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PubMed1987

Surgical treatment of renovascular hypertension caused by arteriosclerosis. II. Influence of preoperative risk factors and postoperative blood pressure response on late patient survival.

This study assesses the late survival of 103 patients with renovascular hypertension caused by arteriosclerosis who underwent reconstructive surgery during the period of 1959 through 1982. It provides a detailed analysis of the influence of preoperative factors and the postoperative blood pressure response to fatal and nonfatal cardiovascular events during follow-up. All patients suffered from severe hypertension. Arteriosclerosis was limited to the renal arteries in 52% of the patients, while 48% showed overt extrarenal arteriosclerosis. Hypertensive target organ damage was present in 68% of the patients. At a mean of 8.5 months postoperatively, 80% of the patients showed beneficial and 20% showed unsatisfactory blood pressure responses. These results were not related to the presence or absence of extrarenal arteriosclerosis. Overall, late (10 years) patient survival was significantly lower than the expected survival of a reference population (79% versus 92%; p less than 0.0001). Late patient survival was not influenced by the absence or presence of extrarenal arteriosclerosis (82% versus 82%) or target organ damage (83% versus 82%), but late survival was significantly better with beneficial (87%) than with unsatisfactory blood pressure responses (67%). This effect was especially conspicuous in the presence of extrarenal arteriosclerosis (88% versus 57%; p = 0.04) but not in its absence (86% versus 74%; p = 0.41). In terms of long-term survival, these findings clearly demonstrate the favorable effect of successful surgical treatment of patients with renovascular hypertension caused by arteriosclerosis. Moreover, they illustrate that the mere presence of preoperative extrarenal arteriosclerosis or target organ damage is not sufficient argument against surgical therapy.

Adult↗
PubMed1994

Peritransplant injury to the myocardium associated with the development of accelerated arteriosclerosis in heart transplant recipients.

Accelerated arteriosclerosis is now the major long-term complication of heart transplantation. Defining the risk factors associated with the development of accelerated arteriosclerosis will provide not only a means of identifying patients at risk for this complication but also clues to the etiology of accelerated arteriosclerosis. The purpose of this study was to examine the relationship between peritransplant myocardial ischemic injury and the development of accelerated arteriosclerosis. In a case-control study we examined the first three endomyocardial biopsies from 50 heart transplant recipients and graded the degree of ischemic injury present in these biopsies. The histologic changes graded in the biopsies included contraction band necrosis, coagulative necrosis, and macrophagic removal of ischemically injured myocytes. Of the 50 recipients included in the study, 25 had angiographic evidence of accelerated arteriosclerosis and 25 did not. In multivariate analysis, which included the number of class I major histocompatibility (MHC) antigen mismatches between the donor and the recipient, the recipient's post-transplant cytomegalovirus status, the donor's age, and the number of rejection episodes, the histologic degree of ischemic injury present in the biopsies emerged as the strongest predictor of the development of accelerated arteriosclerosis (RR 2.6, 95% CI 1.2-5.8, p = 0.02). These results suggest that ischemic injury to the heart during the peritransplant period significantly contributes to the development of accelerated arteriosclerosis in heart transplant recipients and that histologic changes in early posttransplant biopsies can be used to identify recipients at risk of developing accelerated arteriosclerosis.

Adolescent↗
PubMed1994

Arteriosclerosis: its morphology in the past and today.

In a brief historical review the contributions of Rokitansky, Virchow, and Langhans concerning the pathogenesis of arteriosclerosis and the histogenetic puzzle of intimal cells classification are described. Then, some unresolved problems are discussed, especially the localization and distribution of arteriosclerotic plaques, the shape of endothelial cells and the orientation of their nuclei in correlation to local hemodynamic stress under normal and pathologic conditions. Some differences between experimental arteriosclerosis and arteriosclerosis in humans are illustrated by examples. The key role of the endothelium in the development of arteriosclerosis is well founded. According to recent investigations some cells on the surface of human arteriosclerotic plaques appear to be of non-endothelial origin. Arteriosclerosis seems to be a systemic disorder with multiorgan involvement. Individual cases, however, show significant differences in the distribution and extent of lesions. Today, arteriosclerotic research is focused on arteries being most important in clinical investigations. Nevertheless, there are also other arteries with severe arteriosclerotic lesions; for example, the degree of arteriosclerosis in periprostatic arteries is more pronounced than in coronary artery branches of the same size. Finally, the importance of primary prevention of arteriosclerosis is emphasized.

Animals↗
PubMed2001

Smooth muscle cell apoptosis in arteriosclerosis.

