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Atherosclerosis
Kinds of Atherosclerosis Terms modified by Atherosclerosis Selected AbstractsAtherosclerosis in diabetes and insulin resistanceDIABETES OBESITY & METABOLISM, Issue 4 2007Jane E.-B. Atherosclerosis and cardiovascular disease are the major causes of morbidity and mortality in patients with diabetes and those with insulin resistance and the metabolic syndrome. Both conditions profoundly accelerate the development of atherosclerosis and increase the morbidity and mortality of cardiovascular events. The question, therefore, is what are the molecular/biochemical mechanisms that underlie the potentiating influence of diabetes, the metabolic syndrome and/or insulin resistance on the development and progression of atherosclerosis? The following review will focus on the molecular mechanism whereby hyperglycaemia and/or hyperinsulinemia either directly or indirectly promote atherosclerosis. [source] Association analysis of genes in the renin-angiotensin system with subclinical cardiovascular disease in families with Type 2 diabetes mellitus: The Diabetes Heart StudyDIABETIC MEDICINE, Issue 3 2006K. P. Burdon Abstract Aims Cardiovascular disease (CVD) is a major complication of Type 2 diabetes mellitus. The renin-angiotensin system (RAS) and nitric oxide production are both important regulators of vascular function and blood pressure. Genes encoding proteins involved in these pathways are candidates for a contribution to CVD in diabetic patients. We have investigated variants of the angiotensinogen (AGT), angiotensin converting enzyme (ACE), angiotensin type 1 receptor (AT1R) and endothelial nitric oxide synthase (NOS3) genes for association with subclinical measures of CVD in families with Type 2 diabetes mellitus (T2DM). Methods Atherosclerosis was measured by carotid intima-media thickness and calcification of the carotid and coronary arteries in 620 European Americans and 117 African Americans in the Diabetes Heart Study. Because of the role of these systems in blood pressure regulation, blood pressure was also investigated. Results Compelling evidence of association was not detected with any of the SNPs with any outcome measures after adjustments for covariates despite sufficient power to detect relatively small differences in traits for specific genotype combinations. Conclusions Genetic variation of the RAS and NOS3 genes do not appear to strongly influence subclinical cardiovascular disease or blood pressure in this diabetic population. [source] The Relation between the Color M-Mode Propagation Velocity of the Descending Aorta and Coronary and Carotid Atherosclerosis and Flow-Mediated DilatationECHOCARDIOGRAPHY, Issue 3 2010Yilmaz Gunes M.D. Background: To improve clinical outcomes, noninvasive imaging modalities have been proposed to measure and monitor atherosclerosis. Common carotid intima-media thickness (CIMT) and brachial artery flow-mediated dilatation (FMD) have correlated with coronary atherosclerosis. Recently, the color M-mode-derived propagation velocity of descending thoracic aorta (AVP) was shown to be associated with coronary artery disease (CAD). Methods: CIMT, FMD, and AVP were measured in 92 patients with CAD and 70 patients having normal coronary arteries (NCA) detected by coronary angiography. Patients with acute myocardial infarction, renal failure or hepatic failure, aneurysm of aorta, severe valvular heart disease, left ventricular ejection fraction <40%, atrial fibrillation, frequent premature beats, left bundle branch block, and inadequate echocardiographic image quality were excluded. Results: Compared to patients with normal coronary arteries, patients having CAD had significantly lower AVP (29.9 ± 8.1 vs. 47.5 ± 16.8 cm/sec, P < 0.001) and FMD (5.3 ± 1.9 vs. 11.4 ± 5.8%, P < 0.001) and higher CIMT (0.94 ± 0.05 vs. 0.83 ± 0.14 mm, P < 0.001) measurements. There were significant correlations between AVP and CIMT (r =,0.691, P < 0.001), AVP and FMD (r = 0.514, P < 0.001) and FMD and CIMT (r =,0.530, P < 0.001). Conclusions: The transthoracic echocardiographic determination of the color M-mode propagation velocity of the descending aorta is a simple practical method and correlates well with the presence of carotid and coronary atherosclerosis and brachial endothelial function. (Echocardiography 2010;27:300-305) [source] Stanford Type A Aortic Dissection in a Hypertensive Patient with Atherosclerosis of Aorta and AortitisECHOCARDIOGRAPHY, Issue 2 2000DANIELA BEDELEANU M.D., PH.D. Dissection of aorta is a serious condition; the main factors are hypertension and diseases of the connective tissue or of collagen. Aortitis syndrome in combination with hypertension and atherosclerosis in association with ascending aortic dissection is rarely seen. We present the case of a 53-year-old hypertensive patient whose ascending aortic dissection was associated with pericardial effusion without rupture of the aorta and with pleural effusion. Several unusual aspects of transesophageal echocardiography are described. The