Joint swelling as a predictor of death from cardiovascular disease in a population study of Pima Indians

Objective. Markers of inflammation have recently been shown to be predictiv e of cardiovascular disease (CVD). Furthermore, the excess mortality in rhe umatoid arthritis (RA), a disease characterized by chronic polyarthritis, i s chiefly due to death from CVD. With this background, we studied the effec t of inflammation, as reflected by the number of joints with soft tissue sw elling, and rheumatoid factor (RF) seropositivity on CVD-related mortality. Methods. Mortality rates and rate ratios for all-cause and CVD-related deat hs were computed in a longitudinal, population-based cohort of Pima Indians in Arizona from 1965 through 1994. Repeated health examinations were perfo rmed, involving systematic assessment of the features of RA, cardiovascular risk factors, serum titers of RF, as well as mortality. The cohort compris ed 4,120 subjects (1,861 men, 2,259 women) who were examined an average of 3.5 times during a mean followup of 14 years. Results. During the followup period, 182 CVD-related deaths ocurred. The ag e- and sex-adjusted CVD-related mortality rates increased significantly wit h the presence of a higher number of joints with soft tissue swelling (P-tr end = 0.04), and were 2.07 (95% confidence interval [95% CI] 1.30-3.31) tim es as high in those subjects who had 2 or more swollen joints as in those w ho had none. There were no significant additional effects on CVD-related mo rtality when seropositivity for RF or a previous diagnosis of RA were consi dered. In age- and sex-adjusted proportional hazards analyses, which were c ontrolled for possible confounders, the effect of swollen joints remained s ignificant (mortality rate ratio 1.33, 95% CI 1.04-1.71 per category increa se [no swollen joints, 1 swollen joint, at least 2 swollen joints]). Conclusion. Joint swelling is a significant risk factor for CVD-related dea th, independent of other known risk factors including a diagnosis of RA. Th is finding supports the hypothesis that inflammatory mechanisms are importa nt for the development of CVD.