Arteriosclerosis, a paradigmatic age-related disease, encompasses (spontaneous) atherosclerosis, restenosis after percutaneous transluminal coronary angioplasty, autologous arterial or vein graft arteriosclerosis and transplant arteriosclerosis. In all types of arteriosclerosis, vascular smooth muscle cell (SMC) accumulation in the intima is a key event, but abundant evidence also indicates the importance of SMC apoptosis in the development of arteriosclerosis. Because SMC proliferation and apoptosis coincide in arteriosclerotic lesions, the balance between these two processes could be a determinant during vessel remodeling and disease development. Various stimuli, including oxidized lipoproteins, altered hemodynamic stress and free radicals, can induce SMC apoptosis in vitro. As risk factors for arteriosclerosis, these stimuli may also lead to vascular cell apoptosis in vivo. The presence of apoptotic cells in atherosclerotic and restenotic lesions could have potential clinical implications for atherogenesis and contributes to the instability of the lesion. Based on the progress in this field, this review focuses on the mechanism and impact of SMC apoptosis in the pathogenesis of arteriosclerosis and highlights the role of biomechanical stress in SMC apoptosis.

Animals↗
PubMed1998

Exposure of vascular allografts to insulin-like growth factor-I (IGF-I) increases vascular expression of IGF-I ligand and receptor protein and accelerates arteriosclerosis in rats.

BACKGROUND: Accelerated arteriosclerosis limits the survival of transplanted hearts. We hypothesized that insulin-like growth factor-I (IGF-I) is crucial in accelerating transplant arteriosclerosis. Recently, we reported that exposure to IGF-I prior to transplantation accelerates transplant arteriosclerosis in the rat aorta allograft model. Here, we studied the mechanism whereby IGF-I exposure accelerates transplant arteriosclerosis. METHODS: The abdominal aorta was harvested from male Brown Norway rats and exposed to 0, 200, or 500 ng/ml of IGF-I at 37 degrees C for 30 min prior to transplantation to the abdominal position of male Lewis rats. The allografts were harvested 14 days later and processed for immunohistochemical staining for alpha-actin, growth factors (IGF-I, IGF-I receptor, platelet-derived growth factor-BB, and basic fibroblast growth factor), and immunological markers (major histocompatibility complex class II antigen, macrophage, and CD4- and CD8-positive T cells). RESULTS: By 14 days, the ex vivo IGF-I donor aorta treatment with IGF-I increased in a concentration-dependent manner the expression of IGF-I and IGF-I receptor in both the intima and the adventitia. In contrast, the expression of platelet-derived growth factor-BB was decreased in a concentration-dependent manner in the intima while basic fibroblast growth factor remained unchanged. The cell-mediated immune response was not affected by IGF-I at 14 days after transplantation, which suggests that the immune events associated with acceleration of transplant arteriosclerosis may occur at an earlier time. CONCLUSION: Acceleration of transplant arteriosclerosis by exposure to IGF-I is associated with increased IGF-I ligand and receptor expression in the allograft vascular wall. These data further suggest that IGF-I may be a major factor in mediating graft arteriosclerosis.

Actins↗
PubMed2003

Increased expression of transforming growth factor-beta and eosinophil infiltration is associated with the development of transplant arteriosclerosis in long-term surviving cardiac allografts.

BACKGROUND: Transplant arteriosclerosis is a major limiting factor for long-term function of allografts in clinical transplantation. This study investigated the impact of three different protocols capable of inducing long-term allograft survival on the development of transplant arteriosclerosis and immune response in cardiac allografts. METHODS: CBA.Ca (H2k) recipients of fully allogeneic C57/BL10 (H2b) heart grafts received a short-term course of anti-CD154 antibody or were pretreated with anti-CD4 antibody in combination with donor alloantigen in the form of CBK (H2k+Kb) bone marrow or C57BL/10 donor-specific transfusion (DST). Grafts were analyzed on day 40 or 100 after transplantation for transplant arteriosclerosis and expression of interferon-gamma, interleukin (IL)-2, IL-4, IL-10, IL-12p40, inducible nitric oxide synthase, and transforming growth factor (TGF)-beta1 mRNA. Serum was analyzed for the presence of alloantibodies. RESULTS: Intimal proliferation was 62%+/-11% on day 40 in the anti-CD154 group, progressed from 31%+/-10% on day 40 to 68%+/-8% on day 100 in the CBK-bone marrow group, but remained stable at 39%+/-4% in the DST group. Increased transplant arteriosclerosis on day 100 was associated with high intragraft TGF-beta1 mRNA production and eosinophil infiltration, but not alloantibody production. Progressing transplant arteriosclerosis was associated with increased IL-4 expression. CONCLUSION: Treatment protocols for the induction of long-term allograft survival can differ substantially in the extent and kinetics of transplant arteriosclerosis. IL-4 and TGF-beta1 may be two potential therapeutic targets to attenuate the development of transplant arteriosclerosis in the long term.

