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PubMedDate not supplied

Effect of elastase on primary graft patency after femoralpopliteal arterial bypass for arteriosclerosis obliterans: a randomized, controlled study.

METHODS: Studies were carried out on 104 limbs with femoralpopliteal bypasses for arteriosclerosis obliterans (ASO). They were randomized to a group receiving elastase (10800 EL. U. P.O. per day) with an antiplatelet drug (Elastase group, 58 patients) or a group receiving only the antiplatelet drug (Control group, 46 patients). The follow-up period ranged from 24 to 36 months after operation at 22 institutions across Japan. RESULTS: The cumulative graft patency rate was higher in the Elastase group than the Control group, but the difference lacked statistical significance. When autogenous saphenous veins were used, the cumulative graft patency rate was significantly higher in the Elastase group than the Control group. CONCLUSIONS: The present study suggests that elastase is effective in maintaining graft patency in femoralpopliteal arterial bypass when an autogenous saphenous vein is used as a graft.

Aged↗
PubMed1998

Reduced transplant arteriosclerosis in murine cardiac allografts placed in interferon-gamma knockout recipients.

To investigate the functional role of interferon (IFN)-gamma in transplant arteriosclerosis, BALB/c hearts were transplanted in immunosuppressed C57BL/6J recipients with (n = 10) or without (n = 10) targeted IFN-gamma gene deletion. In 55-day heart allografts, IFN-gamma deficiency resulted in a significant decrease in vascular thickening. The severity of intimal thickening measured as the percentage of luminal occlusion (mean +/- SEM) in all elastin stained vessels (n = 410) decreased from 37+/-5% in wild-type recipients to 18+/-5% in IFN-gamma -/- recipients (P < 0.005). In the few diseased vessels in grafts from IFN-gamma -/- recipients, the neointima was more cellular with a 90% increase in the nuclear density. This finding correlated with a 50% reduction in fibrosis estimated by alpha-smooth muscle actin cell accumulation in the neointima. The reduction in severity and altered composition of vascular thickening in grafts from IFN-gamma -/- recipients shows that IFN-gamma contributes to arteriosclerotic development following transplantation.

Animals↗
PubMed1998

[Magnetic resonance arteriography as a method for diagnosing arteriosclerosis of the lower extremities].

The purpose of our study was the evaluation of usefulness of Magnetic Resonance Angiography in diagnostic process in patients with arteriosclerosis of lower extremities and complications such as aneurysms and pseudoaneurysms. 105 patients were examined using 2D TOF method. We concluded the results were very similar as in radiological examinations. The MRA is a very helpful method in evaluation of constriction and occlusion of iliac and femoral arteries and aorta.

Adult↗
PubMed1998

Cardiac allografts from IL-4 knockout recipients: assessment of transplant arteriosclerosis and peripheral tolerance.

To study the role of IL-4 in tolerance induction and transplant arteriosclerosis, BALB/c hearts were transplanted into C57BL/6J wild-type or IL-4 knockout (IL-4(-/-)) recipients. A 30-day course of anti-CD4/8 mAb was used to induce long term graft survival. Primary graft survival was 50% (5 of 10) in IL-4(-/-) recipients comparable to 63% (5 of 8) in wild-type recipients. Mice with allografts surviving >80 days were tested for tolerance by challenge with a second donor or third party (CBA) heart. Secondary donor-strain heart grafts survived >30 days, but showed histologic evidence of ongoing alloimmune response. Third party hearts rejected rapidly. Although immunostaining and 32P RT-PCR assays showed no differences in the mononuclear cell infiltration and T cell activation between IL-4(-/-) and wild-type tolerant recipients, some monokines (IL-12, TNF-alpha, and allograft inflammatory factor-1) were up-regulated in grafts from IL-4(-/-) recipients. Computer-assisted analysis of elastin-stained vessels revealed that the severity of vascular thickening (percentage of luminal occlusion, mean +/- SD, n = 329) was similar in grafts from IL-4(-/-) (63.7 +/- 16.9%) and wild-type (69.5 +/- 17.6%) recipients. Thus, IL-4 deficiency did not alter primary or secondary graft survival, infiltration, or vascular thickening. The selective alterations in monokine expression suggests that alternative pathways are activated and may compensate in IL-4(-/-) mice.

