Universität zu Köln

Hortmann, M., Robinson, S., Mohr, M., Haenel, D., Mauler, M., Stallmann, D., Reinoehl, J., Duerschmied, D., Peter, K., Bode, C. and Ahrens, I. (2017). Circulating HtrA2 as a novel biomarker for mitochondrial induced cardiomyocyte apoptosis and ischemia-reperfusion injury in ST-segment elevation myocardial infarction. Int. J. Cardiol., 243. S. 485 - 492. CLARE: ELSEVIER IRELAND LTD. ISSN 1874-1754

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Abstract

Background: Ischemia-reperfusion (I/R) injury in ST-segment elevation myocardial infarction (STEMI) significantly contributes to overall myocardial damage. As a consequence of I/R injury in the heart, the hightemperature requirement protein A2 (HtrA2) is released from the mitochondrial intermembrane space of cardiomyocytes to the cytoplasm, whereupon it induces apoptosis. Methods: Serum was obtained from STEMI (n = 37), non-ST-segment elevation myocardial infarction (NSTEMI) (n = 20), stable coronary artery disease (CAD) (n = 17) and patients with CAD excluded (n = 9). In STEMI, I/R injury was assessed via measurement of ST-segment resolution. Results: HtrA2 was significantly increased in STEMI compared to NSTEMI, stable CAD and patients with CAD excluded (981.3 (IQR: 543.5-1526.2) pg/mL vs. 494.5 (IQR: 413.8-607) pg/mL vs. 291 (IQR: 239-458.5) pg/mL vs. 692.2 (IQR: 276.6-964.7) pg/mL; p <= 0.0001). STEMI patients with HtrA2 level of at least the median or above had a higher peak creatine kinase (CK) (p = 0.0002) and cardiac troponin T levels (cTnT) (p = 0.0019). Significantly more STEMI patients with HtrA2 levels of at least the median or above were identified as I/R injury (87% vs. 42%; p < 0.0001). Serum HtrA2 demonstrated a superior area under a curve in a receiver operating characteristic analysis for predicting I/R injury compared to CK, creatine kinase myocardial-band (CK-MB) and cTnT levels (AUC = 0.7105 vs. AUC = 0.5632 vs. AUC = 0.5660 vs. AUC = 0.5407 respectively). Conclusion: HtrA2 shows promise as a novel potential biomarker for mitochondrial-induced cardiomyocyte apoptosis and may help to identify I/R injury after STEMI. (C) 2017 Elsevier B.V. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Hortmann, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Robinson, S. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mohr, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Haenel, D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mauler, M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Stallmann, D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Reinoehl, J. UNSPECIFIED UNSPECIFIED UNSPECIFIED Duerschmied, D. UNSPECIFIED UNSPECIFIED UNSPECIFIED Peter, K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Bode, C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ahrens, I. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-217750
DOI:	10.1016/j.ijcard.2017.05.088
Journal or Publication Title:	Int. J. Cardiol.
Volume:	243
Page Range:	S. 485 - 492
Date:	2017
Publisher:	ELSEVIER IRELAND LTD
Place of Publication:	CLARE
ISSN:	1874-1754
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language PERCUTANEOUS CORONARY INTERVENTION; ISCHEMIA/REPERFUSION INJURY; CYTOCHROME-C; CELL-DEATH; DYSFUNCTION; TRIAL; OMI/HTRA2; HEART; CARDIOPROTECTION; CYCLOSPORINE Multiple languages Cardiac & Cardiovascular Systems Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/21775