Home About us Contact
|
Home About us Contact | ||
|
|
||
Atherosclerotic Vascular Disease (atherosclerotic + vascular_disease)
Selected AbstractsAsymmetric dimethylarginine (ADMA): the silent transition from an ,uraemic toxin' to a global cardiovascular risk moleculeEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2005D. Fliser Abstract Endothelial dysfunction as a result of reduced bioavailability of nitric oxide (NO) plays a central role in the process of atherosclerotic vascular disease. In endothelial cells NO is synthesized from the amino acid l -arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as asymmetric dimethylarginine (ADMA). Acute systemic administration of ADMA to healthy subjects significantly reduces NO generation, and causes an increase in systemic vascular resistance and blood pressure. Increased plasma ADMA levels as a result of reduced renal excretion have been associated with atherosclerotic complications in patients with terminal renal failure. However, a significant relationship between ADMA and traditional cardiovascular risk factors such as advanced age, high blood pressure and serum LDL-cholesterol, has been documented even in individuals without manifest renal dysfunction. As a consequence, the metabolism of ADMA by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) has come into the focus of cardiovascular research. It has been proposed that dysregulation of DDAH with consecutive increase in plasma ADMA concentration and chronic NOS inhibition is a common pathophysiological pathway in numerous clinical conditions. Thus, ADMA has emerged as a potential mediator of atherosclerotic complications in patients with coronary heart disease, peripheral vascular disease, stroke, etc., being the culprit and not only an innocent biochemical marker of the atherosclerotic disease process. [source] LPL polymorphism predicts stroke risk in menGENETIC EPIDEMIOLOGY, Issue 3 2002Alanna C. Morrison Abstract Variation in lipid levels has been associated with atherosclerotic vascular disease, including stroke. Genes contributing to interindividual variation in lipid levels may play a role in the etiology of stroke, either through their effects on lipid synthesis and metabolism or through separate pathways. For this reason, we sought to examine the association between polymorphisms in the lipoprotein lipase (LPL) and apolipoprotein E (APOE) genes and subclinical and clinical stroke in the Atherosclerosis Risk in Communities (ARIC) Study. Subclinical stroke was determined by cerebral magnetic resonance imaging (MRI). Subclinical cerebral infarct cases (n = 197) were compared to a stratified random sample identified from individuals participating in the MRI examination (n = 200). Incidence of clinical ischemic stroke was determined by following the ARIC cohort for an average of 7.5 years for potential cerebrovascular events; 218 validated clinical ischemic strokes were identified. A stratified random sample of the ARIC cohort (CRS, n = 964) was used as the comparison group for clinical cases. The LPL S291-carrying genotypes and APOE ,2- and ,4-carrying genotypes were not significantly associated with subclinical or clinical stroke. The LPL X447-containing genotypes were significantly associated with subclinical (odds ratio [OR], 4.32; 95% confidence interval [CI], 1.23,15.15; P = 0.020) and clinical stroke (hazard rate ratio [HRR], 2.57; 95% CI, 1.24,5.34; P = 0.01) in men, both by themselves and after adjustment for multiple stroke risk factors. The LPL S447X polymorphism is significantly associated with subclinical cerebral infarction and incident clinical ischemic stroke in men from a middle-aged American population. This association does not appear to be mediated by triglyceride, high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol levels, or additional stroke risk factors. Genet. Epidemiol. 