Abstract 20372: Therapeutically Reduced Air Pressure Improves Left Ventricular Function After Acute Myocardial Infarction in Mice
Introduction: Humans living at higher elevations have lower risk for myocardial infarction (MI) and better post-MI survival. We have shown that acute reductions in air pressure enhance arterial vasodilation in an endothelium-independent manner ex vivo and reduce afterload in vivo in mice. We hypothesized that afterload reduction induced by mild therapeutically reduced air pressure after acute MI would improve myocardial function.
Methods: Left-anterior descending artery (LAD) ligation was performed on three-month old C57BL6 males mice. Control group mice (n=9) were allowed to recover from the surgery at the averaged atmospheric pressure (754 mmHg) for a period of 7 days. The intervention group mice (n=8) were placed in a custom designed hypobaric pressure chamber to recover from the LAD ligation for 3-hours at 714 mmHg, a pressure chosen to mimic an elevation of 1500 m and avoid hypoxemia. The successful induction of an anterior MI was confirmed by echocardiography 24 hours after the surgery. Intervention group mice were administered 3-hours of hypobaric treatment daily for 7 days. Echocardiographic evaluation of left ventricular (LV) function was performed for all mice on Day 8.
Results: Echocardiography confirmed large anterior MI’s in both groups with no difference in ejection fraction (EF) or cardiac output at day 1. After 7 days of therapeutically lowered air pressure, there was a 14.2±5.3% improvement in EF for intervention group mice (p<0.01 versus Day 1), and no change for control mice. Similarly, cardiac output and stroke volume increased by 11.48±3.9 mL/min and 24.33±8.3 μL, respectively, in intervention group mice (p<0.01 versus Day 1) after 7 days of reduced air pressure treatment while the control mice showed no significant improvement.
Conclusion: We conclude that acute afterload reduction achieved by therapeutically reduced air pressure improves myocardial function after acute MI in mice. This finding may have tremendous translational potential as a novel therapy for acute MI in humans.
Author Disclosures: A. Shahid: None. M.S. McMurtry: None.
- © 2016 by American Heart Association, Inc.