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Examining the Genetic Marker for Ischemic Preconditioning and its Effect on Apoptosis and Autophagy in ST-Elevation vs. Non-ST Elevation Acute Myocardial Infarction

Lacey Maclay, Ziad Faramand, MD, MSc, Imad Al-Ghouleh, PhD, Yvette Conley, PhD, and Salah Al-Zaiti, RN, PhD, University of Pittsburgh, 4200 Fifth Avenue, Pittsburgh, PA 15260 and UPMC, Pittsburgh, PA

Growing evidence suggests that the differences observed in symptomatology, morbidity, and mortality between ST-Elevation Myocardial Infarction (STEMI) and Non-ST-elevation myocardial infarction (NSTEMI) cannot be simply explained by the severity of coronary occlusion. Apoptosis and autophagy are two known pathways that can induce myocardial cell death or cell survival, respectively. Ischemic preconditioning, on the other hand, is a recognized endogenous protective mechanism that can limit the extent of scaring. It remains unknown if the degree of ischemic preconditioning, and subsequently the extent of apoptosis and autophagy, can partially explain the differences observed between STEMI and NSTEMI.

In this exploratory pilot study, we prospectively enrolled consecutive myocardial infarction (MI) patients from a single UPMC-affiliated primary PCI-receiving center. The interventional cardiologist obtained blood samples from each patient using PAX-gene tubes femoral arterial access line prior to the catheterization procedure. qRT-PCR were conducted using TaqMan assays, GAPDH as an endogenous control, and quantified using comparative Ct method. The following three candidate genes were analyzed: 1) EGR1, a suppressor of ischemic preconditioning; 2) BCL-2, an apoptosis inducing gene; and 3) PINK1, an autophagy inducing gene.

Our sample included 29 patients treated for acute MI (Age 67±12; 83% males). Compared to patients with STEMI, those with NSTEMI had attenuated expression of EGR1 (4.7±2.2 vs. 6.9±0.7, p=0.001) and BCL-2 (2.7±1.2 vs. 4.8±1.0, p=0.001), but not PINK1 (5.1±0.7 vs. 3.9±1.6, p=0.096). EGFR1 was significantly correlated with BCL-2 (r=0.657, p<0.001), but not PINK1 (r=0.183, p=0.382).

Compared to NSTEMI, STEMI patients had less ischemic preconditioning and higher apoptosis. The corresponding gene expression differences we observed between STEMI and NSTEMI could explain the differences in morbidity and mortality of each condition. The correlation between ischemic preconditioning and apoptosis provides an insight into the distinct mechanisms of myocardial scarring in these patients which can inform future targeted therapies.




Additional Abstract Information

Presenter: Lacey Maclay

Institution: University of Pittsburgh School of Nursing

Type: Oral

Subject: Nursing & Public Health

Status: Approved


Time and Location

Session: Oral 9
Date/Time: Wed 12:00pm-1:00pm
Session Number: 935
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