Animals↗
PubMed1998

[Control of the progress of arteriosclerosis in high risk subjects treated with mesoglycan. Measuring the intima media].

BACKGROUND: Noninvasive ultrasonic biopsy (UB) can be used to classify arteriosclerotic lesions and their progression in the carotid and femoral bifurcation. Also the evaluation of intima-media thickness (IMT) is useful to quantify the progression of early arteriosclerosis. METHODS: Two randomly selected groups of asymptomatic subjects were included in a 18 month, open study. One group was treated with oral mesoglycan (200 mg/day) and one group was followed-up as control. The two groups were comparable for age and sex distribution. RESULTS: The average UB score was 14.4 +/- 5 in the treatment group and 14.3 +/- 8 in the control group. After 18 months the UB score was 15.7 +/- 4 in the treatment and 16.2 +/- 6 in the control group. The average increase in IMT in 18 months in the treatment group was 0.016 mm equivalent to 0.0106 mm per year. In the control group the average increase was 0.119 equivalent to 0.0793 per year. Therefore the increase in IMT was 7.48 times greater in the control group. These differences were significant (p < 0.05). Two drop-outs were recorded in the treatment group and 1 in the control group. CONCLUSIONS: In conclusion IMT measurements showed a decreased level of IMT progression in subjects under mesoglycan treatment. These results need to be confirmed by a larger randomised study.

Arteriosclerosis↗
PubMed1998

[99mTc-tetrofosmin exercise leg perfusion scintigraphy in arteriosclerosis obliterans (ASO)--assessment of leg ischemia using two phase data acquisition].

Twenty-one patients with arteriosclerosis obliterans (ASO) were studied with 99mTc-tetrofosmin exercise leg perfusion scintigraphy using the delayed administration method. In this method, tracer was injected 4 minutes after termination of symptom-limited repetitive climbing of a stair to validate prolonged vasodilatation in an ischemic lower limb after exercise. Visual and quantitative analyses were performed to evaluate a diseased leg using dynamic and static images. On a posterior whole body image, all cases except one showed decreased foot uptake in the affected side (affected normal ratio; ANR = 0.82 +/- 0.14). On dynamic images, 9 cases showed transient hyper-accumulation (blush phenomenon) only in the thigh of the affected side suggesting that this valuable finding may be a useful diagnostic sign to distinguish a diseased leg. Sensitivity and positive predictive value were 71.4% and 93.8% to detect a diseased leg based on more than one finding of non-visualization of ilio-femoral artery, muscle-soft tissue blush, and early venous return in a dynamic study. Moreover, a low uptake of ANR of below 0.90 in the foot in the static study gave an improved sensitivity of 85.7%. The transit time of the diseased legs (12.0 +/- 3.1 sec.) which was determined as the interval between the time of arterial and venous peak counts was significantly shorter than that of normal legs (17.3 +/- 4.5 sec.; p < 0.0001, paired t-test). The cases with blush phenomenon showed significantly higher thigh ANR (1.04 +/- 0.11) than those without (0.94 +/- 0.08; p < 0.05, unpaired t-test). These results could reflect prolongation of a hypervascular state after exercise in a diseased leg which sometimes induced blush phenomenon at arterial phase and high leg uptake at static phase. This scintigraphy is useful for the detection of a diseased leg as well as for grasping changes of vascular regulation after stress in patients with ASO.

Aged↗
PubMed1998

[Introductory review of diagnostic approach to arteriosclerosis].

Investigation of the pathogenesis of arteriosclerosis and/or atherosclerosis has been progressed using molecular biology. New concepts have been developed and, receptors and substances have been found clinically and experimentally, which have led us to create new methods of evaluating or diagnosing the grade of atherosclerosis lesion. Dealing with the new concepts or knowledge in this symposium, this introductory paper describes an overview of pathogenesis of atherosclerosis, from which the new methods of evaluating or diagnosing lesion has been exploited. The injury to the endothelium leads to endothelial cell dysfunction, which initiates the acceleration of LDL oxidation and increases adherence of monocytes, macrophages and T lymphocytes, migrating subendothelially and causing large foam cells to develop because of lipid accumulation. Macrophages and platelets release many growth factors, which accelerate the growth of vascular smooth muscle cells, forming fibrous plaque. In these pathogenic processes of atherosclerosis, angiotensin II participates in releasing growth factor for cell proliferation and hepatocyte growth factor (HGF) participates in revascularization of the sclerotic lesion, suggesting a candidate marker for atherosclerosis. Hyperlipidemia and hypercoagulation are the major factors in advanced atherosclerosis. Using new methods to evaluate or diagnose lesions, further therapy and prevention for atherosclerosis will progress in future.

