Myotrophin is a more powerful predictor of major adverse cardiac events following acute coronary syndrome than N-terminal pro-B-type natriuretic peptide
Résumé
Myotrophin is a 12 kD protein initially isolated from hypertrophied hearts of spontaneously hypertensive rats and acts by modulating NF{kappa}B activity. We have reported the presence of myotrophin in patients with human systolic heart failure.However its role as a predictor of major adverse cardiac events (MACE) in patients with acute coronary syndrome (ACS) is unclear. We sought to investigate this and compared it to N-terminal pro B type natriuretic peptide (NTproBNP), a marker of MACE. We studied 356 ACS patients (276 men, mean age 63.0 ± 12.8 years, 80.8% STEMI, 19.2% NSTEMI). Blood measurement was made at 25-48hrs after the onset of chest pain.The plasma concentration of myotrophin and NTproBNP was determined using in-house non-competitive immunoassays. Patients were followed-up for the combined endpoint of death, MI or need for urgent revascularisation. Over the median follow up period of 355 days (range 0-645) there were 28 deaths, 27 non-fatal MI and 73 patients required urgent revascularisation. Myotrophin was raised in patients with MACE compared to survivors (Median [Range], fmol/ml, 510.7; [116.0-7445.6] vs. 371.5; [51.8-6990.4] fmol/ml; p=0.001). Using a Cox proportional hazards model myotrophin (HR 1.64, 95% CI: 0.97-2.76, p=0.05) and Killip class above 1 (HR 1.52, 95% CI: 0.93-2.42, p=0.10) were the only independent predictors of MACE. The Kaplan-Meier survival curve revealed a significantly better clinical outcome in patients with myotrophin below the median compared with those with myotrophin above the median (log rank 7.63, p=0.006). After an ACS, levels of myotrophin are more informative at predicting MACE than NTproBNP and may be useful to risk stratify patients.
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