Abstract 15597: Transvascular Mechanical Unloading Combined With Ivabradine Stabilizes Hemodynamics and Strikingly Suppresses the Infarct Size in Acute Myocardial Infarction
Background: Myocardial infarction (MI) remains a leading cause of chronic heart failure (CHF) despite the latest advances of early reperfusion. The presence of unsalvaged myocardium leads to cardiac remodeling and CHF. Thus, there exists unmet needs for new therapies which reduce the infarct size in acute MI. Reducing myocardial oxygen consumption (MVO2) is known to reduce the infarct size in MI. Since MVO2 is mainly determined by the product of left ventricular (LV) work and heart rate (HR), we hypothesized that the combination therapy of transvascular left ventricular assist device (VAD), Impella®, which reduces LV work and bradycardic agent, Ivabradine (IVA), in acute MI reduces the infarct size.
Methods: In 14 anesthetized dogs, we ligated coronary arteries for 180 min and then reperfused. We started VAD and IVA (1mg/kg iv.) one hour after the onset of ischemia. We allocated animals into 3 groups, no support (Control, n=4), VAD (n=5) and the combination of VAD and IVA (VAD+IVA, n=5). We compared the infarct size (infarct area/risk areaх100 (%)) 3 hours after reperfusion.
Results: Compared to Control, IVA significantly reduced HR by 63±19 bpm. In spite of bradycardia, VAD+IVA did not affect arterial pressure (Control: 104.6±21.4, VAD: 81.6±8.4, VAD+IVA: 97.8±7.6 mmHg, n.s.) or left atrial pressure (Control: 9.6±2.5, VAD: 8.7±1.3, VAD+IVA: 10.7±2.5 mmHg, n.s.), because the mechanical support fully compensated the negative hemodynamic impact of bradycardia. The infarct size was marginally reduced in VAD, whereas strikingly reduced to less than half in VAD+IVA (Control: 55.4±5.6, VAD: 40.3±14.7, VAD+IVA: 23.9±10.6%, p<0.01, Fig. 1, 2).
Conclusion: The combination therapy of VAD and IVA in the acute phase of MI dramatically reduces the infarct size without compromising hemodynamics. Since both VAD and IVA are clinically approved modality of treatment, the combination treatment may serve as a readily available powerful therapeutic option for acute MI to prevent CHF.
Author Disclosures: G. Sunagawa: None. K. Saku: None. T. Arimura: None. T. Akashi: None. Y. Murayama: None. T. Sakamoto: None. T. Kishi: None. T. Ide: None. H. Tsutsui: None. K. Sunagawa: None.
- © 2016 by American Heart Association, Inc.