Key result
Induction of PGC-1α expression 72 hours after STEMI was associated with significantly larger necrotic areas (24.91% vs 10.90%) and more severe left ventricular dysfunction.
Cohort (n=38)
No
Absolute Event Rate: 24.91% vs 10.9%
p-value: p=0.012
PGC-1α expression is induced in blood mononuclear cells following STEMI, and higher induction levels correlate with larger infarct size and worse ventricular dysfunction, suggesting its potential as a biomarker for cardiac injury and recovery.
Should not yet alter post-STEMI care; hypothesis-generating for PGC-1α as biomarker of infarct severity.
Following acute myocardial infarction (MI), cardiomyocyte survival depends on its mitochondrial oxidative capacity. Cell death is normally followed by activation of the immune system. Peroxisome proliferator activated receptor γ-coactivator 1α (PGC-1α) is a transcriptional coactivator and a master regulator of cardiac oxidative metabolism. PGC-1α is induced by hypoxia and facilitates the recovery of the contractile capacity of the cardiac muscle following an artery ligation procedure. We hypothesized that PGC-1α activity could serve as a good molecular marker of cardiac recovery after a coronary event. The objective of the present study was to monitor the levels of PGC-1α following an ST-segment elevation acute myocardial infarction (STEMI) episode in blood samples of the affected patients. Analysis of blood mononuclear cells from human patients following an STEMI showed that PGC-1α expression was increased and the level of induction correlated with the infarct size. Infarct size was determined by LGE-CMR (late gadolinium enhancement on cardiac magnetic resonance), used to estimate the percentage of necrotic area. Cardiac markers, maximum creatine kinase (CK-MB) and Troponin I (TnI) levels, left ventricular ejection function (LVEF) and regional wall motion abnormalities (RWMA) as determined by echocardiography were also used to monitor cardiac injury. We also found that PGC-1α is present and active in mouse lymphocytes where its expression is induced upon activation and can be detected in the nuclear fraction of blood samples. These results support the notion that induction of PGC-1α expression can be part of the recovery response to an STEMI and could serve as a prognosis factor of cardiac recovery.
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Fabregat‐Andrés et al. (2011) conducted a cohort in ST-segment elevation acute myocardial infarction (STEMI) (n=38). PGC-1α induction (PGC-1α mRNA 72 h/0 h > 1) vs. No PGC-1α induction (PGC-1α mRNA 72 h/0 h ≤ 1) was evaluated on Infarct size (necrotic area) estimated by late gadolinium enhancement (LGE) on cardiac magnetic resonance (p=0.012). Induction of PGC-1α expression 72 hours after STEMI was associated with significantly larger necrotic areas (24.91% vs 10.90%) and more severe left ventricular dysfunction.
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