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oai:repisalud.isciii.es:20.500.12105/55252024-09-27T09:04:13Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud author Fernandez-Jimenez, Rodrigo author Silva, Jacobo author Martinez-Martinez, Sara author Lopez-Maderuelo, Dolores author Nuno-Ayala, Mario author Garcia-Ruiz, Jose M author Garcia-Alvarez, Ana author Fernandez-Friera, Leticia author Pizarro, Gonzalo author Garcia-Prieto, Jaime author Sanz-Rosa, David author Lopez-Martin, Gonzalo J. author Fernandez-Ortiz, Antonio author Macaya, Carlos author Fuster, Valentin author Redondo, Juan Miguel author Ibáñez, Borja funder Instituto de Salud Carlos III funder Ministerio de Sanidad, Servicios Sociales e Igualdad (España) funder Ministerio de Economía y Competitividad (España) funder Fundación ProCNIC 2017-12-01T07:37:27Z 2017-12-01T07:37:27Z 2015 J Am Heart Assoc. 2015; 4(1):e001218 10.1161/JAHA.114.001218 2047-9980 Journal of the American Heart Association 25609414 http://hdl.handle.net/20.500.12105/5525 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. eng 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 Impact of Left Ventricular Hypertrophy on Troponin Release During Acute Myocardial Infarction: New Insights From a Comprehensive Translational Study journal article URL https://repisalud.isciii.es/bitstreams/cbad955d-3918-441c-992f-89bdeaf48648/download File MD5 c2678855c9f20e6abdea9381923cb6dd 2078398 application/pdf ImpactLeftVentricularHypertrophy_2015.pdf URL https://repisalud.isciii.es/bitstreams/57248b80-dd91-405f-b9d4-bc7cfbabe874/download File MD5 809e2926c50913d9dc63ec3e85dee445 64514 text/plain ImpactLeftVentricularHypertrophy_2015.pdf.txt