SEARCH · PubMed Health

Results for “ARTERIOSCLEROSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMed1975

[Arteriosclerosis: morbid anatomy (author's transl)].

Pathology is a variant of physiology with obstacles. No arterial wall is absolutely impermeable. The basic form of arteriosclerosis results from a disturbance of the lifelong flow of humors ab intima in adventitiam et ex centro in peripheriam (author's "Perfusion theory"). Special forms develop from this basic form. Analysis of postmortem material with special reference to the so-called risk factors allowed us to establish connections between some of these factors and arteriosclerosis, while some other connections, e.g. with smoking, were called in question. It is pointed out that prospective treatment of arteriosclerosis will begin only when the cluster of risk factors can be broken down.

Arteriosclerosis↗

PubMed1985

Selective determination of cholesterol in high density lipoprotein subfractions (HDL2 and HDL3) in patients with cerebral and peripheral arteriosclerosis.

Cholesterol levels in high density lipoprotein subfractions (HDL2 and HDL3) were evaluated in 69 patients (55 males, average age +/- SD 58.3 +/- 8.8, and 14 females, average age +/- SD 63.1 +/- 10.3) with extra-coronary arteriosclerosis (lower limbs, supraaortic trunks and both sites), and in 79 healthy age-matched control subjects. HDL cholesterol was significantly reduced in male and female patients. The HDL cholesterol decrease was due to a fall in both HDL2 and HDL3 cholesterols; nonetheless, an analysis of the HDL2-cholesterol/HDL3-cholesterol ratio disclosed that HDL2 cholesterol was the most reduced. Slightly higher plasma cholesterol and triglyceride levels were found in the patients as well as a higher plasma cholesterol/HDL-cholesterol ratio. On the contrary, the HDL2-cholesterol/HDL3-cholesterol ratio was significantly reduced in the patients. These preliminary findings suggest that, as in ischemic heart disease, the HDL cholesterol reduction in cerebral and peripheral arteriosclerosis is also mainly due to a reduction in the HDL2 subfraction. These results also lend further support to the proposal that determination of the HDL subfractions is useful for a better assessment of the risk profile for arteriosclerosis.

Aged↗

PubMed1978

The natural course of arteriosclerosis in animals and man.

A thorough search for the natural history of arteriosclerosis involving the cerebrum, aorta, and peripheral vessels has been made. The disease's rate of progress has been studied anatomically, clinically, radiologically, and plethysmographically. We conclude that arteriosclerosis is usually associated with other diseases such as diabetes, high blood cholesterol, and hypertension. Heart disease in particular is often the cause of the patient's death, rather than the peripheral arteriosclerotic disease itself. The usually slow development and course of arteriosclerosis indicate that its treatment is largely a medical problem. It seems important to control the various risk factors and to utilize surgical therapy to attack specific lesions which threaten the tissues. A thorough cardiovascular profile of the patient should be compiled and should include a glucose tolerance test and lipoprotein phenotyping.

Aged↗

PubMed1996

Importance of minor histocompatibility antigens in the development of allograft arteriosclerosis.

Although acute rejection has been mostly ameliorated with the use of powerful immunosuppressive drugs, kidney and heart transplants continue to succumb to a more chronic response characterized by intimal lesions in the graft vasculature. This late-stage response is referred to as allograft arteriosclerosis. Allorecognition is clearly involved in the initiation of this response but the relative importance of major histocompatibility (MHC) and minor histocompatibility (mH) antigens remains unclear. By taking advantage of the B10 congenic set of mice and our newly described mouse aortic interposition graft model we have been able to assess the contribution of these antigens to the development of the concentric intimal lesions characteristic of allograft arteriosclerosis. We performed transplants between syngeneic animals, animals which were disparate at both MHC and multiple mH, animals which were disparate at MHC only, and animals which were disparate at multiple mH antigens only. H-Y antigen variation was controlled for by performing all transplants between female mice. In all cases the recipients were C57BL/10 (H-2b) mice. Both cellular infiltration into the intima and resulting intimal thickness were measured at 2, 4, 8, and 13 weeks posttransplant. At all time points, the grafts from MHC disparate only donors showed less severe intimal lesions than the grafts from fully disparate or mH disparate donors. This difference reached statistical significance at 4 and 13 weeks. This suggests that mH antigens are as immunogenic as MHC antigens with respect to the generation of allograft arteriosclerosis. These findings are not unique to vascular grafts and may relate to the importance of indirect antigen presentation in the development of chronic rejection.

