Dual Burdens of RA, MASH Raise CVD Risk: Rayan Salih, MD

Research presented at the recent ASPC 2025 Congress on CVD Prevention shows that among patients who have both rheumatoid arthritis and metabolic dysfunction–associated steatohepatitis (MASH), there are significantly higher rates of non–ST-segment elevation myocardial infarction (NSTEMI), STEMI, worsening heart failure, arrhythmias, and stroke. Rayan Salih, MD, Northeast Georgia Health System, who presented the poster, “Beyond the Liver and Joints: The Synergistic Effect of Rheumatoid Arthritis and Metabolic Dysfunction-Associated Steatohepatitis on Cardiovascular Outcomes: A Propensity Matched Analysis,” explains that inflammation may be the underlying reason for the higher rates of these cardiovascular (CV) conditions. As a result, these high-risk patients need to be treated aggressively and early, she says.

This transcript has been lightly edited for clarity; captions were auto-generated.

Transcript

What CV outcomes were most influenced by the synergistic effect of rheumatoid arthritis and MASH?

This study looked at patients with MASH, also known as MASH cirrhosis previously, and patients who had rheumatoid arthritis. We had these 2 groups compared to patients who only had MASH cirrhosis. We wanted to see if the presence of both of them increases the risk for cardiovascular events. We did the propensity matching, where we basically tried to match the 2 groups to several factors to make the 2 cohorts similar and eliminate confounders. We did that, and we ran the analysis, and we found that the group with both diseases really have significantly higher cardiovascular events, including STEMI, NSTEMI, heart failure exacerbation—all of these are really, really high—even arrhythmias as well, and strokes.

Given the propensity-matched analysis, what key confounding variables may have accounted for the synergistic effect?

We looked at the demographics between the 2 groups. We matched for sex, we matched for age, we matched for race and insurance status to match the socioeconomic status. We also matched for medications, the disease-modifying medications, and also the biological agents, as well as GLP-1 [glucagon-like peptide 1] and prednisone use. These were the 4 medications that we used. We also matched for the common comorbidities between the 2 groups and the common comorbidities that precipitate cardiovascular events, so we can get as clean data as possible. One of the limitations, I think, was the severity of the disease that we can tell because we mainly use ICD-10 [International Classification of Diseases, Tenth Revision] as the coding system for coding now.

What are the implications of these findings for risk stratification and holistic management of CVD in patients with both conditions?

It's an observational study. I wish we could find causality doing these types of studies, but unfortunately, it's just for observation, and we really need to think of that and try to come up with new prospective studies. What I personally think, why both of them are causing all of this? I think they share the common inflammatory condition situation. I think both of the conditions increase the inflammation, the endothelial remodeling, and all of that precipitates the cardiovascular disease. I think we should stratify these groups as really high risk and start really optimizing the comorbidities and all other risk factors, and maybe aggressively start treating these conditions by starting early disease-modifying agents and biological agents, as well as controlling the metabolic aspect by exercising more and eating healthier, so it's all a holistic approach for this situation.