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Updated: May 14, 2026

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Published on: April 19, 2019
A Flexible Wearable Electronics System for Electrocardiographic Assessment of Colchicine Therapy for Post-MI
Weijia Huang1, Xiangfeng Gong2, Maoshuai Yang1
1College of Biomedical Engineering, Sichuan University, Chengdu 610065, China.
Abstract:
Objective: Myocardial infarction (MI) triggers inflammation and fibrosis that drive the progressive impairment of cardiac function. Yet most pharmacological studies still depend on single-time-point histological or imaging endpoints and lack longitudinal, non-invasive assessments of treatment response. Electrocardiography (ECG) detects conduction and repolarization abnormalities tightly associated with myocardial injury and structural remodeling. However, ECG monitoring in mice is limited by rigid or invasive hardware, which restricts its use for longitudinal assessment of cardiac structure and function. Approach: Here, we propose an ECG-based non-invasive post-MI cardiac remodeling assessment approach and develop a flexible electrocardiographic monitoring microsystem (FECMS). Using the anti-remodeling drug (colchicine) therapy in an MI mouse model (Sham n = 4, MI n = 7 survivors, Col n = 7 survivors) for validation, we longitudinally track drug-induced changes in ECG parameters and systematically evaluate their concordance with functional, structural, and molecular indicators of cardiac injury and remodeling. Results: Colchicine treatment induced progressive shortening of the QRS and QT intervals and gradual stabilization of the PR interval. These interval changes were accompanied by increased EF and FS, decreased LVESV, reduced myocardial fibrosis and inflammatory infiltration, and lower plasma troponin I levels at the endpoint. Correlation analyses revealed strong relationships between drug-induced changes in ECG parameters and functional recovery and inhibited structural remodeling. Significance: The FECMS provides a new, non-invasive tool for longitudinal cardiovascular drug evaluation. This approach has the potential to complement or reduce reliance on terminal histological endpoints and to facilitate the optimization of dosing strategies in preclinical cardiovascular pharmacology.
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