BACKGROUND AND HYPOTHESIS: The initial assessment of late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) reflects cardiac damage and is an important prognostic factor in patients with acute ST-elevation myocardial infarction (STEMI). N-Terminal prohormone of brain natriuretic peptide (NT-proBNP) is released following cardiomyocytes injury. However, the relationship between NT-proBNP levels, myocardial damage and clinical outcomes after STEMI has not been well defined. METHODS: Plasma levels of NT-proBNP, troponin I and creatinine kinase (CK) were assessed in 75 patients with STEMI. Echocardiography and CMR were performed prior to hospital discharge. Cardiac damage was quantified using peak biomarker levels and LGE. Patients were followed for a median of 975 days (IQR 823-1098 days) for major adverse cardiac events (MACE) (all-cause mortality, recurrent myocardial infraction, unplanned recurrent revascularization and recurrent hospitalization for heart failure). RESULTS: Plasma levels of NT-proBNP increased following STEMI to peak at 24 hours. The dynamic changes in plasma NT-proBNP were similar to those noted with troponin I and its delayed peak but not those observed with plasma CK levels. Peak NT-proBNP levels correlated positively with indices of myocardial damage such as peak troponin I (R2 =0.38, P <0.001), peak CK (R2 =0.22, P = 0.01) and LGE examination (R2 = 0.46, P <0.001). Peak plasma level of NT- proBNP was strongly predictive of MACE during the follow-up period. CONCLUSIONS: Peak levels of NT-proBNP following STEMI are predictive of the extent of myocardial damage and clinical outcomes. These results suggest an important prognostic role for NT-proBNP assessment in STEMI patients.
BACKGROUND AND HYPOTHESIS: The initial assessment of late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) reflects cardiac damage and is an important prognostic factor in patients with acute ST-elevation myocardial infarction (STEMI). N-Terminal prohormone of brain natriuretic peptide (NT-proBNP) is released following cardiomyocytes injury. However, the relationship between NT-proBNP levels, myocardial damage and clinical outcomes after STEMI has not been well defined. METHODS: Plasma levels of NT-proBNP, troponin I and creatinine kinase (CK) were assessed in 75 patients with STEMI. Echocardiography and CMR were performed prior to hospital discharge. Cardiac damage was quantified using peak biomarker levels and LGE. Patients were followed for a median of 975 days (IQR 823-1098 days) for major adverse cardiac events (MACE) (all-cause mortality, recurrent myocardial infraction, unplanned recurrent revascularization and recurrent hospitalization for heart failure). RESULTS: Plasma levels of NT-proBNP increased following STEMI to peak at 24 hours. The dynamic changes in plasma NT-proBNP were similar to those noted with troponin I and its delayed peak but not those observed with plasma CK levels. Peak NT-proBNP levels correlated positively with indices of myocardial damage such as peak troponin I (R2 =0.38, P <0.001), peak CK (R2 =0.22, P = 0.01) and LGE examination (R2 = 0.46, P <0.001). Peak plasma level of NT- proBNP was strongly predictive of MACE during the follow-up period. CONCLUSIONS: Peak levels of NT-proBNP following STEMI are predictive of the extent of myocardial damage and clinical outcomes. These results suggest an important prognostic role for NT-proBNP assessment in STEMI patients.
Authors: Charlotte Kragelund; Bjørn Grønning; Lars Køber; Per Hildebrandt; Rolf Steffensen Journal: N Engl J Med Date: 2005-02-17 Impact factor: 91.245
Authors: D A Morrow; E M Antman; A Charlesworth; R Cairns; S A Murphy; J A de Lemos; R P Giugliano; C H McCabe; E Braunwald Journal: Circulation Date: 2000-10-24 Impact factor: 29.690
Authors: M Mukoyama; K Nakao; K Hosoda; S Suga; Y Saito; Y Ogawa; G Shirakami; M Jougasaki; K Obata; H Yasue Journal: J Clin Invest Date: 1991-04 Impact factor: 14.808