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Background: The progressive cardiac dysfunction after myocardial infarction (MI) related with left ventricular fibrosis and remodeling. This study investigated whether new ARB ‘Fimasartan’ is able to protect in the post-MI progression of left ventricular (LV) dysfunction and unknown under lining mechanism.
Methods: MI was induced in SD rats by permanent ligation of the left anterior descending artery (LAD). Treatment with Fimasartan (10mg/kg) was initiated 24 hours post-MI and continued for 7 weeks through oral administration. All animals performed baseline echocardiography and then randomly assigned into 3 groups.
Results: In histologic finding, infarct size and fibrosis were significantly decreased in MI+Fima compare to MI. Echocardiography was performed in 1 week and 7 weeks post-MI. LV function was dramatically preserved in MI+Fima compare with MI group (FS, 71.65±1.49% VS 51.77±5.14%). Hemodynamic measurement was observed 3 days after final echocardiography. Results showed great positive (+4526±240 mmHg/sec) and negative dP/dt (-4187±303) in MI+Fima compare with MI group (+3670±239, −3301±280 mmHg/sec, p<0.05 respectively). From microarray, fimasartan treatment dramatically decreased inflammatory signal and increased lipid metabolic relate genes. In addition, mitochondria membrane ion transport and damage response genes were increased.
Conclusions: A new ARB, fimasartan, strongly inhibit LV remodeling and development of cardiac dysfunction in myocardial infarction thorough preserve mitochondria survival. It shows possibility of fimasartan as a clinical treatment option to prevent progression of heart failure after MI.
Poster Hall, Hall C
Saturday, March 18, 2017, 9:45 a.m.-10:30 a.m.
Session Title: From Diet to Drugs: Mechanistic Insight Into Ischemic Heart Disease
Abstract Category: 1. Acute and Stable Ischemic Heart Disease: Basic
Presentation Number: 1202-301
- 2017 American College of Cardiology Foundation