intraoperative biopsy revealed inflammatory aortitis with mural hematoma, without giant cells. The literature concerning aortic dissection and aortitis is reviewed. [source] A systems biology approach to understanding atherosclerosisEMBO MOLECULAR MEDICINE, Issue 3 2010Stephen A. Ramsey Abstract Atherosclerosis, a chronic inflammatory disease of the vascular system, presents significant challenges to developing effective molecular diagnostics and novel therapies. A systems biology approach integrating data from large-scale measurements (e.g. transcriptomics, proteomics and genomics) is successfully contributing to deciphering regulatory networks underlying the response of many different cellular systems to perturbations. Such a network analysis strategy using pathway information and data from multiple measurement platforms, tissues and species is a promising approach to elucidate the mechanistic underpinnings of complex diseases. Here, we present our views on the contributions that a systems approach can bring to the study of atherosclerosis, propose ways to tackle the complexity of the disease in a systems manner and review recent systems-level studies of the disease. [source] Predicting intra-urban variation in air pollution concentrations with complex spatio-temporal dependencies,ENVIRONMETRICS, Issue 6 2010Adam A. Szpiro Abstract We describe a methodology for assigning individual estimates of long-term average air pollution concentrations that accounts for a complex spatio-temporal correlation structure and can accommodate spatio-temporally misaligned observations. This methodology has been developed as part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study funded by the US EPA to investigate the relationship between chronic exposure to air pollution and cardiovascular disease. Our hierarchical model decomposes the space--time field into a "mean" that includes dependence on covariates and spatially varying seasonal and long-term trends and a "residual" that accounts for spatially correlated deviations from the mean model. The model accommodates complex spatio-temporal patterns by characterizing the temporal trend at each location as a linear combination of empirically derived temporal basis functions, and embedding the spatial fields of coefficients for the basis functions in separate linear regression models with spatially correlated residuals (universal kriging). This approach allows us to implement a scalable single-stage estimation procedure that easily accommodates a significant number of missing observations at some monitoring locations. We apply the model to predict long-term average concentrations of oxides of nitrogen (NOx) from 2005 to 2007 in the Los Angeles area, based on data from 18 EPA Air Quality System regulatory monitors. The cross-validated IR2 is 0.67. The MESA Air study is also collecting additional concentration data as part of a supplementary monitoring campaign. We describe the sampling plan and demonstrate in a simulation study that the additional data will contribute to improved predictions of long-term average concentrations. Copyright © 2009 John Wiley & Sons, Ltd. [source] Arterial stiffness in relation to subclinical atherosclerosisEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2009A. Wykretowicz ABSTRACT Background, Increased arterial stiffness or arteriosclerosis, represents a physiological part of ageing. Atherosclerosis is a process that does not affect the arterial bed uniformly but has a variable local distribution and is frequently superimposed on stiffened vessels. We therefore addressed the question of whether any correlation exists between the general characteristics of arterial stiffness or wave reflection and subclinical atherosclerosis as assessed by carotid intima-media thickness (IMT) in a sample of healthy subjects. Methods, A total of 116 healthy subjects (mean age 55 years, 43 female) were evaluated. Arterial stiffness and wave reflection was assessed with the use of digital volume pulse analysis (DVP) and pulse wave analysis (PWA). Subclinical atherosclerosis was assessed by measurement of IMT. Results, Stiffness Index (SIDVP), the measure of general arterial stiffness correlated significantly with IMT (r = 0·37, P < 0·01). IMT correlated significantly with age (r = 0·5, P < 0·0001), waist to hip ratio (WHR) (r = 0·39, P < 0·0001) and mean blood pressure (BPmean) (r = 0·4, P < 0·0001). IMT did not correlate with measures of wave reflection. SIDVP correlated significantly with age (r = 0·32, P < 0·005), WHR (r = 0·36, P < 0·0001), BPmean (r = 0·36, P < 0·0001) and measurements of wave reflection. However analysis of a model which included variables that significantly influenced SIDVP and IMT, such as age, WHR and mean BP showed that arterial stiffness is not independently associated with subclinical atherosclerosis. Conclusions, The indices of subclinical atherosclerosis, arterial stiffness and wave reflection, indicate different aspects of vascular status in otherwise healthy subjects [source] Etiology of and risk factors for