Xia Liu, Lingjie Xu, Li Zhang, Hailin Yang, Qian Xiao
Sarcopenia is independently associated with significantly elevated DCM risk in T2DM patients; the cross-sectional design precludes definitive causal inference and directionality requires prospective longitudinal confirmation. Shared mechanisms-including systemic inflammation, elevated ferritin and uric acid, and potentially common genetic regulatory pathways (hypothesized on the basis of existing literature)-may underlie the muscle-heart dysfunction axis. Routine sarcopenia screening using AWGS 2019 criteria-consistent with the updated AWGS 2025 framework-may facilitate early identification of T2DM patients at elevated DCM risk.
BACKGROUND: Sarcopenia is an emerging complication of type 2 diabetes mellitus (T2DM) characterized by progressive loss of skeletal muscle mass and function. Diabetic cardiomyopathy (DCM) is a distinct cardiac disease in T2DM patients independent of coronary artery disease and hypertension. Whether sarcopenia independently predicts DCM risk in T2DM patients, and whether shared molecular pathways including systemic inflammation and metabolic dysregulation underlie this association, remains unclear.
METHODS: This retrospective cohort study enrolled 400 T2DM patients admitted to the First Affiliated Hospital of Chongqing Medical University between February 2022 and February 2026. Sarcopenia was diagnosed using AWGS 2019 criteria as the primary framework, with concurrent evaluation against the updated AWGS 2025 criteria. DCM was diagnosed by Doppler echocardiography in T2DM patients with myocardial dysfunction after excluding other cardiac etiologies, per clinically established criteria (2024 ESC DCM position statement); this echocardiographic approach, while standard practice, does not carry the tissue-characterization precision of cardiac MRI. Multivariate logistic regression (three sequentially adjusted models), propensity score matching, and prespecified subgroup analyses were performed.
RESULTS: Sarcopenia was identified in 137/400 patients (34.3%) and DCM in 113/400 (28.3%). DCM prevalence was significantly higher in sarcopenic versus non-sarcopenic patients (44.5% vs. 19.8%, p < 0.001). After full adjustment, sarcopenia remained independently associated with DCM risk (adjusted OR = 2.70, 95% CI: 1.72-4.24, p < 0.001; AUC-ROC = 0.812). The association was consistent across all subgroups (all p-interaction > 0.05). Sarcopenic patients exhibited elevated hs-CRP, NT-proBNP, ferritin, and uric acid, with lower vitamin D levels.
CONCLUSION: Sarcopenia is independently associated with significantly elevated DCM risk in T2DM patients; the cross-sectional design precludes definitive causal inference and directionality requires prospective longitudinal confirmation. Shared mechanisms-including systemic inflammation, elevated ferritin and uric acid, and potentially common genetic regulatory pathways (hypothesized on the basis of existing literature)-may underlie the muscle-heart dysfunction axis. Routine sarcopenia screening using AWGS 2019 criteria-consistent with the updated AWGS 2025 framework-may facilitate early identification of T2DM patients at elevated DCM risk.