22:233,242, 2002. © 2002 Wiley-Liss, Inc. [source] Bilateral Axillary Artery Perfusion to Reduce Brain Damage during Cardiopulmonary BypassJOURNAL OF CARDIAC SURGERY, Issue 2 2010Kazuhiro Kurisu M.D. The aim of the present study was to examine the value of bilateral axillary artery perfusion during thoracic aortic and cardiac surgery, and to evaluate the clinical results with a particular focus on cerebral damage. Methods: From March 2002 through December 2007, 24 patients (16 male and eight female; age range, 43 to 84 years) underwent bilateral axillary artery perfusion through side grafts during cardiopulmonary bypass. Aortic surgery, including total arch replacement, hemiarch replacement, and ascending aortic replacement, was performed in 21 patients. Bilateral axillary artery perfusion was also used in three complicated valve surgeries after expanding its indication to cardiac pathology with a diseased aorta, two redo cases with severe atherosclerotic vascular disease, and one case with a porcelain aorta. Results: Bilateral axillary artery perfusion was successful in all patients. There were no complications related to this procedure except in one patient, who suffered from a local fluid retention in one wound, requiring puncture drainage. There was no hospital mortality. No strokes were identified by either clinical assessments or diagnostic imaging. Conclusions: Bilateral axillary artery perfusion is a useful method for protection of the brain during either thoracic aortic or cardiac surgery when the patients have an extensively diseased aorta.,(J Card Surg 2010;25:139-142) [source] Whole-body MR angiography using a novel 32-receiving-channel MR system with surface coil technology: First clinical experienceJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2005Michael Fenchel MD Abstract Purpose To demonstrate the feasibility of detecting atherosclerotic vascular disease using an innovative magnetic resonance angiography (MRA) protocol in combination with a dedicated whole-body MR scanner with new surface coil technology. Materials and Methods A total of 10 volunteers and eight patients with peripheral arterial occlusive disease (PAOD) were examined at 1.5 T. Conventional digital subtraction angiography (DSA) of the symptomatic region was available as a reference standard in all eight patients. Depending on subjects' size, four to five three-dimensional data sets were acquired using an adapted injection protocol. Images were assessed independently by two readers for vascular pathology. Additionally, signal-to-noise ratios (SNRs) and contrast-to-noise ratios (CNRs) were measured. Results Whole-body MRA yielded excellent sensitivity and specificity of more than 95% for both readers with high interobserver agreement (k = 0.93). Surface coil signal reception rendered a high SNR (mean 151.28 ± 54.04) and CNR (mean 120.75 ± 46.47). Despite lower SNR and CNR of the cranial and cervical vessels, a two-step injection protocol exhibited less venous superposition and therefore proved to be superior compared to single-bolus injection. Conclusion Our approach provides accurate noninvasive high-resolution imaging of systemic atherosclerotic disease, covering the arterial vasculature from intracranial arteries to distal runoff vessels. The recently introduced MR scanner and coil technology is feasible to significantly increase the performance of whole-body MRA. J. Magn. Reson. Imaging 2005;21:596,603. © 2005 Wiley-Liss, Inc. [source] Moderate Alcohol Intake in Humans Attenuates Monocyte Inflammatory Responses: Inhibition of Nuclear Regulatory Factor Kappa B and Induction of Interleukin 10ALCOHOLISM, Issue 1 2006Pranoti Mandrekar Background: In contrast to the deleterious effects of chronic excessive alcohol consumption on the liver and cardiovascular system, modest alcohol intake, such as 1 to 2 drinks per day, has benefits on cardiovascular mortality. Little is known about the length of time or the amounts of alcohol consumed that may cause alterations in inflammatory cells such as monocytes that are crucial to atherosclerotic vascular disease. Here, we determine in vivo effects of acute alcohol consumption on inflammatory cytokine production and nuclear regulatory factor ,B (NF- ,B) binding in human monocytes. Methods: Human blood monocytes were isolated by plastic adherence before and after acute alcohol consumption (2 ml vodka/kg body weight). Lipopolysaccharide (LPS)- and superantigen-induced tumor necrosis factor , (TNF ,), interleukin (IL)-1,, and IL-10 production were then determined in monocytes by ELISA. Nuclear regulatory factor- ,B activity of monocytes before and after alcohol consumption was estimated by electromobility shift assay and promoter-driven reporter activity. I,B, was determined by Western blotting in the cytoplasmic extracts. Results: Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF- , and IL-1,, in response to LPS or staphylococcal enterotoxin B stimulation. Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF- ,B in monocytes that regulates the expression of both the TNF- , and the IL-1, genes. Consistent with this, acute alcohol treatment (25 mM) significantly reduced LPS-induced activation of an NF- ,B-driven reporter gene suggesting inhibition of this proinflammatory signaling pathway. Further, LPS-induced I,B, degradation was not affected by acute alcohol consumption indicating an I,B, -independent mechanism, as observed earlier in the in vitro acute alcohol studies. In contrast, monocyte production of the anti-inflammatory cytokine, IL-10, was augmented by acute alcohol intake. Conclusions: Our findings suggest that acute alcohol consumption has dual anti-inflammatory effects that involve augmentation of IL-10 and attenuation of monocyte inflammatory responses involving inhibition of NF- ,B. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis. [source] Alcohol and Atherosclerotic Vascular Disease Risk Factors in French Men: Relationships Are Linear, J-Shaped, and U-ShapedALCOHOLISM, Issue 1 2005Philippe Rouillier Background: Although it is well admitted that alcohol displays a U-shaped relationship with atherosclerotic vascular disease, individual relationships between alcohol and atherosclerosis risk factors may be different and have not been determined precisely for several of them. Methods: A cross-sectional study within the SU.VI.MAX French cohort study was performed to assess the curve of potential relationships between alcohol and atherosclerosis risk factors in 2126 healthy men. Mean daily alcohol intake was derived from 37 alcoholic beverages in twelve 24-hr dietary recalls. Logistic models were adjusted for age. Results: Apolipoprotein B (ApoB), fasting glucose, body mass index, waist-to-hip ratio, and waist circumference displayed a linear relationship with alcohol. The odds ratios and 95% confidence intervals associated with abnormal values of the markers for the highest quintile of alcohol intake were 1.45 (1.06,1.97) for ApoB, 1.98 (1.40,2.80) for fasting glucose, and 1.74 (1.30,2.34) for body mass index. An inverse J-shaped relationship was assumed for ApoA1 and ApoB/ApoA1 ratio, whereas a U-shaped relationship was observed for serum triglycerides and mixed hyperlipidemia. Only the highest quintile of alcohol was associated with hypertension, although the test for linearity was also significant. No association was observed for Lp(a) or homocysteine. Associations were unmodified by further adjustment for carbohydrates, fiber, lipids, tobacco, or exercise. Conclusions: The aggregate of the disparate alcohol risk factor relationships suggests probable net benefit at 15 to 25 g of alcohol/day. [source] Review article: medical management of the liver transplant recipient , a primer for non-transplant doctorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2007A. SETHI Summary Background Survival 10 years after orthotopic liver transplantation now approaches 65%. Consequently, community doctors must manage the metabolic and neoplastic complications of orthotopic liver transplantation in an ageing population. Aims To review common sources of morbidity and mortality in long-term orthotopic liver transplantation recipients, and to make evidence-based recommendations regarding their management. Methods Pertinent studies and reviews were identified by literature search through PubMed. Where evidence-based recommendations could not be gleaned from the literature, expert opinion was obtained from syllabi of national meetings. Results The two most common causes of morbidity and mortality in orthotopic liver transplantation recipients are atherosclerotic vascular disease and de novo malignancy. The pathogenesis of many complications begins before orthotopic liver transplantation, and many are potentially modifiable. Most complications, however, can be directly ascribed to immunosuppressive agents. Despite improvements in our understanding of the pathogenesis and epidemiology of the metabolic and neoplastic complications of orthotopic liver transplantation, remarkably few randomized-controlled studies exist to define their optimal management. Conclusions Orthotopic liver transplantation recipients experience and succumb