cerebral infarction in young adults in western Norway: a population-based case-control studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2004H. Naess We sought to study the etiology of and risk factors for cerebral infarction in young adults in Hordaland County, Norway. All patients aged 15,49 years living in Hordaland County with a first-ever cerebral infarction during 1988,97 were included. Etiology was analyzed in subgroups defined by sex, age (<40 years versus 40 years), circulation territory (anterior versus posterior circulation) and short-term functional outcome [modified Rankin score (mRS) 2 versus mRS > 2]. A questionnaire was used to evaluate possible risk factors amongst the patients compared with an age- and sex-matched control group. The distribution of etiology was significantly different in all subgroups. Atherosclerosis was frequent amongst men (22.8% vs. 4.2%) and patients 40 years (20.8% vs. 2.7%). All patients with microangiopathy had favorable short-term outcome. Significant risk factors were smoking more than 15 cigarettes per day (P < 0.001), hypertension (P = 0.001), and myocardial infarction (P = 0.035). Modifiable risk factors were frequent. [source] Nonconcordance between subclinical atherosclerosis and the calculated Framingham risk score in HIV-infected patients: relationships with serum markers of oxidation and inflammationHIV MEDICINE, Issue 4 2010S Parra Objectives HIV-infected patients show an increased cardiovascular disease (CVD) risk resulting, essentially, from metabolic disturbances related to chronic infection and antiretroviral treatments. The aims of this study were: (1) to evaluate the agreement between the CVD risk estimated using the Framingham risk score (FRS) and the observed presence of subclinical atherosclerosis in HIV-infected patients; (2) to investigate the relationships between CVD and plasma biomarkers of oxidation and inflammation. Methods Atherosclerosis was evaluated in 187 HIV-infected patients by measuring the carotid intima-media thickness (CIMT). CVD risk was estimated using the FRS. We also measured the circulating levels of interleukin-6, monocyte chemoattractant protein-1 (MCP-1) and oxidized low-density lipoprotein (LDL), and paraoxonase-1 activity and concentration. Results There was a weak, albeit statistically significant, agreement between FRS and CIMT (,=0.229, P<0.001). A high proportion of patients with an estimated low risk had subclinical atherosclerosis (n=66; 56.4%). In a multivariate analysis, the presence of subclinical atherosclerosis in this subgroup of patients was associated with age [odds ratio (OR) 1.285; 95% confidence interval (CI) 1.084,1.524; P=0.004], body mass index (OR 0.799; 95% CI 0.642,0.994; P=0.044), MCP-1 (OR 1.027; 95% CI 1.004,1.050; P=0.020) and oxidized LDL (OR 1.026; 95% CI 1.001,1.051; P=0.041). Conclusion FRS underestimated the presence of subclinical atherosclerosis in HIV-infected patients. The increased CVD risk was related, in part, to the chronic oxidative stress and inflammatory status associated with this patient population. [source] Regular or "Super-Aspirins"?JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001A Review of Thienopyridines or Aspirin to Prevent Stroke PURPOSE: To review the evidence for the effectiveness and safety of the thienopyridines (ticlopidine and clopidogrel) compared with aspirin for the prevention of vascular events among patients at high risk of vascular disease. BACKGROUND: Atherosclerosis and resultant cardiovascular disease are important causes of morbidity and mortality in older people. In particular, atherosclerosis of the cerebral arteries can lead to transient ischemic attacks (TIAs) and stroke. Stroke ranks as the third-leading cause of death in the United States and in 1997 was responsible for over 150,000 fatalities.1 In addition to the mortality associated with this disease, stroke is also a leading source of long-term disability in survivors. Nearly 4.5 million stroke survivors are alive today,1 highlighting the fact that primary, but also secondary, prevention are extremely important for minimizing the complications of this illness. DATA SOURCES: Specialized trial registers of the Cochrane Stroke Group and the Antithrombotic Trialist's Collaboration, MEDLINE, and Embase were searched. Additional unpublished information and data were sought from Sanofi, the pharmaceutical company that developed and manufactures ticlopidine and clopidogrel, as well as the principal investigators of the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial,7 the largest of the trials identified. STUDY SELECTION CRITERIA: All unconfounded randomized trials comparing either ticlopidine or clopidogrel with aspirin among patients at high risk of vascular disease (those with symptoms of ischemia of the cerebral, coronary, or peripheral circulations) who were followed for at least 1 month for the recurrence of vascular events were included. DATA EXTRACTION: Data were extracted from four completed randomized trials completed in the past 20 years, which included 