Cardiovascular Risk in Sjögren's Disease: Unraveling the Connection

Primary Sjögren's syndrome confers a reproducible, clinically meaningful increase in cardiovascular events and mortality that has been underrecognized.

That elevation shifts how clinicians should approach routine risk assessment and prevention for affected patients; the following summarizes the epidemiology, putative mechanisms, and practical mitigation strategies.

Multiple population-based cohorts and longitudinal clinical series document a consistent rise in incident atherosclerotic events and cardiovascular mortality among people with primary Sjögren's compared with matched controls; these signals persist after adjustment for some traditional risk factors. The excess risk appears across registry-based and clinic-based cohorts, strengthening confidence in the finding and supporting its relevance to everyday practice.

Systemic inflammation, endothelial injury, and immune-mediated vascular damage are central mechanistic themes that plausibly accelerate atherogenesis in primary Sjögren's. Circulating proinflammatory cytokines and chronic B-cell activation can sustain vascular inflammation; autoantibodies may directly impair vascular function; many patients show endothelial activation, reduced vasoreactivity, and subclinical vascular stiffness consistent with endothelial dysfunction; and an adverse cardiometabolic profile in some individuals compounds risk. These intersecting pathways offer a biologic rationale for the observed excess of clinical cardiovascular events.

Mitigation centers on rigorous control of conventional risk factors alongside attention to systemic inflammation. First, implement routine screening and guideline-directed management of blood pressure, lipids, glycemia, and smoking cessation with the same urgency applied to other high-risk groups. Second, emphasize lifestyle measures—weight management, regular aerobic exercise, and cardioprotective dietary patterns—to reduce modifiable risk. Third, optimize immunomodulatory therapy when clinically indicated to lower inflammatory burden, recognizing that randomized cardiovascular outcome data for Sjögren's-specific agents are limited.

Integrating these steps into care pathways can help reduce overall cardiovascular risk in this population.

Looking ahead, targeted research must test whether inflammation-directed therapies reduce hard cardiovascular outcomes while clinicians adopt routine cardiovascular risk management for patients with primary Sjögren's.

Key Takeaways:

• Primary Sjögren's carries a reproducible, clinically significant increase in cardiovascular events and mortality that has been underappreciated.
• Patients with primary Sjögren's—including those without overt systemic disease—face higher cardiovascular risk and warrant closer surveillance.
• Routine cardiovascular risk assessment and aggressive control of traditional risk factors should be integrated into standard Sjögren's care pathways.