Arteriosclerosis↗
PubMed1976

Mönckeberg's arteriosclerosis revisited: or silver vessels among the old.

This study showed that Mönckeberg's arteriosclerosis was found in 23 patients over the age of 60. Diabetes or probable diabetes mellitus was found in 22 out of 23 of these patients. It is concluded that roentgenographic demonstration of MAS in this age group is highly specific for diabetes mellitus. Further, a pilot study suggests that if MAS is present, without demonstrable plain film evidence of coexistent IAS, the chances of the patient having elevated cholesterol seems to be approximately one quarter that of the general population over 60. His chances of an elevated triglyceride appear to be about half that of the same population group.

Age Factors↗
PubMed1997

[Musical relaxation therapy on the cerebral arteriosclerosis].

The transcranial Doppler and psychological measurement methods were used to evaluate the effect of musical relaxation therapy on the cerebral arteriosclerosis. The results showed that the musical relaxation therapy could improve the cerebral blood flow (physiological), offset the Type A behavior and eliminate the emotional disturbance (psychological), and that its effect was better than that of the control patients. The mechanism of the effect may be related to the 1/f sound wave (physical), abdominal respiration with long expiration and involuntary inspiration (physiological) and the hinting effects of the inducing phrases (psychological).

Aged↗
PubMed1976

Zinc, copper and ceruloplasmin in arteriosclerosis.

High serum levels of Zn, Cu and Ceruloplasmin were found in 13 patients with arteriosclerosis when compared with controls. The Zn/Cu ratio is much higher in arteriosclerotic patients than in healthy subjects.

Adult↗
PubMed1985

The erythrocyte aggregation value as a measure of the risk of myocardial infarction and arteriosclerosis of peripheral arteries.

The erythrocyte aggregation value (AW) has been determined in groups of patients with and without coronary heart disease (CHD) and in a group of apparently normal subjects, using the Metricell apparatus as described by Kachel et al. The following results were obtained: There was a close correlation between the AW and the existence of CHD or arteriosclerosis of peripheral arteries. The precision of the retrospective prediction of CHD by this noninvasive test in male subjects aged over 45 years (total CHD prevalence = 0.494) was: sensitivity = 0.571, specificity = 0.767. The predictive value of positive tests (PVpos) was 0.706, of negative test (PVneg) 0.647. The discriminatory ability of the AW test was superior to that of serum cholesterol determinations or measurement of other CHD risk factors made in the same population. The AW rises exponentially with the total score for risk factors for CHD hazard for the subject. It appears, however, from the insignificant correlations observed that there is no direct connection between the AW and any single risk factor.

Cholesterol↗
PubMed1993

Lipid peroxides and antioxidant defenses in accelerated transplantation-associated coronary arteriosclerosis.

Accelerated coronary artery disease develops in most if not all heart transplant recipients within the first year after transplantation. Increased lipid peroxidation seems to be involved in atherogenesis. In these patients we have investigated whether there is an association between lipid peroxidation, reduced antioxidant defenses, and some conventional coronary risk factors. Lipid peroxides, lipids, uric acid, albumin, antioxidant enzymes and their cofactors (the trace elements selenium, iron, copper, and zinc) have been determined in heart transplant recipients compared with nonrecipients with coronary artery disease. Lipid peroxides (p = 0.002) and uric acid (p = 0.01) were higher and zinc (p = 0.001) was lower in heart transplant recipients. Thirteen of 30 transplant recipients compared with one of 30 nonrecipients (p < 0.001) had very low (less than 10 mumol/L) zinc levels. Antioxidant enzymes and other trace elements were not significantly different. In univariate regression analysis, zinc correlated positively with albumin (p = 0.02) and negatively with lipid peroxides (p < 0.05). Uricemia had a strongly positive correlation with hydroperoxides (r = 0.45; p = 0.0001). In stepwise multivariate regression analysis, lipids, uricemia, creatinine, and zinc were significant (p < or = 0.004) predictors of the lipid peroxide level. Cyclosporine and corticosteroid dosages were significant (p = 0.01) determinants of zinc concentration in the transplant recipients. Although a causal relationship between increased lipid peroxidation and accelerated arteriosclerosis is not definitely demonstrated, the results of this analysis suggest new insights into conventional coronary disease risk factors and possible therapeutic interventions; further controlled trials are needed.

