TY - JOUR
T1 - Blood PGC-1α concentration predicts myocardial salvage and ventricular remodeling after st-segment elevation acute myocardial infarction
AU - Fabregat-Andrés, Óscar
AU - Ridocci-Soriano, Francisco
AU - Estornell-Erill, Jordi
AU - Corbí-Pascual, Miguel
AU - Valle-Muñoz, Alfonso
AU - Berenguer-Jofresa, Alberto
AU - Barrabés, José A.
AU - Mata, Manuel
AU - Monsalve, María
PY - 2015/1/1
Y1 - 2015/1/1
N2 - © 2015 Sociedad Española de Cardiologia. Introduction and objectives Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is a metabolic regulator induced during ischemia that prevents cardiac remodeling in animal models. The activity of PGC-1α can be estimated in patients with ST-segment elevation acute myocardial infarction. The aim of the present study was to evaluate the value of PGC-1α in blood in predicting the extent of necrosis and ventricular remodeling after infarction. Methods In this prospective study of 31 patients with a first myocardial infarction in an anterior location and successful reperfusion, PGC-1α expression in peripheral blood on admission and at 72 hours was correlated with myocardial injury, ventricular volume, and systolic function at 6 months. Edema and myocardial necrosis were estimated using cardiac magnetic resonance imaging during the first week. At 6 months, infarct size and ventricular remodeling, defined as an increase > 10% of the left ventricular end-diastolic volume, was evaluated by follow-up magnetic resonance imaging. Myocardial salvage was defined as the difference between the edema and necrosis areas. Results Greater myocardial salvage was seen in patients with detectable PGC-1α levels at admission (mean [standard deviation (SD)], 18.3% [5.3%] vs 4.5% [3.9%]; P =.04). Induction of PGC-1α at 72 hours correlated with greater ventricular remodeling (change in left ventricular end-diastolic volume at 6 months, 29.7% [11.2%] vs 1.2% [5.8%]; P =.04). Conclusions Baseline PGC-1α expression and an attenuated systemic response after acute myocardial infarction are associated with greater myocardial salvage and predict less ventricular remodeling.
AB - © 2015 Sociedad Española de Cardiologia. Introduction and objectives Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is a metabolic regulator induced during ischemia that prevents cardiac remodeling in animal models. The activity of PGC-1α can be estimated in patients with ST-segment elevation acute myocardial infarction. The aim of the present study was to evaluate the value of PGC-1α in blood in predicting the extent of necrosis and ventricular remodeling after infarction. Methods In this prospective study of 31 patients with a first myocardial infarction in an anterior location and successful reperfusion, PGC-1α expression in peripheral blood on admission and at 72 hours was correlated with myocardial injury, ventricular volume, and systolic function at 6 months. Edema and myocardial necrosis were estimated using cardiac magnetic resonance imaging during the first week. At 6 months, infarct size and ventricular remodeling, defined as an increase > 10% of the left ventricular end-diastolic volume, was evaluated by follow-up magnetic resonance imaging. Myocardial salvage was defined as the difference between the edema and necrosis areas. Results Greater myocardial salvage was seen in patients with detectable PGC-1α levels at admission (mean [standard deviation (SD)], 18.3% [5.3%] vs 4.5% [3.9%]; P =.04). Induction of PGC-1α at 72 hours correlated with greater ventricular remodeling (change in left ventricular end-diastolic volume at 6 months, 29.7% [11.2%] vs 1.2% [5.8%]; P =.04). Conclusions Baseline PGC-1α expression and an attenuated systemic response after acute myocardial infarction are associated with greater myocardial salvage and predict less ventricular remodeling.
KW - infarction
KW - Oxidative metabolism
KW - Oxidative stress
KW - PGC-1α
KW - ST-segment elevation acute myocardial
KW - Ventricular remodeling
U2 - 10.1016/j.recesp.2014.05.020
DO - 10.1016/j.recesp.2014.05.020
M3 - Article
VL - 68
SP - 408
EP - 416
IS - 5
ER -