Although underlying mechanisms of coronary artery ectasia (CAE) are clearly unknown, destruction of extracellular matrix may be responsible for the ectasia formation. Thus, we investigated the role of matrix metalloproteinases (MMP), tissue inhibitor of matrix metalloproteinases (TIMP-1), and inflammatory markers [high-sensitive C-reactive protein, interleukins (ILs)] in CAE patients.
This study consisted of 28 consecutive CAE patients, 27 obstructive coronary artery disease (CAD) patients, and 22 controls with normal coronary arteries undergoing cardiac catheterization. Plasma levels of MMP-3, MMP-9, TIMP-1, and inflammatory markers were measured.
Plasma level of MMP-3 was significantly higher in CAE patients compared with both CAD patients and controls (17.2±6.1, 11.2±3.2, and 9.2±3.4 ng/ml, respectively, both P=0.001) and so did MMP-9 level (27.4±5.9, 24.8±4.4, and 20.6±4.6 ng/ml, respectively, both P<0.05). IL-6 level was also higher in CAE patients than in controls (60.9±22.1 vs. 36.1±21.5 pg/ml, P=0.001) but were comparable in CAE and CAD patients. Plasma high-sensitive C-reactive protein, IL-1, and TIMP-1 levels were similar in three groups. MMP-3 levels correlated with diffuse (r=0.46, P=0.01) and multivessel ectasia (r=0.45, P=0.02).
Our results suggest that the increased level of MMP-3, MMP-9, and IL-6 may be responsible for ectasia formation in patients with CAE.