to the same afflictions of old age as non-transplant patients, but with greater frequency and at an earlier age. Most recommendations regarding surveillance for, and treatment of, medical complications of orthotopic liver transplantation remain based upon expert opinion rather than evidence-based medicine. [source] APOE,4 influences the pathological phenotype of Alzheimer's disease by favouring cerebrovascular over parenchymal accumulation of A, proteinNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2003K. Chalmers The relative amounts of amyloid ,-protein (A,) in cerebral blood vessels and parenchyma vary considerably amongst patients with Alzheimer's disease (AD). Although several mechanisms have been proposed to explain this variability, the underlying genetic and environmental determinants are still unclear, as are the functional consequences. Polymorphisms in APOE, the gene for apolipoprotein E (ApoE), influence the risk of developing AD and of deposition of A, within the brain. We examined the relationship between the APOE genotype and the relative extent of accumulation of A, as plaques within the cerebral parenchyma and in cortical blood vessels in the form of cerebral amyloid angiopathy (CAA), in autopsy brain tissue from 125 AD cases and from 53 elderly, neurologically normal controls of which 19 had CAA without other neuropathological features of AD. In the AD cases, we also assessed whether the severity of CAA was related to the age of onset and duration of dementia, risk factors for atherosclerotic vascular disease, and histologically demonstrable cerebral in-farcts or foci of haemorrhage. The APOE genotype was determined by a standard polymerase chain reaction-based method. Paraffin sections of frontal, temporal and parietal lobes were immunolabelled for A, and the parenchymal A, load (total A, minus vessel-associated A,) was quantified by computer-assisted image analysis. CAA severity was scored for cortical and leptomeningeal vessels. The relevant clinical data were obtained from the database of the South West Brain Bank. In AD, we found the severity of CAA to be strongly associated with the number of ,4 alleles (P < 0.0001) but the parenchymal A, load to be independent of APOE genotype. Cases with severe CAA had a lower parenchymal A, load than had those with moderate CAA (P = 0.003). Neither the severity of CAA nor the parenchymal A, load correlated with age of onset, duration of disease or age at death, and the severity of CAA also did not correlate with the presence of cerebral infarcts or foci of haemorrhage. These findings indicate that possession of the APOE,4 allele favours vascular over parenchymal accumulation of A, in AD. This may influence the pathogenesis of neurodegeneration in ,4-associated AD. [source] Association between serious ischemic cardiac outcomes and medications used to treat diabetes,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 8 2008David J. Margolis MD Abstract Purpose Data on cardiovascular outcomes among treated diabetics have been inconsistent. Our goal was to compare cardiovascular outcomes associated with different treatments for diabetes. Methods This is a retrospective cohort study of diabetic patients at least 40 years of age treated in general practices participating in The Health Information Network (THIN) data system between 2002 and 2006. Our primary outcome was serious atherosclerotic vascular disease of the heart. Results Among all diabetics (N,=,63,579), the fully adjusted hazard ratios of association with our outcome were 1.2 (1.1, 1.3) for insulin, 1.03 (0.97, 1.09) for sulfonylureas, 0.8 (0.7, 0.8) for biguanide, 1.2 (0.99, 1.5) for meglitinide, 0.5 (0.5, 0.6) for thiazolidinediones, and individually 0.6 (0.5, 0.6) for rosiglitazone, and 0.5 (0.4, 0.7) for pioglitazone. Among those individuals newly diagnosed and treated for diabetes after 2002 (N,=,13,576), the adjusted hazard ratios of association with our outcome were 2.4 (2.0, 2.9) for insulin, 1.4 (1.2, 1.7) for sulfonylureas, 0.5 (0.4, 0.5) for biguanide, 0.9 (0.4, 2.1) for meglitinide, 0.8 (0.7, 1.0) for thiazolidinediones, and individually 0.8 (0.6, 1.0) for rosiglitazone, and 0.9 (0.6, 1.4) for pioglitazone. Risk increased as total duration of therapy increased for insulin, sulfonylureas, and biguanide, but decreased with duration for rosiglitazone and