Myotrophin is a 12 kDa protein initially isolated from hypertrophied hearts of spontaneously hypertensive rats and acts by modulating NF-κB (nuclear factor κB) activity. We have reported previously the presence of myotrophin in patients with human systolic heart failure; however, its role as a predictor of MACE (major adverse cardiac events) in patients with ACS (acute coronary syndrome) is unclear. In the present study, we sought to investigate this and compared myotrophin with NTproBNP (N-terminal pro-B-type natriuretic peptide), a marker of MACE. We studied 356 patients with ACS {276 men; mean age, 63.0±12.8 years; 80.6% STEMI [ST segment elevation MI (myocardial infarction)]; and 19.4% NSTEMI (non-STEMI)}. Blood measurement was made at 25–48 h 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 end point of death, MI or need for urgent revascularization. Over the median follow-up period of 355 (range 0–645) days, there were 28 deaths, 27 non-fatal MIs and 73 patients required urgent revascularization. Myotrophin was raised in patients with MACE compared with survivors [510.7 (116.0–7445.6) fmol/ml compared with 371.5 (51.8–6990.4) fmol/ml respectively; P=0.001; values are medians (range)]. Using a Cox proportional hazards model, myotrophin {HR (hazard ratio), 1.64 [95% CI (confidence interval), 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. A 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). In conclusion, after an ACS, levels of myotrophin are more informative at predicting MACE than NTproBNP and may be useful to risk stratify patients.
Skip Nav Destination
Article navigation
February 2007
-
Cover Image
Cover Image
- PDF Icon PDF LinkTable of Contents
Research Article|
January 17 2007
Myotrophin is a more powerful predictor of major adverse cardiac events following acute coronary syndrome than N-terminal pro-B-type natriuretic peptide
Sohail Q. Khan;
1Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, U.K.
Correspondence: Dr Sohail Q. Khan (email [email protected]).
Search for other works by this author on:
Dominic Kelly;
Dominic Kelly
1Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, U.K.
Search for other works by this author on:
Paulene Quinn;
Paulene Quinn
1Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, U.K.
Search for other works by this author on:
Joan E. Davies;
Joan E. Davies
1Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, U.K.
Search for other works by this author on:
Leong L. Ng
Leong L. Ng
1Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, U.K.
Search for other works by this author on:
Publisher: Portland Press Ltd
Received:
July 18 2006
Revision Received:
August 23 2006
Accepted:
October 02 2006
Accepted Manuscript online:
October 02 2006
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2007
Clin Sci (Lond) (2007) 112 (4): 251–256.
Article history
Received:
July 18 2006
Revision Received:
August 23 2006
Accepted:
October 02 2006
Accepted Manuscript online:
October 02 2006
Citation
Sohail Q. Khan, Dominic Kelly, Paulene Quinn, Joan E. Davies, Leong L. Ng; Myotrophin is a more powerful predictor of major adverse cardiac events following acute coronary syndrome than N-terminal pro-B-type natriuretic peptide. Clin Sci (Lond) 1 February 2007; 112 (4): 251–256. doi: https://doi.org/10.1042/CS20060191
Download citation file:
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Biochemical Society Member Sign in
Sign InSign in via your Institution
Sign in via your InstitutionGet Access To This Article
Cited By
Open Access for all
We offer compliant routes for all authors from 2025. With library support, there will be no author nor reader charges in 5 journals. Check here |
![]() |