Adult↗
PubMed1994

Expression of meta-vinculin in human coronary arteriosclerosis is related to the histological grade of plaque formation.

In the present study we demonstrate that the quantitative reduction of meta-vinculin expression parallels histological changes during the course of coronary arteriosclerosis. Immunofluorescence stainings of coronary arteries revealed that vinculin distribution resembled that of other smooth muscle-specific cytoskeletal proteins like alpha-actin, caldesmon or myosin light chain kinase in labeling smooth muscle cells brightly. Although close to arteriosclerotic plaques, the cellularity as measured by the density of nuclei was often not significantly altered. Cells of this location expressed markedly reduced amounts of vinculin, suggesting that they are smooth muscle cells of a synthetic phenotype. To determine the fractional meta-vinculin content in arteriosclerotic lesions, we performed densitometric scanning of immunoblots incubated with anti-vinculin monoclonal antibodies reacting with both meta-vinculin (150 kDa) and vinculin (130 kDa). In parallel, each tissue sample was evaluated histologically for the degree of arteriosclerotic alterations according to the morphometric atheroma score of Stratford et al. (n = 13). In type 1 lesions covering slight intimal thickening, meta-vinculin represented 36% (mean, range 35%-39%) of the total vinculin immunoreactivity. In type 2 lesions consisting of fibrous plaques of up to twice the original artery wall thickness, meta-vinculin accounted for 28% (mean, range 22%-35%) of the total vinculin content. Meta-vinculin was substantially reduced in type 3 lesions (mean 13%, range 8%-18%) which are characterized by extensive atheromatous plaques. Thus, the meta-vinculin/vinculin ratio differed significantly between early, intermediate and advanced phases of coronary arteriosclerotic plaque formation.

Aged↗
PubMed1992

Morphology of graft arteriosclerosis in cardiac transplant recipients.

The morphologic features of graft arteriosclerosis (GA) and other vascular lesions were semiquantitatively evaluated. Five failed cardiac allografts attributable to GA and five other allografts were obtained from nine autopsies and one surgical explanation. The subjects, aged 4.5 to 67 years, had a mean allograft survival of 735 +/- 184 days. A total of 1,174 arterial and 754 venous cross-sections were reviewed. Intimal fibrosis (nine cases, 254 arteries, and 118 veins), fibrofatty plaques (eight cases and 35 arteries), and cellular intima thickening and concentric foam cell lesions (eight cases, 326 arteries, and 20 veins) were seen. Cellular lesions contained T lymphocytes, monocytes, and cells of smooth muscle cell origin detected by staining using the immunoperoxidase technique. Allografts with severe GA had a greater luminal stenosis in epicardial arteries (P less than .05), greater cellular proliferation in large mural arterial lesions (P less than .004), and more foam cell lesions in both arteries (P less than .06) and veins (P less than .03) than other allografts. Medical fibrosis and thinning were present in six allografts. Severity of acute rejection (P less than .01) was correlated with the presence of GA. The morphology and distribution of GA is heterogeneous, with evidence supporting an immune-mediated pathogenesis.

Adult↗
PubMed2006

Impact of coronary endothelial function on the progression of cardiac transplant-associated arteriosclerosis: effect of anti-oxidant vitamins C and E.