pioglitazone. Conclusions Overall, insulin was associated with an increased risk of myocardial infarction. Its risk increased with longer use, and risk emerged with longer use of sulfonylureas and biguanide. Conversely, a protective effect emerged with longer use of rosiglitazone or pioglitazone. Copyright © 2008 John Wiley & Sons, Ltd. [source] C677T polymorphism of methylenetetrahydrofolate reductase gene affects plasma homocysteine level and is a genetic factor of late-onset Alzheimer's diseasePSYCHOGERIATRICS, Issue 1 2004Tomoyuki KIDA Abstract Background:, Elevated plasma homocysteine levels are known as a risk for atherosclerotic vascular disease and venous thrombosis and have been shown as a risk for late-onset Alzheimer's disease (LOAD). Method:, To examine the effect of genetic factors predisposing to elevated plasma homocysteine levels on the occurrence of LOAD, we determined the genotype of a C677T polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene and a variable number tandem repeat (VNTR) spanning exon 13,intron 13 boundary of cystathionine ,-synthase (CBS) gene in patients with LOAD and community-based control subjects. Results:, Logistic regression indicated that the MTHFR-T allele was a risk for LOAD (P < 0.05), independently from apolipoprotein E-,4 (APOE-,4) allele. Kaplan,Meier tests showed that in APOE-,4 non-carriers, individuals with the MTHFR-TT genotype have occurences of LOAD earlier than those with the MTHFR-CC genotype (P < 0.05). Multiple regression analysis indicates that MTHFR-T allele increases plasma homocysteine levels (P = 0.0002), while the number of X chromosomes decreases (P = 0.01). Plasma homocysteine level was not correlated with age, plasma albumin reflecting nutritional condition, and the dose of APOE-,4 allele. The CBS-20 VNTR allele showed the same trend to increase plasma homocysteine level as the MTHFR-T allele, but a risk effect for LOAD was not evident. Conclusion:, A genetic propensity for elevated plasma homocysteine levels, explained by the MTHFR-T allele encoding defective enzymatic function, is involved in the development of LOAD, particularly in APOE-,4 non-carriers, and that homocysteine metabolism could be a preventive target to LOAD in the elderly. [source] Apolipoprotein C-III and E Polymorphisms and Cardiovascular Syndrome, Hyperlipidemia, and Insulin Resistance in Renal TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2002Emilio Rodrigo Hyperlipidemia and insulin resistance frequently develop after renal transplantation, contributing to cardiovascular disease. Individual differences in response based upon genetic variations in proteins regulating lipidic and glucose tolerance metabolism could be expected. In the general population, the S2 allelic variant of the apoprotein (apo) C-III gene has been associated with hypertriglyceridemia and an insulin resistant state, whereas the E4 allele of the apo E has been associated with hypercholesterolemia and atherosclerosis. Its influence in renal transplant patients remains to be seen. In order to assess the impact of apo E and C-III major polymorphisms on atherosclerotic vascular disease, lipid profile and impaired glucose tolerance in renal transplant patients, we studied 110 consecutively examined patients undergoing kidney transplantation (age range 24,73 years). Atherosclerotic complications were detected in 25% of patients, with age, male sex and hypercholesterolemia being significant atherosclerotic risk factors. Among the male patients with E4 allele, the odds ratio for coronary disease and global atherosclerosis were 10.2 (95% CI) and 6.4 (95% CI), respectively. There were no significant differences in the frequency of any of the polymorphisms among patients with dyslipidemia and impaired glucose tolerance. As the number of patients in our sample was small, larger studies are needed to verify these issues. While in the studied population C-III polymorphism appears to have little association with the prevalence of atherosclerotic complications, E4 allele should be considered as a genetic marker of coronary artery disease and global atherosclerosis in renal transplant patients. [source] Retinal vascular findings and penile cavernosal artery blood flowBJU INTERNATIONAL, Issue 9 2003Y. Kawanishi Authors from Japan attempt to correlate retinal vascular changes with cavernosal arterial