22,656 patients.7,10 Two authors independently extracted the data from these trials for the following information: the types of patients enrolled; the entry and exclusion criteria; the randomization method; the number of patients originally allocated to the treatment and control groups; the method and duration of follow-up; the number of patients in each group lost to follow-up; information on compliance with the treatment allocated; the definitions of outcome events; the number of outcome events in each treatment group; and any method used for blinding patients, treating clinicians, and outcome assessors to treatment allocation. MAIN RESULTS: Four completed trials involving a total of 22,656 patients were identified. Aspirin was compared with ticlopidine in three trials (3,471 patients)8,10 and with clopidogrel in one trial (19,185 patients).7 A recent TIA or ischemic stroke was the qualifying event in 9,840 patients, a recent myocardial infarction in 6,302 patients, and symptomatic peripheral arterial disease in 6,514 patients. The average age of the patients was approximately 63, with approximately two-thirds of the patients being male and white. The duration of follow-up ranged from 12 to 40 months. CONCLUSIONS: This systematic review demonstrates that, compared with aspirin, thienopyridines are only modestly more effective in preventing serious vascular events in high-risk patients. For patients who are intolerant of, or allergic to aspirin, the available safety and efficacy data suggest that clopidogrel is an appropriate, but more-expensive, alternative antiplatelet drug. It appears safer than ticlopidine and as safe as aspirin but it should not replace aspirin as the first-choice antiplatelet agent for all patients. Further studies are necessary to determine which, if any, particular types of patients would benefit most and least from clopidogrel instead of aspirin. [source] Surgical Techniques: Transcatheter Aortic Valve Implantation with "No Touch" of the Aortic Arch for the Treatment of Severe Aortic Stenosis Associated with Complex Aortic AtherosclerosisJOURNAL OF CARDIAC SURGERY, Issue 5 2010Rodrigo Bagur M.D. [source] Slowed Progression or Elimination of Atherosclerosis by Low-Frequency Electrical ImpulsesJOURNAL OF CARDIAC SURGERY, Issue 1 2003Ph.D., Valeri Chekanov M.D. In this investigation we demonstrated the slow progression or elimination of atherosclerosis by low-frequency EI in case of moderate atherosclerosis (after eight weeks of HCD). Methods: Series I rabbits (control group) were fed HCD for eight weeks. Series II rabbits were fed HCD for eight weeks and were then switched to normal diet for eight weeks (no EI). Series III rabbits were fed HCD for eight weeks and then switched to a normal diet with simultaneous EI (applied near the abdominal aorta) for eight weeks (3 V, 30 single impulses per minute, 24 hours/day). After euthanization, the level of atherosclerosis, percentage of surface area involved in the atherosclerosis process, and an atherosclerosis score were calculated in the aortic arch, thoracic and abdominal aorta. Results: Statistically significant differences were seen in the level of atherosclerosis in the abdominal aorta between series III animals (0.4 ± 0.2) and the other two groups: 1.5 ± 0.4 in series I (HCD only), 1.2 ± 0.3 in series II (HCD then normal diet). Gross examination of the surface also revealed statistically significant differences (p < 0.05) in the percentage of atherosclerosis between the control series I (30.1 ± 4.1%) and series II (21.3 ± 3.6%), compared with series III (5.5 ± 5.4%). In addition, the atherosclerosis score was also significantly different: 45.8 ± 3.9 in series I, 25.2 ± 6.9 in series II, and 2.2 ± 2.0 in series III (p < 0.05). Conclusion: Our study showed that, when applied near the abdominal aorta, low-frequency electrical impulses decrease atherosclerotic deposition in the abdominal aorta. (J Card Surg 2003; 18:47-58) [source] Race/ethnicity and telomere length in the Multi-Ethnic Study of AtherosclerosisAGING CELL, Issue 3 2009Ana V. Diez Roux Summary Telomere length has emerged as a marker of exposure to oxidative stress and aging. Race/ethnic differences in telomere length have been infrequently investigated. Leukocyte telomere length (LTL) was assessed 981 white, black and Hispanic men and women aged 45,84 years participating in the Multi-Ethnic Study of Atherosclerosis. Direct measurement and questionnaire were used to assess covariates. Linear regression was used to estimate associations of LTL with race/ethnicity and age after adjustment for sex, income, education, smoking, physical activity, diet and body mass index. On average blacks and Hispanics had shorter telomeres than whites [adjusted mean differences (standard error) in T/S ratio compared to whites: ,0.041 (0.018) for blacks and ,0.044 (0.018) for Hispanics]. Blacks and Hispanics showed greater differences in telomere length associated with age than whites (adjusted mean differences in T/S ratio per 1 year increase in age ,0.0018, ,0.0047 and ,0.0055 in whites, blacks and Hispanics respectively). Differences in age associations were more pronounced and only statistically significant in women. Race/ethnic differences in LTL may reflect the cumulative burden of differential exposure to oxidative stress (and its predictors) over the lifecourse. [source] SLE, atherosclerosis and cardiovascular diseaseJOURNAL OF INTERNAL MEDICINE, Issue 6 2005J. FROSTEGĹRD Abstract. Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE-related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE-related atherosclerosis when compared with ,normal' atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in ,normal' atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE-related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions. [source] Immunomodulation of atherosclerosis: myth and realityJOURNAL OF INTERNAL MEDICINE, Issue 3 2000A. Nicoletti Abstract. Nicoletti A, Caligiuri G & Hansson GK (Hôpital Broussais, Paris, and Karolinska Institute, Stockholm). Immunomodulation of atherosclerosis: myth and reality (Minisymposium). J Intern Med 2000; 247: 397,405. Atherosclerosis is an inflammatory disease which displays features of immune activation both locally and systemically. In the present review, we discuss the evidence for immune activation in human disease and experimental models, and survey candidate antigens associated with atherosclerosis. Studies of atherosclerosis in genetic models of immunodeficiency are analysed, as well as immunomodulating therapies and immunization protocols. Based on recent research, it is concluded that immunomodulation represents an interesting approach to the development of new prevention and treatment methods for atherosclerosis. [source] Extracranial Vertebral Artery InterventionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 6 2007DEBABRATA MUKHERJEE M.D. Atherosclerosis is the commonest cause of vertebral artery stenosis and has a predilection for the origin and proximal section of the extracranial portion of the vessel and also the intracranial portion of the vessel. Although it has generally been thought that extracranial vertebral artery (ECVA) disease has a more benign outcome compared to intracranial vertebral artery disease, significant occlusive disease of the proximal vertebral artery is the primary cause of vertebral artery ischemia in a significant proportion of patients. We focus on the interventional management of patients with proximal ECVA disease in this article. [source] Inflammatory Cytokine Imbalance after Coronary Angioplasty: Links with Coronary AtherosclerosisJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2007NATALE DANIELE BRUNETTI M.D., Ph.D. Aim:To investigate release of some inflammatory cytokines (Cys) after coronary angioplasty and its links with coronary atherosclerosis. Methods:Twenty-seven consecutive subjects with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) were enrolled in the study: serial blood samples were taken in order to evaluate plasma concentrations of Interleukin (IL)-2, IL-10, IL-18, TNF,, and IFN, just before PCI at 12 and 24 hours. Patients were then divided, considering balance between each inflammatory Cy and IL-10, an antiinflammatory Cy, into four groups, ranging from a prevalent antiinflammatory response (stable inflammatory Cy,increasing IL-10 values) to a marked inflammatory imbalance (increasing inflammatory Cy,stable IL-10 values). Results:All Cys showed significant increases in plasma concentrations if compared with baseline values. Release curves were not significantly different when comparing subjects with ST-elevation myocardial infarction (STEMI) versus unstable angina,non-STEMI (UA-NSTEMI), diabetics versus controls. Subjects with marked inflammatory response showed a higher incidence of stenosis on left anterior descending (LAD) coronary artery (IL-2 ,2 and IFN, P < 0.05); Cy release was higher in patients with multivessel coronary disease (IL-2 and IFN,, ANOVA P < 0.01). Correlations were also referable between Cys and myocardial enzyme release. Subjects treated with sirolimus-eluting stents (SES) showed significantly lower Cy periprocedure ratio if compared with those treated with bare metal stents. Conclusions:A significant Cy release is detectable after PCI: inflammatory response seems to correlate with both PCI due to plaque instabilization and coronary atherosclerosis. A blunted inflammatory response is detectable in subjects treated with SES. [source] Plaque progression and regression in atherothrombosisJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2007B. IBANEZ Summary., Atherosclerotic disease is a pathological process characterized by the deposition of lipid and other blood-borne material within the arterial wall. The deposition of these materials and the subsequent thickening of the wall may significantly compromise the vessel lumen. Atherosclerosis is a diffuse disease with focal clinical manifestations that are the consequence of thrombotic complications on disrupted atherosclerotic lesions. Until recently, atherosclerosis