Relationship between TRAIL and Left Ventricular Ejection Fraction in Patients with ST-Elevation Myocardial Infarction Treated with Primary Percutaneous Coronary Intervention
Language English Country United States Media electronic-ecollection
Document type Journal Article
PubMed
30112383
PubMed Central
PMC6077671
DOI
10.1155/2018/3709084
Knihovny.cz E-resources
- MeSH
- Biomarkers metabolism MeSH
- ST Elevation Myocardial Infarction physiopathology therapy MeSH
- Myocardial Infarction MeSH
- Percutaneous Coronary Intervention * MeSH
- Middle Aged MeSH
- Humans MeSH
- TNF-Related Apoptosis-Inducing Ligand metabolism MeSH
- Aged MeSH
- Drug-Eluting Stents MeSH
- Stroke Volume * MeSH
- Treatment Outcome MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Biomarkers MeSH
- TNF-Related Apoptosis-Inducing Ligand MeSH
- TNFSF10 protein, human MeSH Browser
BACKGROUND: Apoptosis plays an important role in the myocardial injury after acute myocardial infarction and in the subsequent development of heart failure. AIM: To clarify serum kinetics of apoptotic markers TRAIL and sFas and their relation to left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). METHODS: In 101 patients with STEMI treated with pPCI, levels of TRAIL and sFas were measured in series of serum samples obtained during hospitalization and one month after STEMI. LVEF was assessed at admission and at one month. Major adverse cardiovascular events (MACE, i.e., death, re-MI, and hospitalization for heart failure and stroke) were analysed during a two-year followup. RESULTS: Serum level of TRAIL significantly decreased one day after pPCI (50.5pg/mL) compared to admission (56.7pg/mL), subsequently increased on day 2 after pPCI (58.8pg/mL), and reached its highest level at one month (70.3pg/mL). TRAIL levels on days 1 and 2 showed a significant inverse correlation with troponin and a significant positive correlation with LVEF at baseline. Moreover, TRAIL correlated significantly with LVEF one month after STEMI (day 1: r=0.402, p<0.001; day 2: r=0.542, p<0.001). On the contrary, sFas level was significantly lowest at admission (5073pg/mL), increased one day after pPCI (6370pg/mL), and decreased on day 2 (5548pg/mL). Significantly highest sFas level was marked at one month (7024pg/mL). sFas failed to correlate with LVEF at baseline or at one month. Both TRAIL and sFas showed no ability to predict improvement of LVEF one month after STEMI or a 2-year MACE (represented by 3.29%). CONCLUSION: In STEMI treated with pPCI, TRAIL reaches its lowest serum concentration after reperfusion. Low TRAIL level is associated with worse LVEF in the acute phase of STEMI as well as one month after STEMI. Higher TRAIL level appears to be beneficial and thus TRAIL seems to represent a protective mediator of post-AMI injury.
