Atorvastatin Reload Down Regulates TLR-2 Expression and Reduces the Acute Inflammatory Response in Patients Undergoing Percutaneous Coronary Intervention

Abstract

Abdullah Elttayef Jasim, Sahar A. Majeed, Najah R. Hadi, Khalid I. Amber, Hidhab Jawad.

Coronary artery disease (CAD) is the single most common cause of morbidity and mortality in developed world. PCI with stent implantation is a widely used, safe and effective technique for the treatment of symptomatic ischemic heart disease. Stenting, however, causes significant injury to the vascular wall, resulting in a repair process that requires inflammatory process activation. This study was done to assess the effect of pre PCI atorvastatin reload on toll like receptor 2 expressions with its downstream signaling. A double blind randomized prospective trail in which 60 patients with stable angina pectoris, who are scheduled for an elective PCI at Al-Najaf Center for Cardiac Surgery and Trans Catheter were enrolled and were assigned randomly1:1 into two groups, after an ethical committee of the University of Kufa /Faculty of medicine approval, 30 patients who received low dose atorvastatin 40mg daily without reload (control group). Stent implantation was associated with an elevation in TLR 2 expression in peripheral monocyte in both study groups after stenting but significantly higher expression level was observed among control group than atorvastatin reload group (p<0.05) at 4hrand 12hr post PCI. Inflammatory cytokine (MMP9, MCP-1, and IL-6) were significantly increased after stenting in both study groups (P<0.005) but higher in control group than atorvastatin reload group (p<0.05) also myocardial injury markers (CKMB, troponin I) were significantly higher in control group than atorvastatin reload group (p<0.05). We conclude that atorvastatin reload before coronary artery interventions attenuate toll like receptor 2 expression on peripheral monocyte and significantly reduce serum level of MMP9,MCP-1 and IL-6and cardiac injury markers(CK_MB and cardiac troponin I)