Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
Index Copernicus  – 168.52
MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

Download original text (EN)

Advances in Clinical and Experimental Medicine

2018, vol. 27, nr 2, February, p. 185–191

doi: 10.17219/acem/64464

Publication type: original article

Language: English

Download citation:

  • BIBTEX (JabRef, Mendeley)
  • RIS (Papers, Reference Manager, RefWorks, Zotero)

Oxidative stress markers predict early left ventricular systolic dysfunction after acute myocardial infarction treated with primary percutaneous coronary intervention

Dubravka Rajic1,A,B,C,D, Ivica Jeremic2,3,A,B,C,D, Sanja Stankovic4,B,C,E, Olivera Djuric3,5,C,D, Tatjana Zivanovic-Radnic2,B, Igor Mrdovic1,3,C,E,F, Predrag Mitrovic1,3,A, Dragan Matic1,3,B, Zorana Vasiljevic3,E, Mihailo Matic3,A,E, Milika Asanin1,3,C,E,F

1 Cardiology Clinic, Clinical Centre of Serbia, Belgrade, Serbia

2 Institute of Rheumatology, Belgrade, Serbia

3 School of Medicine, University of Belgrade, Serbia

4 Center for Medical Biochemistry, Clinical Center of Serbia, Belgrade, Serbia

5 Institute of Epidemiology, Belgrade, Serbia

Abstract

Background. Despite successful primary percutaneous coronary intervention (PCI) after ST-segment elevation myocardial infarction (STEMI), some patients develop left ventricular systolic dysfunction (LVSD) and acute heart failure (HF). Identifying patients with an increased risk of developing LVSD by means of biomarkers may help select patients requiring more aggressive therapy.
Objectives. The aim of this study was to evaluate the relationship between the levels of oxidative stress markers and development of LVSD and acute HF early after STEMI.
Material and Methods. The study enrolled 148 patients with the first STEMI, who were treated by primary PCI < 12 h from the onset of symptoms. We assessed the impact of different biomarkers for developing LVSD and acute HF (Killip ≥ 2) including: markers of necrosis – peak creatine kinase (CK), markers of myocardial stretch – B-type natriuretic peptide (BNP), inflammatory markers – C-reactive protein (CRP), leucocyte and neutrophil count, as well as oxidative stress markers – total thiol groups, catalase, superoxide dismutase (SOD) and glutathione reductase (GR).
Results. In multivariate analysis, thiol groups, peak CK, anterior wall infarction, and age were predictors of LVEF ≤ 40%. Out of 16 variables significantly associated with the Killip ≥ 2 in univariate logistic regression analysis, 5 appeared to be independently associated with acute HF in multivariate analysis: catalase, BNP, leucocytes, neutrophil count, and size of left atrium.
Conclusion. In this study, we have shown for the first time that thiol groups and catalase are independent predictors of STEMI complication – LVSD and acute HF, respectively. Beside routine used biomarkers of necrosis and myocardial stretch, thiol groups and catalase may provide additional information regarding the risk stratification.

Key words

oxidative stress, heart failure, acute myocardial infarction, percutaneous coronary intervention, left ventricular systolic dysfunction

References (30)