See more in PubMed
Chen J., Hsieh A. F.-C., Dharmarajan K., Masoudi F. A., Krumholz H. M. National trends in heart failure hospitalization after acute myocardial infarction for medicare beneficiaries 1998-2010. Circulation. 2013;128(24):2577–2584. doi: 10.1161/CIRCULATIONAHA.113.003668. PubMed DOI PMC
Hung J., Teng T. K., Finn J., et al. Trends From 1996 to 2007 in Incidence and Mortality Outcomes of Heart Failure After Acute Myocardial Infarction: A Population-Based Study of 20 812 Patients With First Acute Myocardial Infarction in Western Australia. Journal of the American Heart Association. 2013;2(5):e000172–e000172. doi: 10.1161/JAHA.113.000172. PubMed DOI PMC
Abbate A., Biondi-Zoccai G. G. L., Bussani R., et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. Journal of the American College of Cardiology. 2003;41(5):753–760. doi: 10.1016/S0735-1097(02)02959-5. PubMed DOI
Baldi A., Abbate A., Bussani R., et al. Apoptosis and post-infarction left ventricular remodeling. Journal of Molecular and Cellular Cardiology. 2002;34(2):165–174. doi: 10.1006/jmcc.2001.1498. PubMed DOI
Olivetti G., Quaini F., Sala R., et al. Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving portion of the heart. Journal of Molecular and Cellular Cardiology. 1996;28(9):2005–2016. doi: 10.1006/jmcc.1996.0193. PubMed DOI
Wiley S. R., Schooley K., Smolak P. J., et al. Identification and characterization of a new member of the TNF family that induces apoptosis. Immunity. 1995;3(6):673–682. doi: 10.1016/1074-7613(95)90057-8. PubMed DOI
Suda T., Takahashi T., Golstein P., Nagata S. Molecular cloning and expression of the fas ligand, a novel member of the tumor necrosis factor family. Cell. 1993;75(6):1169–1178. doi: 10.1016/0092-8674(93)90326-L. PubMed DOI
Suliman A., Lam A., Datta R., Srivastava R. K. Intracellular mechanisms of TRAIL: Apoptosis through mitochondrial-dependent and -independent pathways. Oncogene. 2001;20(17):2122–2133. doi: 10.1038/sj.onc.1204282. PubMed DOI
Peter M. E., Krammer P. H. Mechanisms of CD95 (APO-1/Fas)-mediated apoptosis. Current Opinion in Immunology. 1998;10(5):545–551. doi: 10.1016/S0952-7915(98)80222-7. PubMed DOI
Secchiero P., Corallini F., Ceconi C., et al. Potential prognostic significance of decreased serum levels of TRAIL after acute myocardial infarction. PLoS ONE. 2009;4(2) doi: 10.1371/journal.pone.0004442.e4442 PubMed DOI PMC
Osmancik P., Teringova E., Tousek P., Paulu P., Widimsky P. Prognostic Value of TNF-Related Apoptosis Inducing Ligand (TRAIL) in Acute Coronary Syndrome Patients. PLoS ONE. 2013;8(2) doi: 10.1371/journal.pone.0053860.e53860 PubMed DOI PMC
Kawakami H., Shigematsu Y., Ohtsuka T., et al. Increased circulating soluble form of Fas in patients with dilated cardiomyopathy. Japanese Circulation Journal. 1998;62(12):873–876. doi: 10.1253/jcj.62.873. PubMed DOI
Tsutamoto T., Wada A., Maeda K., et al. Relationship between plasma levels of cardiac natriuretic peptides and soluble Fas: Plasma soluble fas as a prognostic predictor in patients with congestive heart failure. Journal of Cardiac Failure. 2001;7(4):322–328. doi: 10.1054/jcaf.2001.30134. PubMed DOI
Niessner A., Hohensinner P. J., Rychli K., et al. Prognostic value of apoptosis markers in advanced heart failure patients. European Heart Journal. 2009;30(7):789–796. doi: 10.1093/eurheartj/ehp004. PubMed DOI
Volpato S., Ferrucci L., Secchiero P., et al. Association of tumor necrosis factor-related apoptosis-inducing ligand with total and cardiovascular mortality in older adults. Atherosclerosis. 2011;215(2):452–458. doi: 10.1016/j.atherosclerosis.2010.11.004. PubMed DOI PMC
Anversa P., Cheng W., Liu Y., Leri A., Redaelli G., Kajstura J. Apoptosis and myocardial infarction. Basic Research in Cardiology. 1998;93(3, supplement):8–12. doi: 10.1007/s003950050195. PubMed DOI
