Attenuation of ST‐segment elevation reflects infarct size reduction by ischemic conditioning in pigs
Authors: Kleinbongard Petra , Amanakis Georgios , Skyschally Andreas , Heusch Gerd 
Published: June 2021

Cardioprotection by ischemic conditioning maneuvers, either locally in the heart or remotely from the heart, reduces infarct size. However, infarct size reduction is seen only hours to days after the acute event. To study the potential of ST‐segment elevation (STE) and its attenuation to reflect infarct size reduction already during ongoing coronary occlusion or early during reperfusion, pigs were subjected to 1 h LAD occlusion and 3 h reperfusion. Cardioprotection was recruited prior to the index ischemia by local ischemic preconditioning (IPC; n=14; 2x3 min LAD occlusion, interspersed by 2 min reperfusion, 15 min prior to ischemia) or remote ischemic preconditioning (RIPC; n=20; 4x5 min / 5 min hindlimb ischemia/reperfusion, 90 min prior to ischemia), during the index ischemia by remote ischemic perconditioning1 (RPER; n=18; 4x5 min / 5 min hindlimb ischemia/reperfusion, starting 20 min after the onset of ischemia), or at the onset of reperfusion by ischemic postconditioning (PoCo; n=9; 4x1 min / 1 min coronary reocclusion/reperfusion at 1 min reperfusion). Pigs without ischemic conditioning served as controls (PLA; n=29). Transmural myocardial blood flow (microspheres), area at risk (blue dye), and infarct size (TTC) were measured. STE amplitude was defined as the voltage difference in a V2‐like ECG lead between a point 30 ms before the P‐wave and one 20 ms after the J‐point.

Area at risk and transmural myocardial blood flow during ischemia were similar among groups, and the cardioprotective maneuvers robustly reduced infarct size (PLA 42±11% of area at risk; mean±SD; IPC 19±10%; RIPC 23±12%; RPER 23±12%; PoCo 22±11%; all p<0.05 vs. PLA). With PLA, STE was markedly increased at 5 min ischemia and this elevation was sustained throughout ischemia. At 10 min reperfusion, STE increased even further, possibly reflecting additional reperfusion injury, followed by a gradual, but incomplete STE recovery over 120 min reperfusion. RIPC and IPC did not impact on STE at 5 min ischemia, but STE was attenuated at 55 min ischemia. With RPER, STE was attenuated immediately after completion of the maneuver at 55 min ischemia. PoCo abolished the further increase of STE at 10 min reperfusion. (see figure)

The infarct size reduction by IPC, RIPC, RPER, or PoCo is robustly reflected in an attenuation of STE. Whereas PoCo and RPER attenuate STE within minutes after completion of the maneuver, the two cardioprotective maneuvers which were performed prior to myocardial ischemia, i.e. IPC and RIPC, did not attenuate STE immediately at 5 min ischemia, but did so at 55 min ischemia. A speculative explanation for such discrepancy is that STE attenuation only reflects protection from irreversible ischemic or reperfusion injury. In any event, STE analysis provides an on‐line estimate of cardioprotection much earlier than a measurement of infarct size.

Support or Funding Information

Supported by: DFG (SFB 1116 B08)

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.