Animals↗
PubMedDate not supplied

Initial lesions of vascular aging disease (arteriosclerosis).

BACKGROUND: In contrast to the well-known morphologic lesions of arteriosclerosis, the initial changes of the disease are less obvious. Commonly, functional disturbances of the endothelium, endothelial dysfunction, are suggested. On the other hand the significance of age-dependent changes in the extracellular matrix with their important role in vessel wall permeability and other features associated with arteriosclerosis should not be overlooked. New topics deal with possible infectious factors, the genetic basis of the disease and the particularities of the unstable atheroma. OBJECTIVE: Alterations in nitric monoxide and endothelin-1 balance of the endothelium are the key events in the initiation of arteriosclerosis induced by oxidized lipoproteins, cigarette smoking and endotoxin. This frequently supposed mechanism contrasts with earlier opinions on the primary alterations in glycosaminoglycan metabolism and other components of the extracellular matrix against atherogenic factors like hypertension, stress and physical inactivity. Based on a survey of the literature and our own experimental experiences, these changes in connection with the morphometrically determined age-conditioned increase in vascular wall thickness and the above-mentioned new topics on arteriosclerosis were analyzed. CONCLUSION: The initial lesions of arteriosclerosis starting in youth seem to be fundamentally different from those beginning in old age. The first step in the development of fatty streaks in the arteries of young people is endothelial dysfunction with a decreased formation of nitric monoxide and an increased expression of adhesion molecules. In comparison the genesis of arteriosclerosis in advanced age is characterized by metabolic changes in the endothelium combined with age-conditioned alterations in the extracellular matrix resulting in faster progression of the disease in old age. The multicausal genesis of arteriosclerosis cannot be doubted even if cooperation with infectious factors cannot be excluded. The histopathologic peculiarities of unstable atheroma are described.

Aged↗
PubMed2004

[Arteriosclerosis and gastoduodenal ulcer].

Recent reports suggested an increase in the occurrence of gastroduodenal ulcers in old age people. And it was reported that gastroduodenal ulcers in old age generation has the characteristics which was different from that in young generation. Namiki et al reported that gastric ulcer in old age generation occurs often at the gastric corpus and is larger and deeper and more often with bleeding comparing with that in young people. Furthermore NSAID ulcer is known to occur more often in old age than in young. Although the pathogenesis of the gastroduodenal ulcer in old age is not clear, a decrease in gastric mucosal blood flow with aging might be related that is possibly due to narrowing of arteries based on arteriosclerosis. Since the report by Virchow that suggested the importance of vessels as a cause for gastric ulcer, many studies indicated the involvement of vessels in the pathogenesis of gastroduodenal ulcer. Until recently, however, there were no methods except autopsy to evaluate the severity of arteriosclerosis, therefore the involvement of arteriosclerosis in the pathogenesis was not clarified. Recently a new device that case evaluate the arteriosclerosis by the measuring pulse wave velocity was developed and is now widely used. We undertook to clarify the relation between arteriosclerosis and gastroduodenal ulcer. The result suggested the involvement of arteriosclerosis in the pathogenesis of gastroduodenal ulcer, especially of NSAID ulcer with bleeding. In this manuscript, we refer to the previous reports that suggest the relation between arteriosclerosis and gastroduodenal ulcer.

Aged↗
PubMed1981

[Reaction time during ageing and in cerebral arteriosclerosis (author's transl)].

Authors studied 142 test persons aged between 54 and 86 years who were, expected for arteriosclerosis, free of any other disease. Severity of arteriosclerosis was assessed by funduscopy and the test persons divided into four groups: without of arteriosclerosis, mild and medium arteriosclerosis, respectively, and severe arteriosclerosis. The automatic measurement of reaction time was repeated in the majority after certain interval. Results of the two examinations have been compared. It has been found that delay of reaction time showed substantial relationship with the severity of cerebral arteriosclerosis and exceeded the relationship with age. Longitudinal examination gave evidence that during aging delay of reaction time showed an even speed, i.e. age does not influence speed of delay. Contrariwise regression was found to be essentially more rapid in the groups with severe arteriosclerosis with poor incipient values.

Age Factors↗