development was envisaged as an incessant progressing process; however, new evidence has shown that atherosclerotic plaque homeostasis is not necessarily a constantly progressing process. There are many data showing that atherosclerotic plaque formation can be slowed, stopped or even reversed. Comprehension of the underlying mechanisms involved in the homeostasis of atherosclerotic plaque (progression/regression) should allow the development of interventions enhancing the regression pathway. Novel imaging technology has allowed the accurate evaluation of plaque progression, vital in the assessment of the efficacy of interventions. In this review we discuss the processes involved in the formation and progression of atherosclerotic lesions, the triggers for plaque disruption, as well as new therapies. We also deal with the potential pathways of plaque regression, as well as tools for accurate serial atherosclerotic quantification. [source] Chemokine Receptor 2 (CCR2) in Atherosclerosis, Infectious Diseases, and Regulation of T-Cell PolarizationMICROCIRCULATION, Issue 3-4 2003ISRAEL F. CHARO ABSTRACT Infiltration of tissues by monocyte-derived macrophages is a prominent component of a wide-range of diseases, including atherosclerosis, glomerulonephritis, encephalitis, infectious diseases, and virtually all syndromes characterized by chronic inflammation. The molecular signals responsible for this directed migration are incompletely understood, but members of the chemokine family, especially the monocyte chemoattractant proteins (MCPs) (MCP-1 to MCP-5) are emerging as key players. Cells that respond to the MCPs do so because they express chemokine receptor 2 (CCR2), the cognate receptor. This review will summarize evidence supporting a key role for CCR2 in the pathogenesis of atherosclerosis, infections with intracellular pathogens, and regulation of the type I adaptive immune response. [source] Guidelines for the optimization of microsurgery in atherosclerotic patientsMICROSURGERY, Issue 5 2006F.A.C.S., Hung-Chi Chen M.D. We review the pathogenesis of atherosclerosis and the issues that must be taken into consideration when performing microsurgery in atherosclerotic patients. Atherosclerosis is a systemic disease, and may affect the success of microsurgery. Atherosclerotic patients have a tendency toward thrombosis, because the nature of the arteries is changed. Such patients are usually old and have additional medical problems. To increase the success rate of microsurgery in atherosclerotic patients, special precautions should be considered. Patients must be evaluated properly for the suitability of microsurgery. The microsurgical technique requires a meticulous approach, and various technical tricks can be used to avoid thrombosis. Recipient-vessel selection, anastomotic technique, and the use of vein grafts are all important issues. Prophylactic anticoagulation is recommended in severely atherosclerotic patients. Close monitoring of the patient and flap is necessary after the operation, as with routine microvascular free-tissue transfers. We conclude that atherosclerosis is not a contraindication for microsurgery. If the microsurgeon knows how to deal with the difficulties in atherosclerotic patients, microsurgery can be performed safely. © 2006 Wiley-Liss, Inc. Microsurgery, 2006. [source] Atherosclerosis and Lipid PeroxidationMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 11 2005László Nagy [source] Modulation of Monocyte-Macrophage Function with ,-Tocopherol: Implications for AtherosclerosisNUTRITION REVIEWS, Issue 1 2002Sridevi Devaraj PhD Cardiovascular disease is the leading cause of morbidity and mortality in the Western world. Monocyte-macrophages are crucial cells in atherogenesis. Several lines of evidence suggest that antioxidants, especially , -tocopherol, have beneficial effects with regard to cardiovascular disease. , -Tocopherol has beneficial effects on cell functions that are pivotal in atherogenesis. , -Tocopherol inhibits platelet aggregation and proinflammatory activity of monocytes. In vitro data also support an effect of , -tocopherol on smooth muscle cell proliferation and endothelial function. Finally, recent data support an effect of , -tocopherol on macrophage function. The mounting evidence from in vitro and in vivo studies provides a sound scientific basis for , -tocopherol supplementation. Further clinical trials are required, however, before a definitive recommendation can be made for primary and secondary prevention of heart disease. [source] Estimating ethnic differences in self-reported new use of antidepressant medications: results from the Multi-Ethnic Study of AtherosclerosisPHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 7 2009Joseph A. C. Delaney PhD Abstract Introduction There is evidence that the utilization of antidepressant medications (ADM) may vary between different ethnic groups in the United States population. Methods The Multi-Ethnic Study of Atherosclerosis (MESA) is a population-based prospective cohort study of 6814 US adults