Targeted therapies in connective tissue diseases (CTDs) have led to improvements of disease-associated outcomes, but life expectancy remains lower compared to general population due to emerging co-morbidities, particularly due to excess cardiovascular risk. Cardiovascular magnetic resonance (CMR) is a noninvasive imaging technique which can provide detailed information about multiple cardiovascular pathologies without using ionizing radiation. CMR is considered the reference standard for quantitative evaluation of left and right ventricular volumes, mass and function, cardiac tissue characterization and assessment of thoracic vessels; it may also be used for the quantitative assessment of myocardial blood flow with high spatial resolution and for the evaluation of the proximal coronary arteries. These applications are of particular interest in CTDs, because of the potential of serious and variable involvement of the cardiovascular system during their course. The International Consensus Group on CMR in Rheumatology was formed in January 2012 aiming to achieve consensus among CMR and rheumatology experts in developing initial recommendations on the current state-of-the-art use of CMR in CTDs. The present report outlines the recommendations of the participating CMR and rheumatology experts with regards to: (a) indications for use of CMR in rheumatoid arthritis, the spondyloarthropathies, systemic lupus erythematosus, vasculitis of small, medium and large vessels, myositis, sarcoidosis (SRC), and scleroderma (SSc); (b) CMR protocols, terminology for reporting CMR and diagnostic CMR criteria for assessment and quantification of cardiovascular involvement in CTDs; and (c) a research agenda for the further development of this evolving field.
. Objectives. A high level of total homocysteine (tHcy) is a risk marker for cardiovascular disease (CVD), and is related to inflammation. We wanted to test the effect of homocysteine‐lowering B‐vitamin therapy, as used in the Western Norway B‐vitamin Intervention Trial (WENBIT), on inflammatory markers associated with atherosclerosis. Design. Single centre, prospective double‐blind clinical interventional study, randomised in a 2 × 2 factorial design. Subjects and methods. Ninety patients (21 female) with suspected coronary artery disease (CAD), aged 38–80 years, were blindly randomised into one of four groups of daily oral treatment with (A) folic acid (0.8 mg)/vitamin B12 (0.4 mg)/vitamin B6 (40 mg), (B) folic acid/vitamin B12, (C) vitamin B6 alone or (D) placebo. Blood samples were collected before and after 6 months of treatment. Results. Before intervention, median levels of the analytes were: tHcy 11.0 μmol L−1, neopterin 8.1 nmol L−1, soluble CD40 ligand (sCD40L) 3.9 ng mL−1, interleukin (IL)‐6 1.9 pg mL−1, C‐reactive protein (CRP) 1.9 mg L−1 and low‐density lipoprotein (LDL) cholesterol 3.3 mmol L−1. tHcy was significantly associated with neopterin (r = 0.49, P < 0.001) and with IL‐6 (r = 0.29, P = 0.01), but not with CRP or sCD40L. Neither treatment with folic acid/B12 nor with B6 induced significant changes in any of these inflammatory biomarkers (P ≥ 0.14). In patients receiving folic acid/B12 (groups A and B), tHcy was reduced with 33% (P < 0.001). Conclusions. In patients with stable CAD, homocysteine‐lowering therapy with B‐vitamins does not affect levels of inflammatory markers associated with atherogenesis. Failure to reverse inflammatory processes, may partly explain the negative results in clinical secondary B‐vitamin intervention trials.
SummaryBackground: Atherosclerosis is considered to be a chronic inflammatory disorder. Several large-scale clinical studies demonstrate that markers of inflammation, such as high-sensitivity C-reactive protein (hsCRP), fibrinogen, and soluble CD40 ligand, are potent and independent predictors of vascular risk.Hypothesis: The study was undertaken to investigate the effect of increasing the statin dose from conventional to aggressive treatment on lipids levels, inflammation, and endothelial function in patients with coronary artery disease (CAD).Methods: We randomized 97 patients to either 20 mg simvastatin or 80 mg atorvastatin. Plasma levels of lipids, hsCRP, fibrinogen, soluble adhesion molecules, and nitric oxide-total were analyzed at baseline and after 6 months of treatment.Results: Lipid values were significantly reduced in both treatment groups, but with significantly greater reduction in the aggressively treated group. Furthermore, aggressive statin treatment significantly decreased hsCRP and fibrinogen, while only small reductions were seen in the conventionally treated group, resulting in significant differences between the two treatment groups (p < 0.001). Nitric oxide-total increased
Summary. Background: Chemokines and platelet activation are both important in atherogenesis. Platelet inhibitors are widely used in coronary artery disease (CAD), and we hypothesized that the platelet inhibitor clopidogrel could modify chemokines in CAD patients. Objectives: We sought to investigate the effect of clopidogrel on the expression of chemokines and chemokine receptors in peripheral blood mononuclear cells (PBMC) in CAD patients. Patients/methods: Thirty-seven patients with stable angina were randomized to clopidogrel (n ¼ 18) or placebo (n ¼ 19). PBMC, blood platelets and plasma were collected at baseline and after 7-10 days in the patients, and in 10 healthy controls. mRNA levels of chemokines and chemokine receptors in PBMC were analyzed by ribonuclease protection assays and real-time reverse transcriptase polymerase chain reaction. Platelet activation was studied by flow cytometry. Results: (i) At baseline, the gene expression of the regulated on activation normally T-cell expressed and secreted (RANTES) chemokines and macrophage inflammatory peptide (MIP)-1b in PBMC, the expression of CD62P and CD63 on platelets and the levels of platelet-derived microparticles (PMP) were elevated in angina patients comparing healthy controls; (ii) markers of platelet activation were either reduced (CD63) or unchanged (CD62P, PMP, b-thromboglobulin) during clopidogrel therapy; (iii) in contrast, clopidogrel significantly up-regulated the gene expression of RANTES and MIP-1b in PBMC, while no changes were found in the placebo group; (iv) a stable adenosine 5¢-diphosphate metabolite attenuated the release of MIP-1b, but not of RANTES, from activated PBMC in vitro. Conclusions: Even if we do not argue against a beneficial role for clopidogrel in CAD, our findings may suggest potential inflammatory effects of clopidogrel in CAD.
Objective To determine whether there are racial differences in social support among patients with knee osteoarthritis (OA) and whether the impact of social support on patient preferences for total knee replacement (TKR) varies by race and gender. Methods 514 white & 285 African-American (AA) patients with knee OA were surveyed. Logistic regression models were performed to determine if the relationship between willingness to undergo TKR and the interaction of patient race and sex were mediated by social support. Results Compared to whites with knee OA, AA patients were less likely to be married (p<0.001), reported less close friends/relatives (p<0.001) and had lower Medical Outcomes Study-Social Support Scale (MOS-SSS) scores (p<0.001). AA patients were also less willing to undergo TKR (62% vs. 80%, p<0.001) than whites. The odds of willingness to undergo TKR was less in white females compared to white males when adjusted for recruitment site, age, income and WOMAC (OR 0.57, 95% CI 0.34–0.96). This difference was no longer significant when further adjusted for marital status, number of close friends/relatives and MOS-SSS score, but the effect size remained unchanged (OR 0.60, 95% CI 0.35–1.02). The odds of willingness to undergo TKR remained much less in AA females (OR 0.35, 95% CI 0.19–0.64) and AA males (OR 0.28, 95% CI 0.14–0.54) compared to white males when controlled for sociodemographic, clinical and social support measures. Conclusions AA patients reported less structural and functional social support than whites. Social support is an important determinant of preference for TKR surgery only among whites.
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