Drs Meissner and Nef contributed equally to this article and should be both considered first authors.
Endogenous stress response in Tako-Tsubo cardiomyopathy and acute myocardial infarction
Article first published online: 9 MAR 2011
© 2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 41, Issue 9, pages 964–970, September 2011
How to Cite
Meissner, J., Nef, H., Darga, J., Kovacs, M., Weber, M., Hamm, C., Möllmann, H., Twerenbold, R., Reiter, M., Heinisch, C., Stelzig, C., Reichlin, T. and Mueller, C. (2011), Endogenous stress response in Tako-Tsubo cardiomyopathy and acute myocardial infarction. European Journal of Clinical Investigation, 41: 964–970. doi: 10.1111/j.1365-2362.2011.02487.x
- Issue published online: 3 AUG 2011
- Article first published online: 9 MAR 2011
- Received 10 September 2010; accepted 11 January 2011
- Acute myocardial infarction;
Eur J Clin Invest 2011; 41 (9): 964–970
Background As the clinical, electrocardiographic and laboratory presentation of Tako-Tsubo cardiomyopathy (TTC) and acute myocardial infarction (AMI) is similar, both entities are in general only distinguishable by coronary angiography. The purpose of this study was to examine the endogenous stress response at presentation, quantified by the copeptin level, of patients with TTC and patients with AMI, as copeptin may be useful in the non-invasive differentiation between both diseases.
Methods We compared the endogenous stress response at initial presentation, quantified by the plasma copeptin levels, in 21 consecutive patients finally diagnosed with TTC and 21 patients finally diagnosed with AMI matched for sex and time since chest pain onset.
Results The prevalence of cardiovascular risk factors and initial cardiac troponin T levels were comparable in TTC and AMI. Copeptin levels were significantly lower in patients with TTC when compared to patients with AMI (median 4·8 [interquartile range, IQR 3·5–13·5] pM vs. 25·6 [IQR 12·1–63·9] pM, P = 0·002). The accuracy for diagnosing TTC as quantified by the area under the receiver operating characteristics curve was significantly higher for copeptin than for cardiac troponin T (0·782 vs. 0·549, P = 0·031). The optimal cut-off value for differentiation between TTC and AMI was found at a copeptin level of 7·8 pM (sensitivity 67% at a specificity of 86%, negative predictive value 72%, positive predictive value 82%).
Conclusions The endogenous stress response, quantified by a novel sensitive biomarker, seems to be different in patients with TTC and AMI. Copeptin levels may be helpful in the non-invasive differentiation between TTC and AMI.