Background Cardiovascular mortality is increased in Rheumatoid Arthritis (RA). This may be due to early development and increased prevalence of Ischaemic Heart Disease (IHD).
Objectives We aimed to assess the prevalence, clinical presentation and risk factors of IHD in RA compared to matched controls.
Methods Prospective, random recruitment of 104 hospital outpatients: 67 RA, 37 osteoarthritis controls. IHD detection: Rose questionnaire, ECG, adenosine-stressed myocardial perfusion SPECT imaging. Assessments: demographics, body mass index (BMI), disease and drug history, Health Assessment Questionnaire (HAQ), current and cumulative inflammatory burden (ESR, CRP), Joint Count, Rheumatoid Factor, von Willebrand Factor (vWF), angiotensin converting enzyme (ACE), lipids, fibrinogen, homocysteine, H. pylori, CMV and C. pneumoniae titers.
Results RA and controls were matched for all classical IHD risk factors (age, sex, family history, smoking, hypertension, lipids, diabetes, BMI) and NSAID use. Despite this, IHD in RA was almost twice as prevalent (49%) as in controls (27%) [p = 0.03] in both sexes, clinically silent in 52% vs 20% [p = 0.003], high risk in 60% vs 70% and present a decade earlier in RA. ESR, CRP, fibrinogen, vWF, ACE were significantly higher in RA [p < 0.001]. By logistic regression, age, male sex, RA and BMI independently predicted IHD in the study population. Within the RA group, patients with IHD had higher age, male sex, blood pressure, triglycerides, BMI, H. pylori titers and steroid use than those without IHD [p < 0.05]; RA duration, activity, seropositivity or functional ability were not significantly different. Age, male sex and BMI were the only independent predictors of IHD in RA.
Conclusion IHD is highly prevalent, clinically silent, occurs early and may be the main cause of increased cardiovascular death in RA. Within a hospital population, RA is an independent risk factor for IHD, with clinical and outcome characteristics similar to type II diabetes. In RA, classical IHD risk factors and systemic inflammation may both play a role. Further research may elucidate the mechanisms involved and help design risk reduction strategies specific to RA.
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