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Matrix metalloproteinases and inflammatory markers in coronary artery ectasia: their relationship to severity of coronary artery ectasia

Dogan, Abdullaha; Tuzun, Nurullaha; Turker, Yasina; Akcay, Selahattina; Kaya, Selcukb; Ozaydin, Mehmeta

doi: 10.1097/MCA.0b013e3283109079
Pathophysiology and Natural History

Objective 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.

Methods 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.

Results 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).

Conclusion 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.

Departments of aCardiology

bMicrobiology, School of Medicine, Suleyman Demirel University, Isparta, Turkey

Correspondence to Associate Professor Abdullah Dogan, MD, Department of Cardiology, School of Medicine, Suleyman Demirel University, Isparta 532100, Turkey

Tel: +90 246 223 8616; fax: +90 246 232 6280;


Received 2 June 2008 Revised 12 July 2008 Accepted 12 July 2008

© 2008 Lippincott Williams & Wilkins, Inc.