Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/5525
Impact of Left Ventricular Hypertrophy on Troponin Release During Acute Myocardial Infarction: New Insights From a Comprehensive Translational Study
Fernandez-Jimenez, Rodrigo CNIC | Silva, Jacobo | Martinez-Martinez, Sara CNIC | Lopez-Maderuelo, Dolores CNIC | Nuno-Ayala, Mario CNIC | Garcia-Ruiz, Jose M CNIC | Garcia-Alvarez, Ana CNIC | Fernandez-Friera, Leticia CNIC | Pizarro, Gonzalo CNIC | Garcia-Prieto, Jaime CNIC | Sanz-Rosa, David CNIC | Lopez-Martin, Gonzalo J. CNIC | Fernandez-Ortiz, Antonio CNIC | Macaya, Carlos | Fuster, Valentin CNIC | Redondo, Juan Miguel CNIC | Ibanez, Borja CNIC
J Am Heart Assoc. 2015; 4(1):e001218
Background-Biomarkers are frequently used to estimate infarct size (IS) as an endpoint in experimental and clinical studies. Here, we prospectively studied the impact of left ventricular (LV) hypertrophy (LVH) on biomarker release in clinical and experimental myocardial infarction (MI). Methods and Results-ST-segment elevation myocardial infarction (STEMI) patients (n=140) were monitored for total creatine kinase (CK) and cardiac troponin I (cTnI) over 72 hours postinfarction and were examined by cardiac magnetic resonance (CMR) at 1 week and 6 months postinfarction. MI was generated in pigs with induced LVH (n=10) and in sham-operated pigs (n=8), and serial total CK and cTnI measurements were performed and CMR scans conducted at 7 days postinfarction. Regression analysis was used to study the influence of LVH on total CK and cTnI release and IS estimated by CMR (gold standard). Receiver operating characteristic (ROC) curve analysis was performed to study the discriminatory capacity of the area under the curve (AUC) of cTnI and total CK in predicting LV dysfunction. Cardiomyocyte cTnI expression was quantified in myocardial sections from LVH and sham-operated pigs. In both the clinical and experimental studies, LVH was associated with significantly higher peak and AUC of cTnI, but not with differences in total CK. ROC curves showed that the discriminatory capacity of AUC of cTnI to predict LV dysfunction was significantly worse for patients with LVH. LVH did not affect the capacity of total CK to estimate IS or LV dysfunction. Immunofluorescence analysis revealed significantly higher cTnI content in hypertrophic cardiomyocytes. Conclusions-Peak and AUC of cTnI both significantly overestimate IS in the presence of LVH, owing to the higher troponin content per cardiomyocyte. In the setting of LVH, cTnI release during STEMI poorly predicts postinfarction LV dysfunction. LV mass should be taken into consideration when IS or LV function are estimated by troponin release.
creatine kinase | hypertrophy | magnetic resonance imaging | myocardial infarction | troponin | PERCUTANEOUS CORONARY INTERVENTION | CREATINE-KINASE ISOENZYMES | MAGNETIC-RESONANCE | CARDIAC INJURY | LABORATORY-ANIMALS | GENERAL-POPULATION | TRANSMURAL EXTENT | ADVERSE OUTCOMES | PROGNOSTIC VALUE | EARLY METOPROLOL
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