Oral Abstract Session
SCMR 22nd Annual Scientific Sessions
Background: A growing number of studies now support the notion that patients experiencing hemorrhagic myocardial infarctions (hMIs) have significantly worse prognoses than those experiencing non-hMIs. Yet, whether hemorrhage is causally connected to the observed adverse outcomes, and if so, whether there are viable approaches which can mitigate the effects of reperfusion hemorrhage are still unknown. Given that therapeutic hypothermia has been shown to be effective in the brain, we hypothesized that localized mild hypothermia to the heart can reduce the effects of hemorrhage and improve left ventricular functional recovery in the setting of hMI. We tested this in a swine model of hMI by imposing mild hypothermia and evaluating the tissue specific and functional changes using serial CMR with appropriate controls.
Methods: Swine (n=6) underwent balloon occlusion of the LAD artery and were reperfused after 90 mins of ischemia. Following 30 mins post-reperfusion, a catheter was inserted into the pericardial space and infused with either normal saline (room temperature, control group) or chilled saline (8°C, experimental group) for 60 minutes. Animals were then recovered and followed-up with CMR on day 3 and day 30 following reperfusion. During CMR studies cine, T2* and LGE images were acquired. Presence and extent of hemorrhage and its remnants were identified on the basis of T2* and LGE images. Left-ventricular ejection fraction (LVEF) was determined from cine datasets.
Results: Both the experimental and control groups showed significant infarction and hemorrhage on day 3 post-MI. Results from representative animals are shown in Fig. 1. In the experimental group (cardiac hypothermia), the remnants of hemorrhage decreased by 85.5% ± 0.4% between day 3 and 30 days post-MI compared to a reduction of 47.3% ± 12.0% in the control group receiving normothermia. In addition, in the animals receiving hypothermia, LVEF increased by 22.8% ± 1.4% between day 3 and 30 days post MI compared to nearly no change (0.6% ± 8.8%) in LVEF in the control group receiving normothermia. This is shown in Fig. 2.
Our early findings are promising and show that mild hypothermia can reduce the hemorrhagic remnants and improve functional recovery in the first month post-MI. Additional follow-up studies are underway to evaluate the continued improvement or stabilization at future timepoints. These early results illuminate an important step towards mitigating the prognostic burden hemorrhagic infarctions pose on MI patients. While future studies are required to uncover the physiological mechanism behind the protective effect of mild hypothermia, our findings pave the first steps in defining a treatment option for hMI patients and establishing a causal connection between hemorrhage and functional recovery of the heart. If the results hold in a larger cohort of animals, it would pave the way for clinical trials aimed at improving functional recovery in hMI patients.