Key result
Peak plasma levels of NT-proBNP following STEMI correlated positively with myocardial damage assessed by late gadolinium enhancement (R = 0.46, P <0.001) and predicted major adverse cardiac events.
Why the study?
The relationship between NT-proBNP levels, myocardial damage assessed by cardiac magnetic resonance imaging, and clinical outcomes after STEMI had not been well defined.
Does peak NT-proBNP level predict the extent of myocardial damage and long-term MACE in patients with STEMI?
Cohort (n=75)
No
Does peak NT-proBNP level predict the extent of myocardial damage and long-term MACE in patients with STEMI?
Peak NT-proBNP levels at 24 hours post-STEMI correlate strongly with myocardial damage on CMR and predict long-term major adverse cardiovascular events.
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.
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Mathbout et al. (2020) conducted a cohort in ST-elevation myocardial infarction (n=75). Peak NT-proBNP level vs. Lower NT-proBNP levels was evaluated on Correlation of peak NT-proBNP with late gadolinium enhancement (LGE) on CMR (R = 0.46, p=<0.001). Peak plasma levels of NT-proBNP following STEMI correlated positively with myocardial damage assessed by late gadolinium enhancement (R = 0.46, P <0.001) and predicted major adverse cardiac events.
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