Ferrari R., Guardigli G., Mele D., Percoco G. F., Ceconi C., Curello S. Oxidative stress during myocardial ischaemia and heart failure. Current Pharmaceutical Design. 2004;10(14):1699–1711. doi: 10.2174/1381612043384718. PubMed DOI
Steg P. G., James S. K., et al. Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC) ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Russian Journal of Cardiology. 2012;33(20):2569–619. PubMed
Feldman L. J., Mazighi M., Scheuble A., et al. Differential expression of matrix metalloproteinases after stent implantation and balloon angioplasty in the hypercholesterolemic rabbit. Circulation. 2001;103(25):3117–3122. doi: 10.1161/01.CIR.103.25.3117. PubMed DOI
Secchiero P., Gonelli A., Corallini F., Ceconi C., Ferrari R., Zauli G. Metalloproteinase 2 cleaves in vitro recombinant TRAIL: potential implications for the decreased serum levels of trail after acute myocardial infarction. Atherosclerosis. 2010;211(1):333–336. doi: 10.1016/j.atherosclerosis.2010.02.024. PubMed DOI
Ashkenazi A., Pai R. C., Fong S., et al. Safety and antitumor activity of recombinant soluble Apo2 ligand. The Journal of Clinical Investigation. 1999;104(2):155–162. doi: 10.1172/JCI6926. PubMed DOI PMC
Jo M., Kim T.-H., Seol D.-W., et al. Apoptosis induced in normal human hepatocytes by tumor necrosis factor- related apoptosis-inducing ligand. Nature Medicine. 2000;6(5):564–567. doi: 10.1038/75045. PubMed DOI
Li J. H., Kirkiles-Smith N. C., McNiff J. M., Pober J. S. Trail induces apoptosis and inflammatory gene expression in human endothelial cells. The Journal of Immunology. 2003;171(3):1526–1533. doi: 10.4049/jimmunol.171.3.1526. PubMed DOI
Ehrlich S., Infante-Duarte C., Seeger B., Zipp F. Regulation of soluble and surface-bound TRAIL in human T cells, B cells, and monocytes. Cytokine. 2003;24(6):244–253. doi: 10.1016/S1043-4666(03)00094-2. PubMed DOI
LeBlanc H. N., Ashkenazi A. Apo2L/TRAIL and its death and decoy receptors. Cell Death & Differentiation. 2003;10(1):66–75. doi: 10.1038/sj.cdd.4401187. PubMed DOI
Toffoli B., Bernardi S., Candido R., Zacchigna S., Fabris B., Secchiero P. TRAIL shows potential cardioprotective activity. Investigational New Drugs. 2012;30(3):1257–1260. doi: 10.1007/s10637-010-9627-8. PubMed DOI
Secchiero P., Candido R., Corallini F., et al. Systemic tumor necrosis factor-related apoptosis-inducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. Circulation. 2006;114(14):1522–1530. doi: 10.1161/circulationaha.106.643841. PubMed DOI
Hallén J., Jensen J. K., Fagerland M. W., Jaffe A. S., Atar D. Cardiac troponin I for the prediction of functional recovery and left ventricular remodelling following primary percutaneous coronary intervention for ST-elevation myocardial infarction. Heart. 2010;96(23):1892–1897. doi: 10.1136/hrt.2009.190819. PubMed DOI
Mayr A., Mair J., Klug G., et al. Cardiac troponin T and creatine kinase predict mid-term infarct size and left ventricular function after acute myocardial infarction: A cardiac MR study. Journal of Magnetic Resonance Imaging. 2011;33(4):847–854. doi: 10.1002/jmri.22491. PubMed DOI
Ohtsuka T., Hamada M., Sasaki O., et al. Clinical implications of circulating soluble Fas and Fas ligand in patients with acute myocardial infarction. Coronary Artery Disease. 1999;10(4):221–225. doi: 10.1097/00019501-199906000-00003. PubMed DOI
Soeki T., Tamura Y., Shinohara H., Sakabe K., Onose Y., Fukuda N. Relation between circulating soluble Fas ligand and subsequent ventricular remodelling following myocardial infarction. Heart. 2003;89(3):339–341. doi: 10.1136/heart.89.3.339. PubMed DOI PMC
Nilsson L., Szymanowski A., Swahn E., Jonasson L. Soluble TNF Receptors Are Associated with Infarct Size and Ventricular Dysfunction in ST-Elevation Myocardial Infarction. PLoS ONE. 2013;8(2) doi: 10.1371/journal.pone.0055477.e55477 PubMed DOI PMC
Risk Stratification of Patients with Acute Coronary Syndrome