Loading
Life sciences · Review
Journal of Clinical Medicine · September 19, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Review.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Background/Objectives: Psoriatic arthritis (PsA) is associated with excess cardiovascular (CV) morbidity, but the supporting literature spans heterogeneous observational, imaging, prediction, therapeutic, and guideline sources. This focused expert narrative review examines clinically relevant evidence for CV burden, risk markers, risk prediction, vascular imaging, treatment safety, and prevention in PsA. Methods: PubMed/MEDLINE was searched through 12 August 2026 using domain-based search blocks, supplemented by EULAR, GRAPPA, and European Society of Cardiology guidance and citation tracking. The final synthesis intentionally prioritized direct human PsA evidence; mixed psoriatic-disease or other immune-mediated evidence was used only when required for clinical context and was labeled as indirect. Embase, Scopus, and Web of Science were not searched; no formal risk-of-bias instrument or certainty-of-evidence grading framework was applied. Results: Conventional CV risk factors remain central. Direct PsA cohorts support associations between disease activity, metabolic abnormalities, and subsequent events, but do not establish incremental predictive value beyond validated risk models. Imaging studies demonstrate frequent subclinical atherosclerosis, yet plaque detection is distinct from event-prediction validation and does not establish benefit from universal screening. Therapeutic evidence is dominated by observational comparisons and low-event randomized-trial syntheses, precluding a causal cardioprotective ranking of drug classes. Conclusions: Current care should combine guideline-based CV prevention with treat-to-target PsA management for rheumatologic outcomes. PsA-specific risk modifiers, imaging-guided prevention, and treatment strategies intended to reduce hard CV outcomes require prospective validation. This article is a selective expert synthesis, not a systematic review, prediction model, or clinical pathway.