Role of Novel Mediators of Inflammation in Left Ventricular Remodeling in Patients With Acute Myocardial Infarction: Do They Affect the Outcome of Patients?

Abstract

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) is a major mechanism for cardiovascular death and disability. A significant number of post-MI patients develop progressive left ventricular enlargement and heart failure and many require heart transplantation and ventricular assist devices. Understanding of the basic mechanisms regulating the reaction to injury is crucial for the development of site-specific cell biological strategies of intervention to both reduce injury and promote repair. To determine whether there are new inflammatory markers having a role in structural remodeling after AMI in patients who applied to the emergency department of this hospital with severe chest pain at the first 12 hours, the authors measured the levels of C-reactive protein (CRP), macrophage colony-stimulating factor (M-CSF) and interleukin-3 (IL-3) in patients with AMI at hospital admission and on day 5. They measured plasma CRP concentrations by using highly sensitive CRP reagent with the immunonephelometric method, and plasma M-CSF and IL-3 concentrations with the help of a commercial enzyme-linked immunoassay test in 30 patients with AMI. Mean plasma CRP, M-CSF, and IL-3 concentrations at admission to the hospital were significantly higher than those on day 5 (5.0 ∓3.1 mg/dL, 119.4 ∓103.6 pg/mL, and 155.1 ∓83.4 ng/mL, respectively, p<0.001 for each value). CRP, M-CSF, and IL-3 were all increased in patients with AMI. These findings suggest that these are new inflammatory markers, which may have important roles in LV remodeling after AMI.