Reperfusion is a common complication of acute myocardial infarction (AMI) that is characterized by tissue damage caused when blood supply returns to the tissue. Transvalvuvar ventricle unloading (LV unloading) is emerging as potential prevention of reperfusion, but its effectiveness not well studied. The objective of this study is to investigate the effect of LV unloading before reperfusion.

This analysis included the results from the STEMI-Door to Unload (STEMI-DTU) trial followed by testing the effects of LV unloading on reperfusion injury, ischemia, cardiac metabolism, and mitochondrial function. The primary outcome of the study was the incidence of ischemic injury before reperfusion.

The findings suggested that LV unloading reduced the infarct size in patients with large anterior ST-Elevation Myocardial Infarction (STEMI). The duration of LV unloading was inversely associated with infarct size in STEMI patients. Preclinical models indicated that LV unloading alleviated the expression of hypoxia-sensitive proteins and myocardial damage due to ischemia. Transvalvular LV unloading (not with venoarterial extracorporeal membrane oxygenation) improved myocardial energy substrate, reduced oxidative stress, and preserved mitochondrial structure and function.

 The research concluded that transvalvular ventricular unloading before reperfusion limits the ischemic injury, along with improving myocardial energy substrate use and preserving mitochondrial function and structure.