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antirheumatics/infarction

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Antirheumatic drug use and the risk of acute myocardial infarction.

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OBJECTIVE To assess the risk of acute myocardial infarction (AMI) associated with the use of disease-modifying antirheumatic drugs (DMARDs) and other medications commonly used in rheumatoid arthritis (RA). METHODS We conducted a nested case-control analysis within a cohort of subjects with RA,

Do antirheumatic drugs increase the risk of acute myocardial infarction?

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Effect of risk factors and antirheumatic drugs on the proliferation of aortic wall cells.

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The proliferation of aortic smooth muscle cells (ASMC) of Wistar rats, impaired by risk factors such as arterial hypertension, diabetes mellitus, atherogenic diet and staphylolysin injections and of normal Wistar rats treated with antirheumatic drugs such as prednisolone and acetylsalicylic acid was
BACKGROUND Multiple studies have observed seemingly unfavorable changes in lipid profiles associated with IL6 receptor antagonists (IL-6R) and some other rheumatoid arthritis (RA) therapies. The real-world cardiovascular disease (CVD) risk associated with the first approved anti IL-6R medication for

The risk of cardiovascular events associated with disease-modifying antirheumatic drugs in rheumatoid arthritis

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Objective: To examine the comparative effects of biologic disease-modifying antirheumatic drugs (bDMARDs) and tofacitinib against conventional synthetic (cs) DMARDs on incident cardiovascular disease (CVD) in patients with rheumatoid
Inflammation of the arterial wall plays a central role in the pathogenesis of atherosclerosis. Among patients with rheumatic diseases, anti-rheumatic medication reduces the incidence of cardiovascular (CV) diseases, but only few studies have addressed their cardioprotective effects on patients with
Background: The aim of this nationwide age- and sex matched longitudinal follow up study is to determine the risk of acute myocardial infarction (AMI) associated with the seropositive rheumatoid arthritis (RA) population in Korea.
Methotrexate, an anti-rheumatic agent, has recently been reported to show an anti-inflammatory action via ecto-5'-nucleotidase- and adenosine-dependent mechanisms. Because ecto-5'-nucleotidase contributes to the production of adenosine and adenosine has a potent cardioprotective effect against
OBJECTIVE To examine disease-modifying antirheumatic drug (DMARD) treatments and estimate risk of a subsequent cardiovascular (CV) event following an initial CV event in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), or psoriasis (PsO). METHODS We analyzed data from MarketScan®
OBJECTIVE Patients with rheumatoid arthritis (RA) are at increased risk of myocardial infarction (MI) compared with subjects without RA, with the increased risk driven potentially by inflammation. Tumour necrosis factor inhibitors (TNFi) may modulate the risk and severity of MI. We compared the risk
BACKGROUND In rheumatoid arthritis (RA), intramuscular (IM) pulsed depomedrone expedites an immediate response to disease modifying antirheumatic drugs (DMARDs). Although IM depomedrone is also widely used to treat disease flares in patients treated with DMARDs, its effect on radiological

Longterm outcomes and treatment after myocardial infarction in patients with rheumatoid arthritis.

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OBJECTIVE To investigate the risk profiles, treatment, and outcomes of patients with rheumatoid arthritis (RA) with myocardial infarction (MI) and matched MI patients without RA. METHODS We used a population-based cohort of Olmsted County, Minnesota, residents with MI from the period 1979-2009. We

Impact of disease activity and treatment of comorbidities on the risk of myocardial infarction in rheumatoid arthritis.

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The aim was to estimate the impact of individual risk factors and treatment with various disease-modifying antirheumatic drugs (DMARDs) on the incidence of myocardial infarction (MI) in patients with rheumatoid arthritis (RA). We analysed data from 11,285 patients with RA, enrolled in the
OBJECTIVE Rheumatoid arthritis (RA) is associated with an increased risk of coronary artery disease, possibly acting via shared mechanisms of inflammation. This study was undertaken to test the hypothesis that the powerful antiinflammatory effect of anti-tumor necrosis alpha (anti-TNFalpha) therapy
OBJECTIVE Pneumonia is a major cause of mortality and morbidity in rheumatoid arthritis (RA). This study was undertaken to determine the rate and predictors of hospitalization for pneumonia and the extent to which specific RA treatments increase pneumonia risk. METHODS RA patients (n = 16,788) were
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