TOPLINE:

Demographic, systemic sclerosis (SSc)-specific, and cardiac factors raised the risk for left ventricular systolic dysfunction (LVSD) in a study of patients with SSc.

METHODOLOGY:

• Researchers used the Johns Hopkins Scleroderma Center Research Registry to identify risk factors for LVSD and predictors of cardiac recovery in patients with SSc.
• A total of 13,209 echocardiograms were analyzed based on 2303 patients with SSc (mean age at disease onset, 42.8 years; 82.6% women), each with at least two echocardiograms.
• Incident LVSD was defined as a decline in LV ejection fraction (EF) from ≥ 50% to < 50%, and severe LVSD was defined as a decline from > 35% to ≤ 35%.
• Data on demographics, features of SSc, organ-specific severity scores, autoantibody profiles, pulmonary function, echocardiography, and comorbidities were collected at baseline and at follow-up visits.

TAKEAWAY:

• During follow-up, 11% of patients with SSc developed incident LVSD (EF < 50%) and 5% developed severe LVSD (EF ≤ 35%); cardiac recovery occurred in 66% of incident LVSD cases and 82% of severe LVSD cases.
• Male sex, higher modified Rodnan skin score, pulmonary hypertension, moderate-to-severe kidney disease, and atrial fibrillation were tied to higher risks for both incident and severe LVSD (P < .05 for all).
• Myopathy and anti-Ku antibodies were exclusively associated with an increased risk for severe LVSD (P = .002 and P = .015, respectively).
• Among patients who developed LVSD, tendon friction rubs and diabetes were linked to a lower likelihood of cardiac recovery (EF ≥ 50%); anti-POLR3 antibodies were linked to a higher likelihood.

IN PRACTICE:

“With early identification, patients at risk for LVSD may be candidates for close monitoring and treatment of arrhythmias or inflammatory myocarditis. Additionally, our study found the important prognostic value of anti-POLR3 regarding the likelihood of cardiac recovery once LVSD has developed,” the authors wrote. 

SOURCE:

This study was led by Ji Soo Kim, PhD, and Rachel S. Wallwork, MD, Johns Hopkins University School of Medicine, Baltimore. It was published online on October 13, 2025, in Arthritis & Rheumatology.

LIMITATIONS:

The study did not systematically collect cardiac comorbidity data throughout the entire study period. It also lacked information regarding whether patients exhibited clinical signs and symptoms of heart failure, or whether LVSD was treated with goal-directed medical therapy. Additionally, the study could not evaluate the influence of overlapping conditions such as idiopathic inflammatory myopathy, autoimmune thyroid disease, or HIV on LVSD. 

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases; National Heart, Lung and Blood Institute; Donald B. and Dorothy L. Stabler Foundation; and other sources. Some authors reported receiving research support, grants, consulting fees, or honoraria from and having other ties with various pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.