Animals↗

PubMed1975

[Contribution to the morphometry of coronary arteriosclerosis (author's transl)].

In 94 cases with and without coronary arteriosclerosis or various cardiac diseases the coronary arteries were pressure fixed, filled with a mixture of barium sulfate and gelatine for coronary angiography and dissected in 1 cm long segments for morphometry. On consecutive cross sections of the three main branches of the coronary arteries the absolute area of lumen, intima and media as well as of the thickness of the intima and media were measured. From the numerous data of the coronary arteries different indices on coronary arteriosclerosis and by correlation to the heart weight also on coronary insufficiency had been calculated. Using these quantitative data age dependent intimal changes could be distinguished convincingly from cases with uncomplicated coronary arteriosclerosis and cases with hypertension or infarcts. Thus in forensic pathology comparative evaluations can be made in regard to the extent, severity and significance of acute and chronic coronary insufficiency.

Acute Disease↗

PubMed1993

Effect of platelet-activating factor (PAF) receptor blockers on smooth muscle cell replication in vitro and allograft arteriosclerosis in vivo.

Platelet-activating factor (PAF) stimulates smooth muscle cell (SMC) replication both in vivo and in vitro. In this study we have investigated whether PAF receptor-blocking molecules modulate SMC replication in vitro and the generation of allograft arteriosclerosis in vivo. SMC cultures were established from baby rat aorta media and fibroblast control cultures from the adventitia. Identification of the cultured cell types was determined both by immunohistochemistry and electron microscopy. Both cell types replicated in culture with 10% fetal calf serum (FCS). The addition of PAF-C18 enhanced, and the addition of three PAF receptor inhibitors--WEB 2086, WEB 2170, and BN 50739--reduced, SMC replication and protein synthesis in a dose-dependent fashion in vitro until toxic concentrations were reached. The most potent of these drugs, WEB 2170, was then delivered at the rate of 12 mg/kg per day to recipients of rat aortic allografts. The responses were quantitated by autoradiography after short-term labeling of the recipients with tritium-labeled thymidine (3H-TdR) and by quantitative morphology. Administration of the PAF receptor blocker had no impact on the replication of the inflammatory cells in the allograft adventitia nor on the replication of SMCs in the media and intima. Administration of the PAF receptor blocker delayed the generation of allograft arteriosclerosis slightly, but not significantly. These results suggest that PAF is not an essential component in the inflammatory cascade leading to allograft arteriosclerosis.

Animals↗

PubMed1990

[15N tracer technical studies of protein metabolism in arteriosclerosis patients].

The incorporation of the stable isotope 15N in plasma proteins and blood cells after oral application of 3 g 15NH4Cl (95 At% 15N) per 70 kg body weight was followed up in 11 patients with ischemic heart disease or peripheral arteriosclerosis and in 7 healthy control subjects. Preliminary results indicate that the turnover of plasma protein, especially fibrin, is elevated in patients with arteriosclerosis. Investigations of platelets intimate a decreased turnover of platelet protein in patients with arteriosclerosis as compared to control subjects. Possible reasons for these alterations are discussed.

Arteriosclerosis↗

PubMed1981

A tentative molecular-biological hypothesis for arteriosclerosis.

