Abstract 17995: NT-proBNP Predicts Myocardial Damage and Correlates With Stem Cell Mobilization in Patients With ST-Eelevation Myocardial Infarction

Abstract

Introduction: N-Terminal prohormone of brain natriuretic peptide (NT-proBNP) is released from cardiomyocytes during injury. However, the relationship between plasma levels, extent of myocardial damage and its correlation with bone marrow stem cell (BMSC) mobilization are poorly understood. Methods: Plasma levels of NT-proBNP (pg/ml), troponin I (ng/ml) and CK (IU/L) were assessed in 76 patients with ST-elevation myocardial infarction (STEMI) at baseline (time of successful primary percutaneous intervention) then at 6, 12, 24, and 48-hour intervals. Levels of circulating Lin-/CD45- cells that are positive for CXCR4, CD34 and CD133 (BMSCs) were examined at the same time points using flow cytometry. Echocardiography and cardiac MRI (CMR) were performed prior to hospital discharge for assessment of cardiac function and scar size. Extent of myocardial damage was quantified using peak biomarker levels and gadolinium enhancement on CMR. Results: Patients characteristics were consistent with the typical demographics for STEMI population (Panel A). Plasma levels of NT-proBNP increased steadily following STEMI to peak at 24 hours (Panel B). Peak NT-proBNP levels correlated positively with indices of myocardial damage such as peak troponin I (r=0.6, P<0.001), peak CK (r=0.3, P=0.04) and late gadolinium enhancement on CMR examination (r=0.54, P=0.02) (Panels C-E). NT-proBNP levels correlated negatively with left ventricular ejection fraction and volume on echocardiography and CMR. There was strong correlation between peak NT-proBNP levels and peak numbers of circulating BMSCs such as Lin-/CD45-/CXCR4+ BMSCs (r=0.6, P<0.001) (Panel F). Conclusion: Peak levels of NT-proBNP following STEMI are predictive of the extent of myocardial damage quantified by cardiac biomarkers or CMR. NT-proBNP levels are also associated with the extent of BMSC release, raising the possibility that it has a role in initiating the myocardial reparative process following STEMI.