Low homoarginine levels in the prognosis of patients with acute chest pain

Background The endogenous amino acid homoarginine predicts mortality in cerebro‐ and cardiovascular disease. The objective was to explore whether homoarginine is associated with atrial fibrillation (AF) and outcome in pa
Background The endogenous amino acid homoarginine predicts mortality in cerebro‐ and cardiovascular disease. The objective was to explore whether homoarginine is associated with atrial fibrillation (AF) and outcome in patients with acute chest pain.
Methods and Results One thousand six hundred forty‐nine patients with acute chest pain were consecutively enrolled in this study, of whom 589 were diagnosed acute coronary syndrome (ACS). On admission, plasma concentrations of homoarginine as well as brain natriuretic peptide (BNP), and high‐sensitivity assayed troponin I (hsTnI) were determined along with electrocardiography (ECG) variables. During a median follow‐up of 183 days, 60 major adverse cardiovascular events (MACEs; 3.8%), including all‐cause death, myocardial infarction, or stroke, were registered in the overall study population and 43 MACEs (7.5%) in the ACS subgroup. Adjusted multivariable Cox regression analyses revealed that an increase of 1 SD of plasma log‐transformed homoarginine (0.37) was associated with a hazard reduction of 26% (hazard ratio [HR], 0.74; 95% CI, 0.57–0.96) for incident MACE and likewise of 35% (HR, 0.65; 95% CI, 0.49–0.88) in ACS patients. In Kaplan–Meier survival curves, homoarginine was predictive for patients with high‐sensitivity assayed troponin I (hsTnI) above 27 ng/L (P<0.05). Last, homoarginine was inversely associated with QTc duration (P<0.001) and prevalent AF (OR, 0.83; 95% CI, 0.71–0.95).
Conclusion Low plasma homoarginine was identified as a risk marker for incident MACEs in patients with acute chest pain, in particular, in those with elevated hsTnI. Impaired homoarginine was associated with prevalent AF. Further studies are needed to investigate the link to AF and evaluate homoarginine as a therapeutic option for these patients.
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Metadaten
Author:Dorothee Atzler, Christina Baum, Francisco Ojeda, Till Keller, Kathrin Cordts, Renate B. Schnabel, Chi‐un Choe, Karl Johannes Lackner, Thomas Münzel, Rainer H. Böger, Stefan Blankenberg, Edzard Schwedhelm, Tanja Zeller
URN:urn:nbn:de:hebis:30:3-403277
DOI:http://dx.doi.org/10.1161/JAHA.115.002565
Parent Title (English):Journal of the American Heart Association
Publisher:New York, NY
Place of publication:American Heart Association
Document Type:Article
Language:English
Date of Publication (online):2016/04/13
Date of first Publication:2016/04/13
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2016/06/10
Tag:acute coronary syndrome; atrial fibrillation; homoarginine; l‐arginine:glycine amidinotransferase
Volume:5
Issue:e002565
Pagenumber:14
First Page:1
Last Page:14
Note:
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License http://creativecommons.org/licenses/by-nc/4.0/, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. 
HeBIS PPN:421413174
Institutes:Medizin
Dewey Decimal Classification:610 Medizin und Gesundheit
Sammlungen:Universitätspublikationen
Licence (English):License LogoCreative Commons - Namensnennung-Nicht kommerziell 4.0

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