In view of the fact that complications of arteriosclerosis are the most frequent causes of death in industrialized societies, its etiology is of enormous interest. The widely held lipid theory (detrimental effects of cholesterol) has been attacked because it cannot account for such facts as the homeostatic relationship of endogenous and exogenous cholesterol: for the "normal" cholesterol content of the early atheroma; for the distribution of the lesions, their spotty occurrence and their "programmed" appearance. Arteriosclerosis is part of the normal processes of aging which are related to molecular-biological changes. Autoimmune processes and the effects of extrachromosomal organisms of the genome (viruses, plasmids, viroids) are clinically of interest. Arteriosclerotic lesions are probably influenced by autoimmune processes; the variability and specificity of the non-chromosomal organisms may explain the location of the lesions; the end of the incubation period of the organisms may be responsible for the programmed appearance of clinical symptoms. The lipid changes are probably part of the adaptive mechanisms counteracting the rapid destruction of the vessels following the DNA alterations. Arteriosclerosis is part of normal evolution.

Aging↗

PubMed1997

Investigation on arteriosclerosis among population in a rare earth area in south China.

An ophthalmofunduscope was used to investigate arteriosclerosis among villagers aged 20-40 yr old in two rare earth areas in Ganzhou, Jiangxi Province. It was noted that the occurrence of arteriosclerosis of the fundus aculi was significantly high (P < 0.05-0.01), the detection of serum cholesterol (CHO) was remarkably increased (P < 0.01), and the level of IgM was also elevated. However, high-density lipoprotein (HDL) remained at a low level. The effect of taking rare earth elements (REE) could be direct or indirect, thus causing an increase in cholesterol and interfering with the synthesis of high-density lipoprotein. Furthermore, rare earth could also cause immunogenic damage to the vascular wall. All of these could facilitate the formation of arteriosclerosis.

Adult↗

PubMed2004

[Münster age- and retina study (MARS). Association between risk factors for arteriosclerosis and age-related macular degeneration].

BACKGROUND: The association between arteriosclerosis and age-related macular degeneration (AMD) has only been examined in a few studies and the data is still very inconsistent. METHODS: A cross sectional study was initiated with 730 patients from the Münster age and retina study (MARS) which examines patients in the age range 60 to 80 years old who were referred by ophthalmologists from the Muenster area. Patients with narrow angle glaucoma were excluded. All patients underwent a standardized ophthalmoscopic examination und were classified into four groups: group 1 without AMD ( n=190), group 2 with unilateral or bilateral early forms of AMD ( n=340), group 3 with unilateral late forms of AMD ( n=139) and group 4 with bilateral late forms of AMD ( n=50). By means of these groups it was tested if there was a significant difference between the different risk factors for arteriosclerosis. RESULTS: The mean age was 72 years and 58% were women and the sex distribution within the different groups did not differ significantly (all trend tests with p>0.1). General risk factors for arteriosclerosis such as diabetes, body-mass-index and hypertension did not differ significantly (all trend tests with p>0.1). The number of smokers increased significantly with the severity of AMD ( p=0.02). Furthermore, various lipids were examined, adjusted for age and sex and showed significant decrease of HDL ( p=0.087) and significant increases of the HDL/LDL quotient ( p=0.0007) and the non-sober triglyceride values ( p=0.0058) correlated with the severity of AMD. CONCLUSIONS: There was a highly significant, direct association of indicators of dyslipidemia such as increasing HDL/LDL quotient and decreasing HDL with the severity of AMD. These results were underlined by increased triglyceride levels even if they were taken non-sober. The results must be interpreted with caution due to the explorative character of the evaluation.

Age Distribution↗

PubMed1990

Arteriosclerosis of the gastroepiploic and internal thoracic arteries.

Arteriosclerosis of the right gastroepiploic artery (GEA) and the internal thoracic artery (ITA) were compared by pathological observation. Specimens were obtained from 35 patients who underwent coronary artery bypass grafting with simultaneous use of these two kinds of arterial grafts. Degree of arteriosclerosis was classified in five categories: 0, normal; 1, luminal narrowing less than 25%; 2, luminal narrowing between 25% and 50%; 3, luminal narrowing greater than 50%; and 4, overt atherosclerosis with ulceration or calcification. The number of arteries with degree 0, 1, 2, 3, and 4 was 16 (46%), 15 (43%), 3 (9%), 0, and 1 (3%) in GEA and 27 (77%), 8 (23%), 0, 0, and 0 in ITA, respectively. Incidence of degree 0 was higher in ITA, but differences were not significant. The mean wall thickness was 0.30 +/- 0.13 mm in GEA and 0.21 +/- 0.07 mm in ITA (p less than 0.05). In 23 patients who underwent postoperative angiography, all 46 arterial grafts were patent without focal stenosis. We conclude that GEA has slightly more intimal thickening than ITA, but significant luminal narrowing caused by arteriosclerosis is rare. Gastroepiploic artery can be expected to be a suitable conduit for coronary artery bypass grafting.