from 4 different ethnic groups. After excluding baseline users of ADM, we examined the relation between baseline depression and new use of ADM for 4 different ethnicities: African,Americans (n,=,1822), Asians (n,=,784) Caucasians (n,=,2300), and Hispanics (n,=,1405). Estimates of the association of ethnicity and ADM use were adjusted for age, study site, gender, Center for Epidemiologic Studies Depression Scale (CES-D), alcohol use, smoking, blood pressure, diabetes, education, and exercise. Non-random loss to follow-up was present and estimates were adjusted using inverse probability of censoring weighting (IPCW). Results Of the four ethnicities, Caucasian participants had the highest rate of ADM use (12%) compared with African,American (4%), Asian (2%), and Hispanic (6%) participants. After adjustment, non-Caucasian ethnicity was associated with reduced ADM use: African,American (HR: 0.42; 95% Confidence Interval (CI): 0.31,0.58), Asian (HR: 0.14; 95%CI: 0.08,0.26), and Hispanic (HR: 0.47; 95%CI: 0.31,0.65). Applying IPCW to correct for non-random loss to follow-up among the study participants weakened but did not eliminate these associations: African,American (HR: 0.48; 95%CI: 0.30,0.57), Asian (HR: 0.23; 95%CI: 0.13,0.37), and Hispanic (HR: 0.58; 95%CI: 0.47,0.67). Conclusion Non-Caucasian ethnicity is associated with lower rates of new ADM use. After IPCW adjustment, the observed ethnicity differences in ADM use are smaller although still statistically significant. Copyright © 2009 John Wiley & Sons, Ltd. [source] Vertebral artery atherosclerosis: a risk factor in the use of manipulative therapy?PHYSIOTHERAPY RESEARCH INTERNATIONAL, Issue 3 2002Jeanette Mitchell BSc (Physiotherapy), MSc Senior Lecturer Abstract Background and Purpose Vertebrobasilar insufficiency, a direct result of compromised blood flow in the vertebrobasilar circulation, may be caused by stretching and/or compression of the vertebral arteries, particularly if superimposed on underlying atherosclerosis of the vessels. This is an important consideration when using manipulative therapy techniques. The aim of the present study was to investigate the incidence of atherosclerosis and to calculate the relative associated decrease in blood flow in the third and fourth parts of the vertebral artery, in a sample of the adult population. Method A laboratory-based experimental investigation was used to study 362 vertebral arteries from embalmed adult cadavers that were routinely processed for light microscopic study. The incidence of each grade of atherosclerosis in the vessels was recorded. Atherosclerosis was classified as grades 0,5, where Grade 0 represented no atherosclerosis and Grade 5 a fully developed plaque occluding more than 75% of the vessel lumen. From mean measurements of 188 of these arteries, the estimated decrease in luminal cross-sectional area and the relative decrease in blood flow in the atherosclerotic vessels were calculated. Results The highest incidence of atherosclerosis found was Grade 3 (third part of the vertebral artery (VA3): 42.0%; fourth part of the vertebral artery (VA4): 35.2%). An estimated decrease in artery luminal cross-sectional area to 6.2% of normal in Grade 5 atherosclerosis was found. Because blood flow is proportional to the fourth power of the vessel radius, relative decreases in blood flow in grades 1,5 atherosclerosis from 100% to 0% (with critical closing pressure in vessels), respectively, are likely to occur. Conclusions These data suggest that, as significant numbers of the sample showed marked (Grade 3+) atherosclerosis, concomitant with decreased blood flow in the vertebral arteries, this population is at risk for developing vertebrobasilar insufficiency. Because other Western populations may be similarly at risk, particular care should be taken when considering the use of rotational manipulative therapy techniques in treatments of the cervical spine. Copyright © 2002 Whurr Publishers Ltd. [source] Subclinical Atherosclerosis: Evolving Role of Carotid Intima-Media ThicknessPREVENTIVE CARDIOLOGY, Issue 4 2010FRCPC, Farouk Mookadam MD Cardiovascular risk factors have utility in risk prediction but have limitations in predicting individual risk. Identifying an individual's risk remains a challenge. Emerging technologies such as carotid artery ultrasonography and measures of carotid intima-media thickness (CIMT) may be useful in identifying the susceptible patient who may benefit from more aggressive preventive therapy. This screening test is noninvasive, reproducible, inexpensive, and radiation-free. Recent data have improved our understanding of the application of CIMT as a screening tool for cardiovascular disease. CIMT measurement may place an individual into a higher- or lower-risk category, allowing for appropriate institution of preventive strategies. Prev Cardiol. 2010;13:186,197.