Abstract 19073: Moderate Hypothermia Reduces Infarct/Injury Size and Preserves Myocardial Function Following Acute Ischemia-Reperfusion Injury
Background and Purpose: Several recent animal and post-hoc human studies have indicated that mild hypothermia provides cardiac protection after a STEMI insult. However, there is insufficient data regarding the influence of pre-reperfusion temperature on the degree of protection. We thus evaluated the dose response of pre-reperfusion temperature (35 & 32C) and the mitigation of ischemic-reperfusion injury using an endovascular cooling catheter.
Methods & Results: Thirteen adult Yorkshire swine underwent 60 minute ischemia reperfusion (IR) injury (left anterior descending coronary artery) with intravascular cooling administered before reperfusion. The swine were split into 3 groups defined by core temperature before reperfusion: a) 32C, b) 35C and C) 38C (control). Cardiac MRI (CMR, 3T GE Inc.) was performed at day 0 and 6 days post-IR for function, T2 injury, and delayed gadolinium enhancement scar volumes (DEMRI, d6 only), which were analyzed using CMR42 software (Circle CVI, Inc). Hearts were stained for scar and area at risk (AAR) by TTC. On day 6, infarct size reduction was found to be dose-dependent (Figure 1B) when compared to 38C. There was good agreement between TTC & MRI-derived infarct size (correlation r=0.75, p<0.005). While all groups displayed similar TTC AAR volumes, which reflect the anatomic ischemia region (Figure 1A), both 35C (n=4) and 32C (n=5) hearts displayed significantly smaller T2 MRI AAR (Figure 1C), indicating reduced injury. EF on d6 was preserved in both cooling groups (Change in EF%: 32C, -14.6±7.6%; 35C, -15.6±6.9%; 38C, -23±8.6%, p>0.05), however, segmental wall thickening suggests residual myocardial stunning at this subacute d6 timepoint.
Conclusion: Pre-reperfusion hypothermia to 35C and 32C reduces T2 myocardial edema and infarct size compared to 38C, and may lead to improved functional outcomes. Additional subjects are warranted to fully evaluate the temperature-dependent characteristic of the reduction in infarct size.
Author Disclosures: R. Dash: Other Research Support; Modest; Zoll Inc.. Y. Matsuura: None. B. Holt: Employment; Significant; Zoll, Inc.. A. Tachibana: None. J. Lyons: None. F. Ikeno: None. M.V. McConnell: Other Research Support; Modest; GE Healthcare. A.C. Yeung: None. U. Illindala: Employment; Significant; Zoll, Inc.. P.C. Yang: None.
- © 2014 by American Heart Association, Inc.