Abstract
The present study aimed to evaluate the plasma concentration of pro and antiangiogenic factors and their role in the pathogenesis of coronary artery abnormal dilation (CAAD). We measured the plasma concentration of matrix metalloproteinase-8 (MMP-8), transforming growth factor beta 1 (TGF-β1), Angiopoietin-2, vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) using a sandwich ELISA technique in the plasma of patients with coronary artery abnormal dilation (CAAD, Group 1), coronary artery disease (CAD, Group 2), and normal coronary arteries (NCA, Group 3). Patients suffering from CAAD showed significantly higher plasma concentrations of VEGF (p = 0.002) than those from the control group. Both pathological angiogenesis and inflammation appear to be crucial in the pathogenesis of aneurysmal dilatation of the coronary arteries.
Highlights
Coronary artery abnormal dilation (CAAD) is one of the uncommon cardiovascular disorders with an incidence range of 0.15–5.3% of patients undergoing coronary angiography [1]
Our study aimed to evaluate the role of angiogenic processes in the pathogenesis of coronary artery abnormal dilation (CAAD) by assessing plasma levels of matrix metalloproteinase-8 (MMP-8), transforming growth factor beta 1 (TGF-β1), Angiopoietin-2, vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) in patients with CAAD compared to those in age- and sex-matched patients with stable angina and obstructive coronary artery disease (CAD), and control subjects with angiographically normal coronary arteries (NCA)
No patient in the control group was indicated for dual antiplatelet therapy (DAPT) (p < 0.001)
Summary
Coronary artery abnormal dilation (CAAD) is one of the uncommon cardiovascular disorders with an incidence range of 0.15–5.3% of patients undergoing coronary angiography [1]. This pathology has been described interchangeably using two terms: coronary artery aneurysm (CAA) and coronary artery ectasia (CAE) [2]. These synonymously used terms refer to two different phenotypes. CAA is defined as a focal dilatation with a diameter of 1.5 times the adjacent normal coronary artery, whereas the term CAE describes similar but more diffused lesions [3]. Less common causes are Kawasaki disease, diagnostic or interventional coronary angiography, inflammatory and infectious arteritis, connective tissue disease, aortic dissection, tumor metastases, trauma, and congenital malformation
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