blood flow. They studied patients with erectile dysfunction, but excluded patients with previous pelvic surgery, pelvic injury or diabetes. They found that penile changes can be anticipated from retinal vascular changes seen on fundoscopy. OBJECTIVE To assess the correlation between retinal vascular findings and penile cavernosal arterial blood flow, as it is probable that systemic atherosclerotic vascular disease is important in male erectile dysfunction (ED), and being systemic, it might be possible to evaluate the extent of atherosclerosis from retinal vascular findings. PATIENTS AND METHODS The study included 75 patients with ED; any with a history of pelvic injury, pelvic surgery, or diabetes mellitus were excluded. All patients gave fully informed consent. Ocular fundus photographs were taken with an automatic-focus fundus camera under amydriatic conditions. Three ophthalmologists, unaware of the patients' detailed data, evaluated the photographs using Hyman's classification to evaluate retinal vascular findings. Blood flow in the penile cavernosal artery was measured with colour Doppler ultrasonography, and the peak systolic velocity used as a haemodynamic variable. Correlations among the peak systolic velocity, retinal vascular findings and vascular risk factors (including hypertension, age, cigarette smoking, and hyperlipidaemia) were investigated using multivariate analysis. RESULTS Of the 75 patients, 72 (96%) had both right and left retinal vascular images of sufficient quality for evaluation; 37 were classified as normal and 35 as Grade I, while no patient was Grade II. From a logistic regression multivariate analysis, the peak systolic velocity was the only significant factor correlating with retinal vascular findings, with an odds ratio of 3.34. In contrast, hypertension, age, cigarette smoking and hyperlipidaemia did not correlate significantly with the retinal vascular findings. Similarly, the retinal vascular finding was the only significant factor correlating with the peak systolic velocity of cavernosal blood flow (odds ratio 3.28) and again hypertension, age, cigarette smoking and hyperlipidaemia were not significant factors. CONCLUSIONS These findings support the assumption that penile erectile function is one of the diseases of atherosclerosis, and emerges nearly simultaneously with retinal vascular disease. It is possible to predict penile arterial conditions in patients with ED from their retinal vascular findings. Thus, amydriatic fundoscopy, a simple practical examination, may be helpful for primary physicians in diagnosing and treating ED. [source] Association between serum lipoprotein (a) level and progression of non-proliferative diabetic retinopathy in Type 2 diabetesACTA OPHTHALMOLOGICA, Issue 5 2009Hideharu Funatsu Abstract. Purpose:, To investigate independent risk factors related to the progression of non-proliferative diabetic retinopathy (NPDR) for Japanese Type 2 diabetic patients. Methods:, One hundred and six patients with NPDR were followed up for 2 years. Diabetic retinopathy (DR) was determined by colour fundus photography. Multivariate logistic regression analysis was performed to assess variables independently associated with the progression of NPDR. Serum concentrations of novel risk factors for atherosclerotic vascular disease, including lipoprotein (a) [Lp(a)] and fibrinogen, were measured. Results:, Thirty-three patients (31%) had progressed by two scale steps or more in 2 years. The progression of NPDR was significantly associated with HbA1c [odds ratio (OR) 2.12; 95% confidence interval (CI) 1.14,4.87], systolic blood pressure (OR 1.72; 95% CI 1.14,2.91), Lp(a) (OR 2.70; 95% CI 1.09,5.12) and fibrinogen (OR 1.68; 95% CI 1.03,3.08). Multivariate logistic regression analysis showed that HbA1c (OR 1.74; 95% CI 1.12,3.21) and Lp(a) level (OR 1.90; 95% CI 1.06,4.33) were significant and independent predictors of the progression of NPDR. Conclusion:, These data suggest that serum Lp(a) level is an independent risk factor for the progression of NPDR in Type 2 diabetes patients. We recommend that further prospective validation of our findings be undertaken to confirm these observations. [source] Androgens, insulin resistance and vascular disease in menCLINICAL ENDOCRINOLOGY, Issue 3 2005D. Kapoor Summary Type 2 diabetes mellitus is increasing globally