Management of an acute myocardial infarction (AMI) focuses on restoring oxygen supply to limit myocardial damage, however ischemia-reperfusion injury (IRI) remains a major determinant of mortality in AMI. No studies have targeted initially reducing left ventricular stroke work (LVSW) to limit IRI in AMI. The Impella CP axial-flow pump reduces LVSW. We tested the hypothesis that first reducing myocardial work and delaying coronary reperfusion reduces infarct size by activating cardioprotective signaling pathways.
Methods:
AMI was induced by occlusion of the left anterior descending artery (LAD) via angioplasty for 90 minutes in 50kg male Yorkshire swine (n=5/group). In Group 1, the LAD was reperfused for 120 minutes. In Group 2, after 90 minutes of ischemia the Impella CP device was activated and the LAD left occluded for an additional 60 minutes (150 minutes of LAD occlusion total), followed by 120 minutes of reperfusion. The Impella CP was active throughout reperfusion. Western blot analysis quantified myocardial kinase activity.
Results:
Compared to Group 1, Group 2 had a reduced LVSW, LV end-diastolic volume and end-diastolic pressure after reperfusion [Fig A]. Group 2 showed increased myocardial phosphorylation of cardioprotective kinases: AKT, ERK, GSK3β and STAT-3 [Fig B]. Compared to Group 1, the percent myocardial infarct size normalized to the area at risk (AAR) was reduced in Group 2 (73+13% vs 42+15%, p=0.02).
Conclusion:
We report the potential benefit of primarily unloading the heart and delaying coronary reperfusion to salvage myocardium in AMI. This is the first report to examine the impact of the Impella CP on cardioprotective signaling in the heart.
Comments on "Quantification of myocardial infarct size after coronary reperfusion by serum cardiac myosin light chain II in conscious dogs".
