# Getting to the heart of cardiovascular complications associated with inflammatory arthritis

## TL;DR

This paper explores how inflammatory arthritis, like rheumatoid arthritis, increases cardiovascular disease risk and highlights new therapeutic approaches.

## Contribution

The paper introduces a mechanistic basis for exploring FPR2-targeted therapies to address cardiovascular complications in inflammatory arthritis.

## Key findings

- Inflammatory arthritis is linked to increased cardiovascular disease risk and poor patient outcomes.
- Current CVD therapies may not be fully effective for patients with arthritis-related heart complications.
- FPR2-targeted therapies offer a potential new treatment avenue for these patients.

## Abstract

Inflammatory arthritis encompasses a group of autoimmune diseases, including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) (Hammaker and Firestein, 2018). Although the exact etiology remains elusive, these conditions are thought to result from an overactive immune response to an unknown antigen, leading to joint pain, swelling, and deformity. Among these, RA is the most prevalent, affecting approximately 1% of the world’s population (Di Matteo et al, 2023). A hallmark of RA is its association with elevated rates of cardiovascular disease (CVD), which significantly increases morbidity and mortality and shortens patients’ life expectancy and quality of life (Semb et al, 2020). Although the prognosis for RA has improved markedly over the past two decades due to advanced treatment options, the lack of targeted therapies for CVD complications in RA patients remains a critical clinical challenge. Finally, guideline-based therapies for CVD are based on the etiology of the disease, which is hypertension or coronary artery disease. How well these therapies work in patients with cardiac complications of RA is incompletely understood.

Hong Shi and Brian H. Annex discuss the study by Margraf et al, in this issue of EMBO Mol Med, that investigates the interplay between inflammatory arthritis and cardiovascular disease, and provides a mechanistic basis for exploring FPR2-targeted therapies.