Atherosclerosis exacerbates arrhythmia following myocardial infarction: Role of myocardial inflammation

Background Atherosclerotic animal models show increased recruitment of inflammatory cells to the heart after myocardial infarction (MI), which impacts ventricular function and remodeling. Objective The purpose of this study was to determine whether increased myocardial inflammation after MI also contributes to arrhythmias. Methods MI was created in 3 mouse models: (1) atherosclerotic (apolipoprotein E deficient [ApoE–/– ] on atherogenic diet, n = 12); (2) acute inflammation (wild-type [WT] given daily lipopolysaccharide [LPS] 10 μg/day, n = 7); and (3) WT (n = 14). Sham-operated (n = 4) mice also were studied. Four days post-MI, an inflammatory protease-activatable fluorescent probe (Prosense680) was injected intravenously to quantify myocardial inflammation on day 5. Optical mapping with voltage-sensitive dye was performed on day 5 to assess electrophysiology and arrhythmia susceptibility. Results Inflammatory activity (Prosense680 fluorescence) was increased approximately 2-fold in ApoE+MI and LPS+MI hearts vs WT+MI ( P