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|Title:||Myotrophin is a more powerful predictor of major adverse cardiac events following acute coronary syndrome than N terminal pro B type natriuretic peptide|
|Authors:||Khan, Sohail Q.|
Quinn, Paulene A.
Davies, Joan E.
Ng, Leong L.
|Citation:||Clinical Science, 2007, 112(4), pp.251-6|
|Abstract:||Myotrophin is a 12 kD protein initially isolated from hypertrophied hearts of spontaneously hypertensive rats and acts by modulating NFκB 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.|
|Description:||This is the authors' final draft of the paper published as Clinical Science, 2007, 112(4), pp.251-256. The final published version is available from http://www.clinsci.org/cs/112/0251/cs1120251.htm|
|Appears in Collections:||Published Articles, Dept. of Cardiovascular Sciences|
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