Psoriatic arthritis (PsA) is an independent risk factor for cardiovascular (CV) disease, according to a meta-analysis of 11 observational studies.
About 33,000 PsA patients were included in studies that assessed the overall risk of CV diseases. Analysis of five cohort studies found a 55% increased risk of incident CV events compared with the general population (pooled RR 1.55, 95% CI 1.22-1.96), reported Lihi Eder, MD, PhD, of the University of Toronto, and colleagues.
In limiting the analysis to the three studies that fully adjusted for demographics and CV risk factors, the risk of developing CV events remained statistically significant (pooled OR 1.84, 95% CI 1.12-3.02, P=0.02), the researchers reported online in Arthritis Care & Research.
In addition, the results were similar when excluding the three studies that were not published as full-text articles (pooled OR 1.49, 95% CI 1.19-1.87). Substantial heterogeneity was observed among studies (I2= 83.3%, P<0.001).
Current risk algorithms, such as the Framingham risk score, underestimate actual CV risk in patients with chronic inflammatory conditions. These algorithms do not consider the independent risk entailed with the chronic inflammatory process.
Among patients with psoriasis, the risk of CV disease has been shown to be about 40% higher than in the general population. However, few studies have evaluated this risk among patients with PsA, and the available evidence is conflicting. No recommendations on risk modification have been formulated, "and these patients are managed according to national guidelines for the general population," which "could potentially lead to underestimation of the actual cardiovascular risk," Eder and colleagues wrote.
They therefore conducted a systematic literature review to identify studies of patients with PsA and their risks for CV diseases such as coronary artery disease and myocardial infarction (MI), cerebrovascular disease, and heat failure.
In the six studies in which MI was assessed, including approximately 26,000 PsA patients, a 68% increased risk of MI was found in patients with PsA (pooled OR 1.68, 95% CI 1.31-2.15). The level of heterogeneity in these studies was high (I2=90%, P<0.001).
Analysis restricted to the four longitudinal cohort studies found a 57% increased risk of incident MI in patients with PsA compared with the general population (pooled RR 1.57, 95% CI 1.19-2.06).
The overall magnitude of the risk for incident MI found in this systematic review was similar to that reported in patients with severe psoriasis (pooled RR, 1.7), the authors noted, but higher than the reported risk for mild psoriasis (pooled RR, 1.29).
Eight studies assessed the risk of cerebrovascular events among about 32,000 PsA patients, and these studies had a lower degree of heterogeneity than that observed for the other outcomes (I2= 58.9%, P=0.01). There was a 22% increased risk of cerebrovascular events in patients with PsA (pooled OR 1.22, 95% CI 1.05-1.41).
The pooled OR was higher in cohort studies than in cross-sectional studies (OR 1.38 versus 1.11, P=0.02). The risk of incident cerebrovascular events was increased by 38% in patients with PsA compared with the general population in an analysis that was restricted to the three cohort studies (pooled RR 1.38, 95% CI 1.25-1.52).
Four studies assessed the risk of heart failure in PsA patients, and found a 31% increased risk of heart failure in patients with PsA compared with the general population (OR 1.31, 95% CI 1.11-1.55).
"It is now widely accepted that atherosclerosis, the underlying process resulting in cardiovascular events, is strongly linked with chronic low-grade vascular inflammation that results from an interaction between immune mechanisms and metabolic abnormalities within the vessel wall," they wrote. Studies in patients with PsA have found abnormalities in several stages of atherogenesis compared with nonpsoriatic controls.
Several limitations were noted. Inclusion of both cross-sectional studies and cohort studies contributed to a heterogeneity in the pooled estimates to some extent, although risk estimates were reported separately for each, except for heart failure. Additional sources of heterogeneity included differences in clinical settings, case definitions of PsA, definitions of outcomes, methods of events ascertainment, and the degree of adjustment for potential confounders. Furthermore, only one study made an attempt to estimate CV risk by PsA severity, and only two studies reported the baseline PsA disease activity measures.
The authors have received support from Janssen Canada, the Krembil Foundation, and the Canadian Institutes of Health Research.
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