and is an established risk factor for the development of atherosclerotic vascular disease. Insulin resistance is the hallmark feature of type 2 diabetes and is also an important component of the metabolic syndrome. There is evidence to suggest that testosterone is an important regulator of insulin sensitivity in men. Observational studies have shown that testosterone levels are low in men with diabetes, visceral obesity (which is strongly associated with insulin resistance), coronary artery disease and metabolic syndrome. Short-term interventional studies have also demonstrated that testosterone replacement therapy produces an improvement in insulin sensitivity in men. Thus hypotestosteronaemia may have a role in the pathogenesis of insulin-resistant states and androgen replacement therapy could be a potential treatment that could be offered for improvements in glycaemic control and reduction in cardiovascular risk, particularly in diabetic men. [source] Comparative study on antibodies to human and bacterial 60 kDa heat shock proteins in a large cohort of patients with coronary heart disease and healthy subjectsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2001Z. Prohászka Background Recent observations indicate an association between antibodies against mycobacterial heat shock protein (hsp65) and coronary heart disease (CHD). Previously, we reported on marked differences in antigen specificity and complement activating ability of anti-hsp65 antibodies and auto-antibodies against human heat shock protein, hsp60. Here, we investigated whether there are differences between antih-sp65 and anti-hsp60 antibodies in their association with CHD. Design We measured by ELISA the levels of antibodies to hsp65, hsp60 and E. coli -derived GroEL in three groups: Group I, 357 patients with severe CHD who underwent by-pass surgery; Group II, 67 patients with negative coronary angiography; Group III, 321 healthy blood donors. Antibodies against Helicobacter pylori were also measured by commercial ELISA. Results As calculated by multiple regression analysis, the levels of anti-hsp60 auto-antibodies were significantly higher in Group I compared to Group II (P = 0·007) or Group III (P < 0·0001). By contrast, although concentrations of anti-hsp65 and anti-GroEL antibodies in Group I were higher than in Group III, no significant differences between Group I and Group II were found. Antibodies to the two bacterial hsp strongly correlated to each other, but either did not correlate or weakly correlated to hsp60. In Group I, serum concentrations of anti- H.pylori antibodies significantly correlated with those of anti-hsp65 and anti-GroEL antibodies but they did not correlate with the anti-hsp60 antibodies. Conclusion As to their clinical relevance, a remarkable difference become evident between antibodies to human hsp60 and antibodies against bacterial hsp in the extent of association with CHD. On the basis of these findings and some pertinent literature data, an alternative explanation for the association between high level of anti-hsp antibodies and atherosclerotic vascular diseases is raised. [source] Combination antiplatelet therapy in patients with peripheral arterial disease: Is the best therapy aspirin, clopidogrel, or both?,,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue S1 2009Emile R. Mohler III MD Abstract Patients with peripheral arterial disease (PAD) are at increased risk of atherothrombotic events. Antiplatelet therapy and risk-factor modification represent the basis of treatment to prevent the ischemic events associated with PAD. The efficacy of aspirin in the secondary prevention of myocardial infarction and stroke has been demonstrated in a large number of trials. More recently, however, the clinical benefit of clopidogrel compared with aspirin in patients with PAD was confirmed. Many clinical trials have evaluated the efficacy of combination antiplatelet therapy in the prevention of recurrent ischemic events in patients with atherosclerotic vascular diseases. Although the results of these studies appear promising, the benefits resulting from dual antiplatelet therapy are counterbalanced by a significant increase in bleeding. Further studies are needed to establish the optimal antiplatelet therapy in the management and prevention of PAD. © 2009 Wiley-Liss, Inc. [source] | ||||||||||