Key result
Colchicine lowers IL-6 and improves left atrial mechanical function in rheumatic mitral valve disease.
Why the study?
Rheumatic heart disease is characterized by persistent low-grade inflammation that contributes to atrial dysfunction, but whether colchicine reduces inflammation and improves left atrial mechanical function was unknown.
Does colchicine reduce interleukin (IL)-6 at 6 months in patients with chronic moderate-to-severe rheumatic mitral valve disease?
RCT (n=90)
Double-blind
1:1
Does colchicine reduce interleukin (IL)-6 at 6 months in patients with chronic moderate-to-severe rheumatic mitral valve disease?
Colchicine significantly attenuates systemic inflammation and improves left atrial mechanical function and NYHA functional status in patients with chronic rheumatic mitral valve disease.
Answers are grounded in this paper and cite their sources.
May warrant colchicine to reduce IL-6 and improve LA function/NYHA in rheumatic mitral valve disease; extends anti-inflammatory therapy to valvular heart disease.
BACKGROUND: Rheumatic heart disease is increasingly recognized as an immunologically active condition characterized by persistent low-grade inflammation contributing to atrial dysfunction. OBJECTIVES: The authors aimed to evaluate whether colchicine reduces systemic inflammation and improves left atrial (LA) mechanical function in chronic rheumatic mitral valve disease. METHODS: In this prospective, double-blind, randomized controlled trial, 90 patients with chronic moderate-to-severe rheumatic mitral valve disease were randomized (1:1) to colchicine (0.5 mg twice daily) or placebo for 6 months in addition to standard therapy. The primary outcome was change in interleukin (IL)-6 at 6 months. Secondary outcomes included changes in other inflammatory markers, LA strain parameters, NYHA functional class, and correlations between inflammatory markers and LA mechanics. RESULTS: Colchicine significantly reduced inflammatory markers (IL-6, high-sensitivity C-reactive protein, erythrocyte sedimentation rate; all P < 0.001). IL-6 decreased from 98.0 (86.9-112.1) to 11.2 (7.3-21.5) pg/mL in the colchicine group, while increasing in placebo (P < 0.001). LA reservoir strain improved significantly (23.6% ± 2.0% vs 16.5% ± 1.6%, P < 0.001). IL-6 showed strong inverse correlation with LA reservoir strain (r = -0.65, P < 0.001). Functional status improved, with 69.2% of NYHA functional class III patients improving to class II. CONCLUSIONS: Colchicine significantly attenuates systemic inflammation and improves LA mechanical function and functional status in chronic rheumatic mitral valve disease, supporting an inflammation-driven atrial myopathy phenotype.
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Gupta et al. (2026) conducted an RCT in chronic moderate-to-severe rheumatic mitral valve disease (n=90). Colchicine vs. placebo was evaluated on change in interleukin (IL)-6 at 6 months (p=<0.001). Colchicine significantly reduced IL-6 levels (decreasing to 11.2 pg/mL vs an increase with placebo; P<0.001) and improved left atrial mechanical function in rheumatic mitral valve disease.
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