Matthew Banks

Excess recurrent cardiac events in rheumatoid arthritis patients with acute coronary syndrome

Background: Cardiovascular mortality is increased in rheumatoid arthritis. Possible reasons include an increased incidence of ischaemic heart disease or worse outcome after acute coronary syndrome (ACS). Objectives: To assess the outcome of ACS in rheumatoid arthritis compared with case matched controls in the context of underlying cardiac risk factors, clinical presentation, and subsequent management. Methods: 40 patients with rheumatoid arthritis and ACS identified from coronary care admission registers between 1990 and 2000 were case matched as closely as possible for age, sex, classical cardiovascular risk factors, type and severity of ACS, and admission date (±3 months) with 40 controls. A standardised proforma was used for detailed case note review. Results: Age, sex, other cardiovascular risk factors, and type and severity of presenting ACS were not significantly different between cases and controls. Recurrent cardiac events were commoner in rheumatoid arthritis (23/40, 57.5%) than controls (12/40, 30%) (p = 0.013); there were 16/40 deaths in rheumatoid arthritis (40%) v 6/40 (15%) in controls (p = 0.012). Recurrent events occurred earlier in rheumatoid arthritis (log rank survival, p = 0.05). Presentation with chest pain occurred in all controls compared with 33/40 rheumatoid patients (82%) (p = 0.006); collapse occurred in one control (2.5%) v 7/40 rheumatoid patients (17.5%) (p = 0.025). Treatment during the ACS was not significantly different in the two groups. Conclusions: Recurrent ischaemic events and death occur more often after ACS in rheumatoid arthritis. Atypical presentation is commoner in rheumatoid arthritis. There is an urgent need to develop identification and intervention strategies for ACS specific to this high risk group.

Risk assessment for coronary heart disease in rheumatoid arthritis and osteoarthritis

Background: The risk of coronary heart disease (CHD) is increased in rheumatoid arthritis (RA). The reasons for this remain unknown, but traditional risk factors for CHD identified in the general population may be important contributors. Objective: To assess comparatively the prevalence of traditional CHD risk factors and the absolute 10‐year CHD risk in patients with RA or osteoarthritis (OA) without known cardiovascular co‐morbidity. Methods: Consecutive Caucasian hospital outpatients with RA (n=150) or OA (n=100) aged 40–75 years were assessed for known cardiovascular co‐morbidity, age, sex, smoking status, presence of diabetes mellitus (DM), height, weight, systolic blood pressure (BP), total cholesterol (TC) and HDL cholesterol. Absolute 10‐year CHD risk for each individual was calculated using the Joint British Societies CHD risk calculator. Results: Prevalence and distribution of known cardiovascular co‐morbid conditions were similar in RA (56/150, 37%) and OA (34/100, 34%). The resulting subgroups of patients without known co‐morbidity (RA: n=94; OA: n=66) were not significantly different for age, sex, DM, smoking, systolic BP or TC: HDL cholesterol ratio. There was no significant difference in the absolute 10‐year CHD risk between RA and OA (15.6±11.0 versus 14.8±9.3, p=0.63). However, a significant proportion of patients without known cardiovascular disease in both the RA and OA subgroups had a 10‐year CHD risk above the 15% or 30% risk levels, indicating the need for possible or definite intervention respectively. Over 80% of RA patients had at least 1 CHD risk factor that could be modified. Conclusion: Absolute 10‐year CHD risk was not different between RA and OA patients in this study. Substantial numbers of RA and OA patients have potentially modifiable CHD risk factors present. We suggest that CHD risk should be assessed and modifiable risk factors addressed in the routine rheumatology clinic setting.

THE ROLE OF ENDOTHELIAL CELL DYSFUNCTION IN THE CARDIOVASCULAR MORTALITY OF RA

Rheumatoid patients present clinically with chronic inflammatory immune arthritis but die of the same cardiovascular (CVS) disease as the normal population. Recent studies emphasize the increased frequency and earlier development of CVS involvement in RA. The mechanisms of this accelerated atherosclerosis are the subject of active research. The hypothesis that rheumatoid vasculitis is a major factor has been pursued through studies in primary systemic vasculitis. These reveal diffuse endothelial dysfunction occurring across a spectrum of vasculitis and involving more than one vascular bed. This may relate to cytokines such as TNFα that are both prominent in rheumatoid inflammation and important in the upregulation of endothelium in innate immune responses. Endothelial injury or dysfunction is widely accepted as the initial factor in atheroma. Its occurrence in vasculitis leads us to propose a model for RA where this dysfunction is the essential first step on which other factors, ranging from adverse lipid profiles to specific T-cell subsets, may build accelerated atherogenesis related to the rheumatoid inflammation.

Hypertension is not a disease of the left arm: a difficult diagnosis of hypertension in Takayasu's arteritis.

Hypertension and its cause may be missed by failure to measure blood pressure in both arms. We report a case of Takayasu’s arteritis where diagnostic confusion arose because there was a failure to detect a difference in blood pressure between the arms.