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Cardiovascular Risk in Axial Spondyloarthritis

sheireyes13@gmail.com
Nov 11, 2026 12:12 pm

When a patient with axial spondyloarthritis patient sits in your clinic, their joint inflammation is only half the story. To truly achieve disease control, one should ask: “Am I consistently and aggressively screening them all for cardiovascular risk?"

Prior studies have already illustrated the increased cardiovascular morbidity and mortality in axSpA attributable to systemic inflammation and traditional cardiovascular risk factors. This relationship has given rise to strategies that help mitigate this heightened risk including investigations on newer therapies that address positive effects on cardiovascular outcome apart from efficacy and safety. 

Dr. Ates and colleagues (abstract #1339) presented a cross-sectional study evaluating the association between coronary artery calcification (CAC) burden, disease activity, inflammatory markers and patient-reported outcomes in axSpA patients. Data was collected prospectively from axial spondyloarthritis registries of University Hospitals. 

Patients were classified into 2 groups based on CAC scores: group A had scores <99 and stratified as normal to mild atherosclerotic disease while group B had scores >100 and stratified as moderate to high disease. 

Out of the thirty-nine (39) patients who fulfilled the ASAS criteria for axSpA, 31 had CAC scores <99 and 8 with CAC scores >100. Baseline and clinical characteristics were similar for both groups.  

Study results show that patients with elevated CAC (group B) had significantly worse physical function (p = 0.043) and higher sleep disturbance scores (p = 0.032). No significant differences were observed for BMI, HLA-B27 status, CRP, ESR, BASDAI, PGA, cardiovascular risk factors, NSAID use, or biologic therapy between groups. According to the investigators, the higher CAC burden associated with worse physical function and greater sleep disturbance suggests that these may contribute to increased coronary artery disease risk and potentially represent disease-specific modifiable risk factors. 

Meanwhile, Dr. Madeleine Gertz and colleagues evaluated cardiovascular events burden between r-axSpA and nr-axSpA in a retrospective cohort study (abstract #2317). The r-axSpA subgroup had significantly higher smoking prevalence, lesser females and fewer White patients. They reported a total of 55 CV events, with arrhythmias being the most common followed by valvular disease (n=7), PE (n=6), aortic atherosclerosis (n=5), DVT (n=5), CVA/TIA (n=4), CHF (n=3), MI (n=2), and PAD (n=2). Patients who developed CV events were significantly older, had later onset of disease and diagnosis, higher opioid use and less likely to be female. Other factors such as race, hypertension, diabetes, lipid profle, BMI, smoking status, alcohol and drug use showed no significant differences. In the multivariable logistic models, r-axSpA was associated with 4-5 times higher odds of developing cardiovascular events compared to nr-axSpA but was not statistically significant. This may be explained by the small sample size therefore larger prospective studies are needed to further elucidate and validate the relationship between axSpA subtypes and CV outcomes. 

While it is difficult to generate robust conclusions regarding cardiovascular risk in the abstracts presented above, the results consistently highlight the burden of subclinical atherosclerosis and CV burden in axSpA. 

In the rheumatology clinic, patients present with pain and systemic inflammation. We aim for complete disease control and remission through a comprehensive management strategy—one that aggressively targets the underlying immunologic drivers while simultaneously addressing non-immune comorbidities, such as cardiovascular risk. 

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