In recent years, numerous studies have explored the cardiovascular involvement, risk, management, and treatment in psoriatic arthritis (PsA). This increased interest arises from the recognition that, while joint and skin manifestations are the primary features of PsA, the disease is also associated with a significantly greater burden of cardiovascular diseases (CVDs).^1,2 The heightened CVD risk in PsA patients reflects their elevated cardiovascular risk, as compared with the general population. Although it is partly linked to a higher prevalence of traditional cardiovascular risk factors, such as hypertension, dyslipidemia, diabetes, and obesity, additional contributors include disease‑specific clinical and laboratory markers, such as elevated erythrocyte sedimentation rate, C‑reactive protein levels, disease activity, and disability indices.^3,4 The aim of this editorial is to highlight a study published in this issue of Polish Archives of Internal Medicine by Nowakowski et al,⁵ which explores the impact of clinical characteristics in PsA patients, including disease phenotypes of polyarthritis, oligoarthritis, and axial PsA, as well as the influence of current treatments, such as nonsteroidal anti‑inflammatory drugs (NSAIDs), on cardiovascular risk and related conditions. The authors emphasized that PsA is a chronic inflammatory disease, with inflammation closely linked to the increased prevalence of CVD in PsA patients, as compared with the general population. The study suggests that systemic inflammation significantly contributes to the elevated cardiovascular risk observed in PsA, in addition to traditional risk factors, such as arterial hypertension (affecting 25.09% of the study patients) and obesity (affecting 23.97% of the study patients). These traditional factors (hyperlipidemia, hypertension, and diabetes mellitus), further amplify the relative risk of CVD in PsA patients. The findings of the study indicate that the cardiovascular risk in PsA is also influenced by medications used to manage the disease activity, and by specific clinical joint phenotypes. The oligoarthritis phenotype was associated with hypertension, a predictor of cardiovascular comorbidity, and was linked to frequent and prolonged use of NSAIDs. Additionally, the patients in this cohort who were diagnosed with any cardiovascular condition, as well as those with hypertension, were more frequently treated with glucocorticoids (GCs), either currently or in the past. A recent study including patients with rheumatoid arthritis and PsA, suggested that systemic inflammation and GC use independently increase the risk of major adverse cardiovascular events.⁶ Based on this evidence, an optimal cardiovascular risk assessment and joint phenotype stratification should be fundamental in the clinical management of PsA. Assessing cardiovascular risk and identifying the clinical joint phenotype should therefore be key strategies for properly diagnosing and treating PsA patients. Cardiovascular risk estimation is typically made using conventional algorithms and imaging techniques. Traditional algorithms, including Framingham and Systemic Coronary Risk Estimation scales, often fall short to accurately evaluate cardiovascular risk in many patients with PsA.^7,8 This limitation leads to inadequate risk stratification and poses challenges for effective clinical management, particularly for individuals classified into a low or intermediate risk group. The optimal algorithm for assessing cardiovascular risk in PsA patients in clinical practice remains uncertain, especially given the inherent limitations of the existing tools. The findings presented by Nowakowski et al⁵ are corroborated by original research conducted by various groups.^9-11 Moreover, the discussed work indicates that treatment with NSAIDs and GCs impacts cardiovascular risk and the associated comorbidities. The strengths of this study include the novel insights it provides into identifying cardiovascular risk in PsA patients,⁸ as well as its practical value in aiding clinicians to identify risk factors, joint subsets, and medications contributing to the increased cardiovascular risk. However, the work also has limitations, which include not addressing the role of comorbidities such as depressive disorders that are highly prevalent in the PsA population and significantly affect CVD outcomes.^12,13 In conclusion, the study showed that patients with hypertension frequently present with oligoarthritis, and the use of GCs emerges as a significant predictor of cardiovascular comorbidities. The association between NSAIDs, GCs, and cardiovascular complications highlights the need to avoid these treatments, particularly in patients with pre‑existing traditional risk factors. This aspect was emphasized in the 2023 update of the European Alliance of Associations for Rheumatology (EULAR) recommendations for PsA management,¹⁴ which introduced notable changes concerning the use of GCs and NSAIDs due to their potential adverse effects on cardiometabolic health and cardiovascular risk. The taskforce specifically recommended restricting NSAID use to a maximum of 4 weeks and strongly discouraged the use of systemic GCs. These changes highlight the growing focus on cardiovascular protection in PsA patients, positioning it as a central consideration in clinical decision‑making, on par with other key manifestations of the disease. Additionally, the findings of Nowakowski et al⁵ emphasize that hyperlipidemia remains an underdiagnosed condition in PsA patients in real‑world settings, warranting greater attention from health care providers. This gap in clinical management is likely influenced by multiple factors, such as limited awareness among physicians and patients, inadequate patient education, and clinical workload pressures. Ultimately, persistent inflammation, combined with treatments such as NSAIDs and GCs, increase the risk of cardiovascular events in PsA patients. The 2010 EULAR recommendations for cardiovascular management in inflammatory arthritis highlight the critical importance of controlling the disease activity to mitigate cardiovascular risks.¹⁵ This recommendation reflects the established link between inflammation and the elevated cardiovascular risk observed in PsA. Furthermore, it is closely related to other recommendations, such as reducing GC use to the lowest effective dose (and tapering when feasible) and prescribing NSAIDs with heightened caution, particularly in patients with existing cardiovascular risk factors or confirmed CVD. Nowakowski et al⁵ underscored the importance of clinicians prioritizing the identification of this comorbidity and thoroughly assessing cardiovascular risk factors to prevent mismanagement based on joint‑specific clinical subsets. Notably, the existing tools and scoring systems often fail to accurately reflect the elevated cardiovascular risk in PsA patients during routine care. Therefore, the availability of reliable clinical markers could significantly enhance clinical practice. Further exploration of cardiovascular impact in this population is essential for identifying specific clinical subsets and tailoring treatment approaches.