Over the past few years, it has been recognized that the risk of cardiovascular disease (CVD) is increased in patients with psoriatic arthritis (PsA).^1-3 Cardiovascular comorbidities in PsA augment the burden of the disease, affecting the quality of life and life expectancy.^4,5 Indeed, a systematic literature review and meta‑analysis showed increased CVD‑related mortality and morbidity in PsA,² attributed to cardiovascular events, such as myocardial infarction and heart failure. Interplay of traditional cardiovascular risk factors and disease activity–associated factors lead to CVD in PsA patients.⁶ Thus, patients with PsA more frequently have classic cardiovascular risk factors, such as hypertension, dyslipidemia, obesity, or metabolic syndrome than healthy individuals,^2,7 and atherosclerosis is more prevalent in PsA patients than in the general population.⁶ A meta‑analysis of 39 studies, including more than 150 000 PsA patients, showed that 34% of the individuals had hypertension, 29% had metabolic syndrome, 27% obesity, and 24% hyperlipidemia.⁴ Obesity is associated with a higher risk for CVD morbidity and mortality,⁸ as it affects proinflammatory cytokine production, such as tumor necrosis factor (TNF) and interleukin‑6, as well as secretion of adipokines (leptin, adiponectin) leading to a low level of chronic systemic inflammation.⁹ Obesity in PsA patients may cause repetitive microtrauma on the joints due to increased weight burden, leading to enthesal and synovial inflammation.¹⁰ It has been linked to a higher disease activity, and is a negative predictor for optimal response to TNF inhibitors.¹¹

The association between PsA and metabolic syndrome may be attributed to shared inflammatory pathways. Patients with PsA present more frequently insulin resistance and diabetes mellitus (DM) than the general population, while increased disease activity may lead to a higher risk of developing DM.

The risk of CVD in PsA has been further documented in a large population‑based longitudinal study involving 8706 patients with PsA, 41 752 patients with rheumatoid arthritis, 138 424 patients with psoriasis, and 81 573 controls. After adjustment for classic risk factors, the risk of major cardiovascular events was higher in the PsA patients not receiving disease‑modifying antirheumatic drugs (DMARDs) than in the controls (hazard ratio, 1.24; 95% CI, 1.03–1.49).¹² Effective treatment of PsA has been associated with a beneficial outcome on CVD risk,² leading to reduced indices of subclinical atherosclerosis, with substantial evidence coming from studies where methotrexate and TNF inhibitors were used.

In this issue of Polish Archives of Internal Medicine, Nowakowski et al¹³ report the results of a cross‑sectional, real‑life study in PsA patients concerning the relationships between cardiovascular comorbidities, clinical phenotype, and treatment. The prevalence of cardiovascular comorbidities in PsA patients treated with steroids and nonsteroidal anti‑inflammatory drugs (NSAIDs) was increased. In addition, oligoarthritis and current use of steroids predicted cardiovascular comorbidities. The study showed that hypertension, dyslipidemia, and obesity were the most prevalent comorbidities. Furthermore, PsA patients with any CVD had a longer disease duration, were older, and had higher body mass index (BMI) than those without cardiovascular comorbidities. Increased level of C‑reactive protein and indices of the disease activity were also found in PsA patients with CVD, indicating that systemic inflammation combined with classic risk factors and metabolic alterations play a pivotal role in CVD pathogenesis. The authors showed that oligoarthritis was associated with cardiovascular comorbidities. In this subgroup of PsA patients, the use of DMARDs is usually limited or delayed, prolonging the inflammatory burden and augmenting the cardiovascular risk.

Furthermore, patients with any CVD were more frequently treated with glucocorticoids, and their current use was a predictive factor for cardiovascular comorbidities. The recent guidelines for PsA treatment limit the use of steroids only to local injections.¹⁴ This recommendation was derived from the scarce data on prescription of systemic glucocorticoids in PsA as well as their adverse effects especially in patients with cardiovascular risk factors. Nowakowski et al,¹³ however, present real‑life data, where management decisions vary among practitioners. In addition, for patients with the longstanding disease it is difficult to discontinue steroids, as they are cortico‑dependent or have limited access to novel therapies. On the other hand, they may represent a group of PsA patients with the more active disease.

NSAIDs offer symptomatic relief to PsA patients with peripheral arthritis or axial disease and their short‑term use is recommended.¹⁴ However, the long‑term safety issues of NSAIDs use must be considered. Nowakowski et al¹³ showed that a vast majority of patients on NSAIDs had heart failure. It is well known that patients with and without CVD, treated with NSAIDs have an increased risk of CVD, including arterial hypertension, myocardial infarction, and heart failure. The absolute risk varies depending on the baseline cardiovascular risk, and the choice and dose of NSAID.¹⁵ The mechanism underlying the increased cardiovascular risk is associated with cyclooxygenase 2 inhibition and the subsequent reduction in prostaglandin I2 by the vascular endothelium, which leads to little or no inhibition of potentially prothrombotic platelet thromboxane A2 production. To minimize the risk for adverse cardiovascular events in patients treated with NSAIDs, the lowest effective dose for the shortest duration should be used.

Cardiovascular comorbidities are frequent in PsA and should be identified and controlled early, because they can affect treatment effectiveness and the outcome of the disease. All patients should be screened for classic cardiovascular risk factors (eg, lipid levels, blood pressure, and smoking), metabolic dysfunction, and DM. Modification of these risk factors should be a part of PsA management. Thus, control of blood pressure and dyslipidemia, cessation of smoking, as well as weight loss in patients with elevated BMI are recommended. Furthermore, the target of PsA treatment is remission or, alternatively, low disease activity. Early and aggressive management can improve the outcome of the disease and modify the cardiovascular risk.