Matrix Metalloproteinases and Cardiac Remodelling in Smokers with Acute Coronary Syndrome

Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) regulate extracellular matrix remodeling and contribute to the pathogenesis of coronary artery disease (CAD). This study examined the associations between MMP-2, MMP-9, and TIMP-3 and coronary atherosclerotic burden and cardiac function among smokers and non-smokers across the CAD spectrum. A total of 180 male participants were enrolled and divided into six groups (n = 30 per group): acute coronary syndrome (ACS) smokers, ACS non-smokers, chronic coronary syndrome (CCS) smokers, CCS non-smokers, control smokers, and control non-smokers. Serum MMP-2, MMP-9, and TIMP-3 levels were measured using ELISA. Coronary artery plaque severity was assessed using the Gensini score, while cardiac function was evaluated by echocardiography. MMP-9 and TIMP-3 levels were significantly higher in CCS patients than in controls, regardless of smoking status. MMP-9 showed significant positive correlations with the Gensini score in smokers (r = 0.556, p < 0.001) and non-smokers (r = 0.596, p < 0.001) and remained independently associated with coronary plaque severity in both groups. TIMP-3 was independently associated with the Gensini score only in non-smokers (B = 0.667, p = 0.031). Higher MMP-9 levels were independently associated with reduced left ventricular ejection fraction and adverse diastolic parameters. Overall, MMP-9 was independently associated with coronary atherosclerotic burden and cardiac dysfunction, supporting its potential as a biomarker of CAD severity. ACS, rather than smoking status, appeared to have a greater influence on cardiac dysfunction.