CONICET | Buscador de Institutos y Recursos Humanos

Background and Aims. Many studies suggest that the different steps of the atherosclerotic process may be mediated by metalloproteases (MMPs). MMP-9 and MMP-2, which are highly expressed in the vulnerable regions of the atherosclerotic plaques, have been suggested to be causally involved in plaque rupture. In another manner linked with LDL, lipoprotein-associated phospholipase A2 (Lp-PLA2) hydrolyzes phospholipids generating proinflammatory and proatherogenic products. Our aim was to evaluate plasma activity of MMP-2 and 9, as well as Lp-PLA2, in subjects with coronary artery stenosis in comparison with controls and to correlate these activities with lipoprotein profile and general biomarkers of inflammation. Methods. Forty two subjects who had undergone coronary angiography were divided into two groups: patients with coronary vessels with at least 45% stenosis (CAD [coronary artery disease], n=24) and patients without angiographically detectable coronary artery disease (controls, n =18). Plasma activity of MMP-2 and MMP-9 was measured and correlated with markers of systemic inflammation (hs-CRP), subendothelial inflammation (Lp-PLA2) and lipoprotein profile. Results. Plasma activity of both MMPs was consistently higher in patients than in controls ( p<0.01). Pro-MMP-2 (r =0.34, p<0.01) and MMP-9 (r =0.51, p <0.02) activities correlated with apoprotein B. Pro-MMP-2 correlated with hs-CRP (r =0.47, p <0.01) and inversely with HDL cholesterol (r =-0.35, p <0.02). No differences were observed in Lp-PLA2 between patients and controls (15.2± 4.0 vs. 15.4±4.5 mmol/mL/h, p=NS, respectively), and no correlation was observed with MMPs. Conclusions. MMP activity was higher in CAD than in controls. The correlation observed between pro-MMP-2 and high-sensitive C-reactive protein (hs-CRP) may be due to specific systemic inflammatory processes. No correlation was observed between Lp-PLA2 and MMPs.Many studies suggest that the different steps of the atherosclerotic process may be mediated by metalloproteases (MMPs). MMP-9 and MMP-2, which are highly expressed in the vulnerable regions of the atherosclerotic plaques, have been suggested to be causally involved in plaque rupture. In another manner linked with LDL, lipoprotein-associated phospholipase A2 (Lp-PLA2) hydrolyzes phospholipids generating proinflammatory and proatherogenic products. Our aim was to evaluate plasma activity of MMP-2 and 9, as well as Lp-PLA2, in subjects with coronary artery stenosis in comparison with controls and to correlate these activities with lipoprotein profile and general biomarkers of inflammation. Methods. Forty two subjects who had undergone coronary angiography were divided into two groups: patients with coronary vessels with at least 45% stenosis (CAD [coronary artery disease], n=24) and patients without angiographically detectable coronary artery disease (controls, n =18). Plasma activity of MMP-2 and MMP-9 was measured and correlated with markers of systemic inflammation (hs-CRP), subendothelial inflammation (Lp-PLA2) and lipoprotein profile. Results. Plasma activity of both MMPs was consistently higher in patients than in controls ( p<0.01). Pro-MMP-2 (r =0.34, p<0.01) and MMP-9 (r =0.51, p <0.02) activities correlated with apoprotein B. Pro-MMP-2 correlated with hs-CRP (r =0.47, p <0.01) and inversely with HDL cholesterol (r =-0.35, p <0.02). No differences were observed in Lp-PLA2 between patients and controls (15.2± 4.0 vs. 15.4±4.5 mmol/mL/h, p=NS, respectively), and no correlation was observed with MMPs. Conclusions. MMP activity was higher in CAD than in controls. The correlation observed between pro-MMP-2 and high-sensitive C-reactive protein (hs-CRP) may be due to specific systemic inflammatory processes. No correlation was observed between Lp-PLA2 and MMPs.