Aged↗

PubMed1977

Inhibition of spontaneously developing arteriosclerosis in female breeder rats by adrenalectomy.

In order to determine whether the adrenal glands play a primary or secondary role in the pathogenesis of the spontaneous arteriosclerosis which occurs in repeatedly bred rats, sexually mature female, Sprague-Dawley rats were adrenalectomized and maintained during four successive pregnancies. Some of the breeders were treated with deoxycorticosterone (DOCA) and 0.5% saline. The adrenalectomized breeders did not develop arteriosclerosis, beta cell degranulations, or those which has accesory or regenerated adrenal glandular tissue. Surprisingly, intact DOCA-treated breeders also showed inhibition of arterial disease but they did have fatty livers and beta cell degranulation. Body and organ weights, serum enzymes, lipids, glucose, BUN, and corticosterone were elevated in breeder rats but not to such high levels as is usual in repeatedly bred rats. These findings demonstrate that the presence of the adrenal glands is essential for the pathogenesis of the spontaneous arteriosclerosis, fatty liver, and beta cell degranulation which occurs in repeatedly bred, female rats.

Adrenal Glands↗

PubMed1990

Lipoprotein abnormalities in patients with extra-coronary arteriosclerosis.

Serum levels of lipids, lipoproteins and apolipoproteins A-I and B were evaluated in 102 patients (75 males and 27 females; ages 58 +/- 8 and 61 +/- 7 years (mean +/- SD), respectively) with arteriosclerosis of the lower limbs of supra-aortic trunks. Compared to findings in 64 healthy, age-matched control subjects, male patients in both groups had significantly higher serum triglyceride levels (+42%, P less than 0.05), while female patients with lower limb arteriosclerosis showed significantly increased cholesterol and triglyceride concentrations (+19%, P less than 0.01 and +82%, P less than 0.05, respectively). LDL-triglycerides were also increased in all patients. HDL-cholesterol was significantly decreased in male patients with arteriosclerosis of the lower limbs (-27%, P less than 0.01) and the supra-aortic trunks (-28%, P less than 0.01), and in females of both groups (-26%, P less than 0.01 and -20%, P less than 0.01, respectively); in terms of percent, HDL2-cholesterol was reduced 2-fold compared to HDL3-cholesterol. Patient apolipoprotein A-I and B levels were unchanged. In male and female patients, correlations between triglycerides and HDL-cholesterol as well as HDL2-cholesterol were negative, but not significant; on the other hand, both correlations were negative and significant in male controls, while only the correlation between triglycerides and HDL2-cholesterol was negative and significant in the female controls. Since HDL-cholesterol, and in particular HDL2-cholesterol, concentrations seem closely related to the intravascular catabolism of triglyceride-rich lipoproteins, the absence of a significant correlation between these parameters in the patients suggests a possible alteration in this metabolic process.

Apolipoproteins↗

PubMed1993

Perforin expression localizing cytotoxic lymphocytes in the intimas of coronary arteries with transplant-related accelerated arteriosclerosis.

Accelerated arteriosclerosis is the major long-term complication of cardiac transplantation. It has been demonstrated recently that accelerated arteriosclerosis is caused, in part, by rejection-related, cell-mediated immunity. However, the role of cytotoxic T lymphocytes in this process is a subject of controversy. Perforin is a specific marker of functionally active cytotoxic lymphocytes because it is a functional component of the cytotoxic granules of these cells. We examined 11 coronary arteries from seven autopsied and four retransplanted heart transplant recipients for the presence of perforin-containing lymphocytes. Immunohistochemical stains for perforin were performed using a monoclonal antibody against human perforin. Eight of the 11 coronary arteries examined were found to contain perforin-positive cells. These perforin-positive cells were present in subendothelial spaces of the coronary arteries, and the staining seen was cytoplasmic and granular. The granules often were polarized to the endothelial surface. Furthermore, the cells identified were usually in close proximity to, or in direct contact with, coronary artery endothelial cells. These results suggest that cell-mediated endothelial injury by perforin-positive cytotoxic lymphocytes may contribute to the development of accelerated arteriosclerosis in heart transplant recipients.

