Cardiovascular disease (CVD) is the most common cause of death in RA as in the general population. According to most epidemiological reports, death due to CVD is more frequent in RA than in the general population with standardised mortality ratios (SMR:s) ranging from 1.3–2.4. Several of the studies are community based. The largest increase, SMR 3.64, was reported in women aged 15–49. Some studies have reported increased death due to ischaemic heart disease (IHD) while reports on cerebrovascular disease are contradictory. In 606 patients with RA followed-up after 16 years we found an SMR for CVD of 1.57 and for IHD 1.54. Cardiovascular morbidity in RA is less investigated. However, current epidemiological data implicate increased prevalence of cardiovascular (CV) events and increased IHD morbidity in RA. These findings are supported by physiological studies. In 39 RA patients with medium-term disease, we found indications of increased atherosclerosis as measured by intima media thickness (IMT) of the carotid artery, presence of plaques and aortic cusp sclerosis compared to controls. Established cardiovascular risk factors do not contribute prominently to CVD in RA. Recent studies have reported increased prevalence of hypertension and higher blood pressure in RA compared to controls. Hypertension could also predict CV events and death. The prevalence of diabetes mellitus, however, appears to be similar to the general population. Smoking has been reported to predict RA per se, but reports on the prevalence of smoking in RA are contradictory. Several studies have reported decreased lipid levels in active RA with quantities inversely related to the acute phase reaction. Lipoprotein (a), was however increased and in patients with high levels related to inflammatory variables. Concerning the use of corticosteroids, epidemiological reports have failed to identify their use as a risk factor for CVD in RA. In a retrospective cohort study on 211 patients with early RA, followed-up after 19–21 years, we found the inflammatory activity at disease onset (ESR, haptoglobin), and during disease progression, to predict cardiovascular event. In contrast to a report on increased risk of death due to CVD following the use of methotrexate, we found DMARDs, and specifically antimalarials, to be protective. Vasculitis, overt or subclinical, has been suggested to be one cause of CVD in RA and in a recent report RA per se actually was shown to predict IHD independently. A population based study showing that the number of swollen joints could predict death from CVD further implicated a harmful impact of the inflammatory activity on the vascular system. The etiopathogenetic basis for this harmful effect still has to be elucidated.

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