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Abstract
Acute myocardial infarction (AMI) triggers the mobilization of stem/progenitor cells from bone marrow (BMSPCs) into peripheral blood (PB). N-Terminal prohormone of brain natriuretic peptide (NT-proBNP) is released from cardiomyocytes during injury. However, the relationship between NT- proBNP 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 72 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 BMSCs especially Lin- /CD45- cells that are positive for CXCR4, CD34 and CD133 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: Plasma levels of NT-proBNP increased steadily following STEMI to peak at 24 hours. 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 (DE) on CMR examination (r=0.54, P=0.02). There was strong correlation between peak NT-proBNP levels and peak numbers of circulating BMSCs such as Lin-/CD45-/CXCR4+ BMSCs. CD34+ cells counts correlate well with DE on CMR and poor clinical outcomes, while CD133 and KDR cells counts, which are reparatory cells did not correlate with DE on CMR but they could predict good clinical outcomes in these patientsI