Abstract 20734: Infliximab Mediates Functional Recovery in a Porcine Model of Acute Myocardial Infarction
Introduction: Myocardial infarction (MI) and resultant heart failure represent a major cause of morbidity and mortality. Thrombolytics and reduction in door-to-balloon times have increased rates of acute survival, however, with a subsequent increase in the incidence of ensuing ischemic cardiomyopathy. This may in large part be due to the fact that myocardial injury activates a local inflammation diminishing the innate regenerative response following MI. This study aims to evaluate the influence of TNF-α inhibition to alter the balance away from inflammation and towards regeneration in the setting of acute MI.
Hypothesis: Systemic administration of Infliximab will diminish scar size and preserve myocardial function in a porcine model of acute MI.
Methods: A porcine model of acute MI was generated via inflation of an angioplasty balloon catheter in the mid-LAD for 90 min (n=9). Infliximab was delivered intravenously upon reperfusion at 5 mg/kg. Hemodynamics, intracardiac/transthoracic echocardiography were monitored throughout the procedure and at one month follow-up. Hearts were harvested, cut into 1 cm thick cross sections and stained with Masson’s Trichrome to visualize and volumetrically quantify scar size.
Results: Left ventricular ejection fraction of the treated group was significantly improved compared to untreated (62.1 ± 3.0 % vs. 39.9 ± 3.2 %, P<0.001). Diastolic wall thickness (0.71 ± 0.09 cm vs. 0.37 ± 0.12 cm, P<0.01) and fractional shortening (27.6 ± 1.9 % vs. 15.7 ± 1.4 %, P<0.001) were also significantly improved for treated vs. untreated respectively. Scar size was significantly less in the treated group (8.31 ± 3.03 % vs. 17.41 ± 3.04 %, P<0.05).
Conclusion: These results demonstrate that systemic Infliximab therapy is effective in preventing structural remodeling, while preserving contractility of the heart post infarction.
Author Disclosures: C. Livia: None. S. Yamada: None. R.D. Singh: None. M. Rihal: None. P. Stalboerger: None. T. Witt: None. C. Rihal: None. A. Terzic: None. A. Behfar: None.
- © 2016 by American Heart Association, Inc.