patients with stable angina pectoris after myocardial infarction.

BACKGROUND: Plasma concentrations of D-dimers show the extent of intravascular fibrinolysis of cross-linked fibrin. Higher concentrations of D-dimers are found in the plasma of arteriosclerosis patients with increased fibrin metabolism. The present study was performed in order to investigate whether there is a relationship between the severity of arteriosclerosis and fibrinolytic activity indicated by plasma levels of D-dimer. METHODS: The study populations consisted of 1112 men and 299 women with stable angina pectoris, on average 36+/-5.6 days after a myocardial infarction, as well as 326 men and 138 women with no clinical signs of cardiovascular disease. In addition to cardiological and angiological examinations, the lipid status and levels of fibrinogen, plasma viscosity, F 1+2, plasminogen, plasminogen activator inhibitor-1, D-dimer, and C-reactive protein of the participants were determined. RESULTS: The plasma concentration of D-dimers increases with age, both in the group with coronary artery disease and in the control group, with the female gender showing consistently higher concentrations in both groups. D-dimers correlate with other parameters of the lipid and coagulation systems, which explains 32.0% and 39.2% of the variance in D-dimer values in men and women, respectively. A significant increase in the level of D-dimers can be found in participants with generalized arteriosclerosis, with a left ventricular ejection fraction </=40% as well as those with left-ventricular aneurysm. CONCLUSION: This study indicates that there is increased fibrinolytic activity in patients with severe arteriosclerosis. This finding gives further support to the hypothesis that D-dimer concentration is dependent on the amount of fibrin associated with arteriosclerotic thrombi. However, because of the low specificity and wide overlap of D-dimer values between patients and controls, enhanced D-dimer values are of limited relevance above and beyond other lipid metabolism risk indicators for coronary artery disease or coronary artery disease and peripheral arterial occlusive disease.

Adult↗

PubMed1995

[Arteriosclerosis of the thoracic aorta as a source of systemic emboli. A clinico-pathologic study].

The significance of the thoracic aorta as a source of systemic emboli in addition to other sources of embolism remains unexplained. A study of 120 consecutive necropsies (65 men, 55 women; mean age 71 [29-94] years) analysed the possible correlation of the severity of arteriosclerosis of the aorta, the carotid arteries and the arteries at the base of the brain as well as cardiac changes, with potential sources of emboli and with proven emboli (n = 39). Complex and fibrous plaques in the arch of the aorta, ipsilateral carotid artery stenoses, a history of atrial fibrillation and heart weight correlated significantly with emboli on both uni- and multivariant analysis. But the presence of calcified and complex plaques in the descending aorta, as well as moderate and severe arteriosclerosis in the arteries at the base of the brain, correlated significantly only on univariant analysis. Ischaemic brain lesions had been clinically silent in twelve of 32 cases, while visceral emboli had been silent in nine out of ten cases. -It is concluded from these data that, in addition to the cardiac chambers and arteriosclerosis of the arteries at the base of the brain, advanced arteriosclerosis of the aortic arch is an important source of systemic emboli. As many of the emboli remain silent, their incidence is probably underestimated clinically.

Adult↗