Adolescent↗

PubMed1985

A possible cause of arteriosclerosis.

A new etiology of arteriosclerosis is proposed. This theory has emerged from the inability of current theories to account for the spontaneously occurring disease and from numerous factual anomalies uncovered by recent research. It is suggested that arteriosclerosis is a chronic infectious disease caused by an infestation of blue-green algae, and that the natural history, histopathologic changes, and many apparently contradictory facts associated with arteriosclerosis are explained by such an etiologic agent. If correct, a radical shift in our understanding of the disease is required. Certain observations and forecasts are made based upon this infection theory.

Animals↗

PubMed1986

Ecology and arteriosclerosis.

An ecological theory of arteriosclerosis invokes antirisk factors dependent on infections and parasitic infestations through the medium of immunoglobulins. Dysglobulinemia modifies blood cholesterol, platelet function, hemostasis, and biophysics of the blood in the vessels. This could explain the differences in epidemiology of arteriosclerosis between northern developed countries and tropical countries, and the present frequency of coronary heart disease in developed countries. Arteriosclerosis is conditioned by environmental factors other than diet.

Arteriosclerosis↗

PubMed1995

Expression of CD11b and ICAM-1 in an in vivo model of transplant arteriosclerosis.

Adhesion molecules play a crucial role in transplant rejection in regulating the interaction of inflammatory cells with cells in the vascular wall. In an aortic transplantation model, we have previously analysed the early adhesion process (7.5 min to 24 h) and the impact of cold ischaemia time (1-24 h) upon transplant arteriosclerosis during the first 2 months after transplantation in the rat. The aim of this investigation was to study adhesion molecules in accelerated transplant arteriosclerosis in a rat model by analysing the immunohistochemical expression of CD11b and ICAM-1 up to 2 months and followed by a semiquantitative evaluation and multivariant analysis. Antigen expression of CD11b and ICAM-1 adhesion molecules was stronger in the aortic allografts than in the ischaemia-induced syngeneic aortic grafts in the whole vessel wall. Neither ICAM-1 nor CD11b antigen expression correlated significantly with time periods of ischaemia/reperfusion injury in allogeneic or syngeneic aortic transplants. CD11b and ICAM-1 are induced by allogeneic stimuli in transplanted aortas suggesting a role in the pathogenesis of transplant arteriosclerosis. Our findings have implications for understanding the role of cell adhesion activation in the vascular wall subject to chronic graft rejection.

Animals↗

PubMed2004

Pulse wave velocity as an indicator of arteriosclerosis in hemodialysis patients.

Studies were performed to examine whether pulse wave velocity (PWV) is a useful indicator of arteriosclerosis in hemodialysis (HD) patients. In total, 72 patients were enrolled. Annual changes in PWV were compared to clinical parameters and therapeutic maneuvers. PWV increased in diabetic patients faster than non-diabetics (35 +/- 10 cm/s/month versus 10 +/- 4 cm/s/month, P < 0.05). Changes in PWV showed strong correlations to triglyceride level exposed during observation period (r = 0.50, P < 0.05) and HD duration (r = 0.46, P < 0.05). In addition, we found that PWV of some patients decreased (regressors), while the others increased (non-regressors). Regressors more frequently received combined treatment with angiotensin blockade and lipid-lowering drugs or vitamin E-coated dialyzers than non-regressors (P < 0.05). Our data demonstrate that PWV is useful as a marker of arteriosclerosis in HD patients. Furthermore, the present results suggest that combined treatment with both angiotensin inhibition and lipid-lowering drugs or vitamin E-coated membrane would slow the progression of arteriosclerosis in HD patients.

Antioxidants↗