©2010 Wiley Periodicals, Inc. [source] Role of Potential Immune Targets in Atherosclerosis for Vaccine DevelopmentPREVENTIVE CARDIOLOGY, Issue 4 2008Nandini Venkatesan PhD First page of article [source] Antioxidant Intake and Coronary Atherosclerosis: Consider a "Foods First" ApproachPREVENTIVE CARDIOLOGY, Issue 2 2006Dianne A. Hyson PhD No abstract is available for this article. [source] Proteomic analysis of human vessels: Application to atherosclerotic plaquesPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 6 2003Mari Carmen Duran Abstract Atherosclerosis is a chronic disease that affects medium and large arteries. This process originates from the interaction between cells of the arterial wall, lipoproteins and inflammatory cells, leading to the development of complex lesions or plaques that protrude into the arterial lumen. Plaque rupture and thrombosis result in acute clinical complications such as myocardial infarction and stroke. Owing to the heterogeneous cellular composition of the plaques, a proteomic analysis of the whole lesion is not appropriate. Therefore, we have studied the proteins secreted by human carotid atherosclerotic plaques, obtained by endarterectomy. Normal artery segments and different regions of the surgical pieces (noncomplicated plaque, complicated plaque with thrombus) were cultured in protein-free medium and the secreted proteins (supernatants) analyzed by two-dimensional gel electrophoresis. Normal artery segments secreted a moderate number of proteins (42 spots). However in the two-dimensional (2-D) gels (pH 3,10) of segments bearing a plaque, the number of spots increased markedly (154). The number of spots also increased (202) in the 2-D gels of artery segments with a ruptured plaque and thrombus. Thus, the more complicated the lesion, the higher the number of secreted proteins, suggesting the production of specific proteins relating to the complexity of the atherosclerotic lesion. [source] Novel biomarkers of atherosclerosis and cardiovascular risk in autoimmune diseases: Genomics and proteomics approachesPROTEOMICS - CLINICAL APPLICATIONS, Issue 2 2009Chary López-Pedrera Professor Abstract Atherosclerosis (AT) and cardiovascular disease (CVD) are enhanced in autoimmune diseases such as antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). The reason for this accelerated process is still debatable and, although traditional risk factors are more prevalent in those patients than in general population, they do not fully explain that enhanced risk. Inflammatory components of the immune response, mainly interleukins, TNF-,, and IFN-,, as well as some autoantibodies, including anti-oxidized low density lipoproteins (anti-oxLDL), anti-beta-2-Glycoprotein 1 (anti- ,2GPI), anti-Heat shock proteins 60/65 (anti-HSP60/65), and anti-oxLDL/,2GPI have been shown to play a leading role in the pathogenesis of both, AT and CVD. However, the role of the autoantibodies in accelerated AT in autoimmune disease patients is still controversial. Recently, DNA microarray and proteomic-based approaches have made substantial breakthrough into the study of various rheumatic diseases, thus allowing for the discovery of previously unknown proteins involved in CVD including some that may be suitable to be used as biomarkers. Herein, we review recent genomics and proteomic approaches that have been applied to the study of autoimmune diseases with atherosclerotic and CV risk. The pharmacogenomics and pharmacoproteomics studies given over to the analysis of ancient and new drugs used to relieve the physiopathology associated to these complex diseases are also discussed. [source] Protective Effect of the Immunosuppressant Sirolimus Against Aortic Atherosclerosis In Apo E-Deficient MiceAMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2003M. Merle Elloso Atherosclerosis is a chronic inflammatory disease that develops in response to injury to the vessel wall, and is augmented by hypercholesterolemia. To further delineate the role of the immune system and local factors in this process, we assessed the effects of the immunosuppressant sirolimus (Rapamycin, RAPAMUNE®, Wyeth, Collegeville, PA) on atherosclerosis in the apoE-deficient (apoE KO) mouse, a well-accepted model of cardiovascular disease. ApoE KO mice were fed a high fat diet and sirolimus was administered. After 12 weeks, atherosclerotic lesions and plasma lipoproteins were measured. The expression of cytokines associated with atherosclerosis was also examined. All groups demonstrated plasma total cholesterol (TC) >1100 mg/dL. Sirolimus treatment was associated with a 30% increase in LDL-cholesterol (LDLc) and a dose-dependent elevation in HDL-cholesterol (HDLc). Despite increased LDLc, aortic atherosclerosis was markedly reduced in all sirolimus-treated groups. Sirolimus treatment resulted in decreased expression of IL-12p40, IFN-, and IL-10 mRNA. In contrast, TGF-,1 was elevated. Sirolimus significantly reduced atherosclerosis in apo E-KO mice; this effect is independent of, and obviates, elevated plasma TC and LDLc. Sirolimus might therefore be of benefit on atherosclerosis in patients undergoing therapy, independent of any impact on circulating lipids. [source] | ||||||||||||||||||||||||||||||||||||||||||||||