Abstract 15509: Left Ventricular Unloading by Left Ventricular Assist Device and Bradycardic Agent Synergistically Reduces Oxygen Consumption in Myocardial Infarction
Introduction: Reducing myocardial oxygen consumption (MVO2) in acute myocardial infarction (AMI) limits infarct size because the imbalance between oxygen supply and demand is the fundamental pathophysiology of ischemia. Since MVO2 is determined by the product of left ventricular pressure-volume area (PVA) and heart rate (HR), we hypothesized that the combination of left ventricular assist device (LVAD), which reduces PVA, and bradycardic agent, Ivabradine (IVA, selective If channel inhibitor), synergistically reduces MVO2 while avoiding the negative hemodynamic impacts resulting from bradycardia.
Methods: In 4 mongrel dogs, we occluded the left circumflex coronary artery for 1 hour, measured PVA and MVO2 by the Fick’s rule and compared those among 6 conditions: Control (no LVAD or IVA), partial LVAD (p-LVAD: LVAD halves pulse pressure), and total LVAD (t-LVAD: totally LVAD dependent circulation) in the presence and absence of IVA (1mg/kg, iv). We used transvascular LVAD, Impella®, for left ventricular unloading.
Results: IVA without LVAD reduced HR (% reduction against Control: -43 ± 8%, p<0.01), whereas significantly decreased mean arterial pressure (90.7±13.8 vs. 54.9±15.2 mmHg, p<0.05) and increased left atrial pressure (11.5±3.1 vs. 20.0±4.9 mmHg, p<0.05). Those negative hemodynamic impacts disappeared when IVA was combined with LVAD. PVA was marginally reduced in p-LVAD, while markedly reduced in t-LVAD (Control: 1747±503, p-LVAD: 1310±637, t-LVAD: 196±50 mmHg▪ml, p<0.05) and so was MVO2 (Fig. 1, dark bars). IVA nearly halved MVO2 in every supported condition (Fig. 1, red bars). As anticipated, PVA linearly increased MVO2. IVA decreased MVO2 for given PVA (Fig. 2).
Conclusions: LVAD suppresses MVO2 via the reduction of PVA and IVA suppresses MVO2 via the reduction of HR. The combination of LVAD and IVA synergistically reduces MVO2 without compromising hemodynamics. This strategy will provide a new clinical tool in the management of AMI.
- Myocardial infarction
- Pressure – volume relation
- Ventricular assist devices
- Heart rate/Heart rate variability
Author Disclosures: K. Saku: None. G. Sunagawa: None. T. Arimura: None. T. Kakino: None. T. Sakamoto: None. T. Akashi: None. Y. Murayama: None. T. Kishi: None. H. Tsutsui: None. K. Sunagawa: None.
- © 2016 by American Heart Association, Inc.