The Cardiovascular Dimension of Psoriatic Arthritis

Psoriatic arthritis (PsA) has traditionally been described as an inflammatory joint disease associated with psoriasis. However, increasing evidence shows that its impact extends beyond the musculoskeletal system. Cardiovascular disease is now recognized as one of the most significant comorbidities in PsA, contributing meaningfully to long-term morbidity and mortality.

A recent narrative review in Autoimmunity Reviews synthesizes evidence on the epidemiology, biological mechanisms, and clinical management of cardiovascular risk in PsA, providing a closer look at the interplay between systemic inflammation, metabolic comorbidities, and treatment exposures. Here’s a quick summary of what it found.

Elevated Cardiovascular Risk in PsA
Patients with PsA experience higher rates of cardiovascular disease than the general population. Over half of patients develop at least one comorbidity, and cardiovascular conditions are among the most prevalent. Meta-analytic evidence shows increased overall mortality in PsA, with cardiovascular disease representing a major contributor. One analysis reported a relative risk of death of 1.74 compared with the general population, while cardiovascular mortality alone showed a relative risk of 1.84.

Cardiovascular events occur more frequently as well. Across observational studies, the incidence of cardiovascular disease in PsA is approximately 43% higher than in the general population, with overall cardiovascular risk increased by roughly 55%. Risks of myocardial infarction, cerebrovascular disease, and heart failure are all elevated.

Subclinical vascular abnormalities are also common. Studies summarized in the review report increased carotid plaque burden, greater carotid intima-media thickness, arterial stiffness, and impaired endothelial function in PsA populations. However, these abnormalities are observed even among patients without traditional cardiovascular risk factors, indicating that inflammatory disease activity contributes directly to vascular injury.

Inflammatory and Metabolic Drivers
Chronic systemic inflammation is a central link between PsA and cardiovascular disease. Cytokines involved in psoriatic inflammation, including TNF-α, IL-1, and IL-6, promote endothelial dysfunction, oxidative stress, and atherosclerotic plaque formation.

Inflammation also alters lipid metabolism. Research has identified reduced high-density lipoprotein cholesterol together with elevated apolipoprotein B and oxidized low-density lipoprotein in PsA populations, producing a pro-atherogenic lipid profile that may correlate with disease activity.

Metabolic syndrome further amplifies cardiovascular risk. Between 24-58% of patients with PsA meet criteria for metabolic syndrome, compared with roughly 15-24% of the general population. Hypertension, dyslipidemia, and obesity occur more frequently in PsA cohorts, reflecting the combined effects of inflammatory and metabolic dysregulation.

Depression also contributes to cardiovascular risk in psoriatic disease. Prevalence estimates vary widely, but evidence from broader cardiovascular research associates depression with higher risks of myocardial infarction, stroke, and cardiovascular mortality. Behavioral factors, neuroendocrine activation, and inflammatory pathways are believed to contribute to this relationship.

Treatment Effects and Clinical Implications
PsA therapies can influence cardiovascular risk in different ways. Nonsteroidal anti-inflammatory drugs and systemic glucocorticoids reduce inflammation but may worsen metabolic parameters or increase cardiovascular risk when used long term. Current European Alliance of Associations for Rheumatology guidance recommends limiting prolonged use of these agents because of potential cardiometabolic effects.

Disease-modifying antirheumatic drugs may provide more favorable cardiovascular profiles. Methotrexate reduces systemic inflammation and has been associated with improvements in endothelial function. Other therapies, such as TNF inhibitors, have been linked with slower progression of atherosclerosis and reduced rates of major cardiovascular events in observational studies. Evidence for IL-17 and IL-23 inhibitors remains mixed, while the phosphodiesterase-4 inhibitor apremilast has shown potential metabolic benefits in some patients. JAK inhibitors require caution; regulatory authorities have issued cardiovascular safety warnings based on findings in other inflammatory diseases.

Risk Assessment and Management
Given the substantial cardiovascular burden associated with PsA, regular cardiovascular risk assessment is recommended. Clinicians typically rely on established tools such as SCORE2, QRISK3, or PREVENT equations, although these instruments may underestimate risk in inflammatory arthritis populations. Imaging approaches, including carotid ultrasound, may help identify subclinical atherosclerosis in selected patients.

Management requires simultaneous control of inflammatory disease activity and traditional cardiovascular risk factors. Lifestyle interventions, along with pharmacologic treatment of hypertension, dyslipidemia, and diabetes, remain essential components of prevention. Multidisciplinary collaboration between rheumatologists, cardiologists, and other specialists can help address the complex drivers of cardiovascular risk in this population.

Recognition of PsA as a systemic inflammatory disease with cardiovascular consequences is reshaping clinical priorities. Integrating cardiovascular risk assessment into routine rheumatology care may improve long-term outcomes for patients living with psoriatic arthritis.

Reference:
Atzeni F, Rodríguez-Carrio J, Alciati A, Tropea A, Marchesoni A. Cardiovascular risk in psoriatic arthritis: How can we manage it? Autoimmun Rev. 2025;24:103889. doi:10.1016/j.autrev.2025.103889