BACKGROUND: Excessive vascular oxidant stress has been implicated in cardiac transplant-associated arteriosclerosis (TxAA). In a recent placebo-controlled study of 40 cardiac transplant recipients, vitamin C 500 mg twice a day and vitamin E 400 IU twice a day for 1 year retarded the progression of TxAA, as assessed by intravascular ultrasound (IVUS). Endothelial dysfunction is a key feature of TxAA and reflects oxidant stress. We hypothesized that coronary endothelial dysfunction portends greater TxAA progression and a larger therapeutic response to anti-oxidant vitamins. METHODS: In this pre-specified analysis, the 40 cardiac transplant recipients were categorized according to normal or abnormal coronary endothelial vasomotor function at baseline, as assessed by acetylcholine (10(-8) to 10(-6) mol/liter). The effect of anti-oxidant vitamins within these two groups of patients was assessed by the change in intimal index over 1 year using IVUS. RESULTS: With placebo (n = 21), the increase in intimal index was greater in the presence vs absence of endothelial dysfunction (11 +/- 3% vs 5 +/- 1%, p < 0.05). Among patients with endothelial dysfunction (n = 21), the intimal index increased 11 +/- 3% with placebo, but decreased -1 +/- 2% with vitamins (p = 0.002). Among patients with normal endothelial function (n = 14), the intimal index increased 5 +/- 1% with placebo and 1 +/- 1% with vitamins (p < 0.05). CONCLUSIONS: Endothelial dysfunction indicates rapid TxAA progression, even in the statin era. Although anti-oxidant vitamins reduce disease progression in patients with normal or abnormal endothelial function, the magnitude of benefit is larger in patients with endothelial dysfunction.

Antioxidants↗
PubMed2005

Role of progenitor cells in transplant arteriosclerosis.

To date, chronic transplant dysfunction (CTD) is recognized as the major cause of transplant loss long term after transplantation. CTD has the remarkable histologic feature that the luminal areas of the intragraft arteries become obliterated as a result of occlusive neointima formation. Neointimal lesions contain predominantly vascular smooth muscle cells (VSMCs) and extracellular matrix admixed with inflammatory cells. At the luminal side, neointimal lesions are covered with a monolayer of endothelial cells (ECs). The etiology of transplant arteriosclerosis (TA) is largely unknown, and adequate prevention and treatment protocols are not available. In contrast to the largely accepted "response-to-injury" hypothesis for the development of TA that attributes an important role to graft-derived ECs and VSMCs, recent data indicate that host-derived vascular progenitor cells play a major role in the development of TA. The process leading to TA appears to be heterogeneous, and neointimal ECs and VSMCs can be recruited from different sources, possibly depending on the severity and duration of vascular damage. These data suggest a significant role of host-derived circulating EC/VSMC progenitor cells, which may be partly bone marrow derived. Circulating vascular progenitor cells are potential targets for therapeutic intervention to ameliorate TA development. Therefore, identification of mediators and cellular mechanisms that promote recruitment of vascular progenitors to sites of injury is warranted to dissect their detrimental and possible beneficial effects in the development of TA.

Cell Proliferation↗
PubMed2006

Antisense ERK1/2 oligodeoxynucleotide gene therapy attenuates graft arteriosclerosis of aortic transplant in a rat model.

UNLABELLED: Chronic rejection is a major cause of transplant loss that is effected by the extracellular signal-regulated kinases (ERK) pathway. This study investigated the effects of antisense ERK1/2 oligodeoxynucleotide(ODN) gene therapy on chronic rejection. METHODS: Lewis (RT1(1)) rats served as recipients of Brown-Norway (BN, RT1n) grafts. The BN rat abdominal aortas were harvested and orthotopically grafted into Lewis rats. The recipients were divided into three groups: (1) control group (n = 9), (2) random ODN transfer group (n = 10), and (3) antisense ODN transfer group (n = 10). At day 60 after transplantation, the recipients were sacrificed; the grafted aortas were evaluated histologically and immunohistochemically. ERK1/2 protein expression in the grafts was determined using Western Blot assays. Serum levels of slCAM-1 were detected by ELISA. RESULTS: In the control group and random ODN transfer group, we observed a remarkable degree of intimal hyperplasia and inflammatory cell infiltration, including macrophages and T cells. Compared with the control group, antisense ERK1/2 ODN gene therapy resulted in a significant reduction in neointimal proliferation (P < .01), inhibition of ERK1/2 protein expression (P < .01), decreased graft infiltration with CD4+ T lymphocytes (P < .01), CD8+ T lymphocytes(P < .05), and ED-1 macrophages (P < .01) with decreased serum levels of sICAM-1 (P < .05). We obtained a negative correlation between ERK1/2 expression and immune cell infiltration or ICAM-1 level. CONCLUSIONS: Antisense ERK1/2 gene therapy can attenuate graft arteriosclerosis so as to protect aortic allografts. The protection seemed to correlate with inhibition of inflammatory infiltration, implying that the ERK1/2 signal transduction pathway plays an important role in the process of chronic vascular rejection.

Animals↗