  1. Hamdan A, Kornowski R, Solodky A, Fuchs S, Battler A, Assali AR. Predictors of left ventricular dysfunction in patients with first acute anterior myocardial infarction undergoing primary angioplasty. Isr Med Assoc J. 2006;8:532–535.
  2. Świątkiewicz I, Magielski P, Woźnicki M, et al. Occurrence and predictors of left ventricular systolic dysfunction at hospital discharge and in long-term follow-up after acute myocardial infarction treated with primary percutaneous coronary intervention. Kardiol Pol. 2012;70:329–340.
  3. Frangogiannis NG, Youker KA, Rossen RD, et al. Cytokines and the microcirculation in ischemia and reperfusion. J Mol Cell Cardiol. 1998; 30:2567–2576.
  4. McClements BM, Weyman AE, Newell JB, Picard MH. Echocardiographic determinants of left ventricular ejection fraction after acute myocardial infarction. Am Heart J. 2000;140:284–290.
  5. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart. Eur Heart J. 2012;33:1787–1847.
  6. Bayes-Genis A, Ordonez-Llanos J. Multiple biomarker strategies for risk stratification in heart failure. Clin Chim Acta. 2015;443:120–125.
  7. De Boer RA, Daniels LB, Maisel AS, Januzzi JL. State of the art: Newer biomarkers in heart failure. Eur J Heart Fail. 2015;17:559–569.
  8. Kundi H, Ates I, Kiziltunc E, et al. A novel oxidative stress marker in acute myocardial infarction; Thiol/disulphide homeostasis. Am J Emerg Med. 2015;33:1567–1571.
  9. Bagatini MD, Martins CC, Battisti V, et al. Oxidative stress versus antioxidant defenses in patients with acute myocardial infarction. Heart Vessels. 2011;26:55–63.
  10. Dieterich S, Bieligk U, Beulich K, Hasenfuss G, Prestle J. Gene expression of antioxidative enzymes in the human heart: Increased expression of catalase in the end-stage failing heart. Circulation. 2000;101: 33–39.
  11. Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33:2569–2619.
  12. Matetzky S, Novikov M, Gruberg L, et al. The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA. J Am Coll Cardiol. 1999;34:1932–1938.
  13. Sheehan FH, Braunwald E, Canner P, et al. The effect of intravenous thrombolytic therapy on left ventricular function: A report on tissue-type plasminogen activator and streptokinase from the Thrombolysis in Myocardial Infarction (TIMI Phase I) trial. Circulation. 1987;75:817–829.
  14. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1–39.
  15. Sedlak J, Lindsay RH. Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman’s reagent. Anal Biochem. 1968;25:192–205.
  16. Góth L. A simple method for determination of serum catalase activity and revision of reference range. Clin Chim Acta. 1991;196:143–151.
  17. Sun M, Zigman S. An improved spectrophotometric assay for superoxide dismutase based on epinephrine autoxidation. Anal Biochem. 1978;90:81–89.
  18. Hosmer DW, Hjort NL. Goodness-of-fit processes for logistic regression: Simulation results. Stat Med. 2002;21:2723–2738.
  19. Gaggin HK, Januzzi JL. Biomarkers and diagnostics in heart failure. Biochim Biophys Acta. 2013;1832:2442–2450.
  20. Bhave PD, Hoffmayer KS, Armstrong EJ, et al. Predictors of depressed left ventricular function in patients presenting with ST-elevation myocardial infarction. Am J Cardiol. 2012;109:327–331.
  21. Kadota K, Yui Y, Hattori R, Murohara Y, Kawai C. Decreased sulfhydryl groups of serum albumin in coronary artery disease. Jpn Circ J. 1991;55:937–941.
  22. Liu T, Schroeder HJ, Wilson SM, et al. Local and systemic vasodilatory effects of low molecular weight S-nitrosothiols. Free Radic Biol Med. 2016;91:215–223.
  23. Maron BA, Tang SS, Loscalzo J. S-nitrosothiols and the S-nitrosoproteome of the cardiovascular system. Antioxid Redox Signal. 2013;18: 270–287.
  24. Richards AM. B-type natriuretic peptides and ejection fraction for prognosis after myocardial infarction. Circulation. 2003;107:2786–2792.
  25. Talwar S, Squire IB, Downie PF, et al. Profile of plasma N-terminal proBNP following acute myocardial infarction; Correlation with left ventricular systolic dysfunction. Eur Heart J. 2000;21:1514–1521.
  26. Ben-Dor I, Haim M, Rechavia E, et al. Serum NT-proBNP concentrations in the early phase do not predict the severity of systolic or diastolic left ventricular dysfunction among patients with ST-elevation acute myocardial infarction. Angiology. 2007;57:686–693.
  27. Takahashi T, Hiasa Y, Ohara Y, et al. Relation between neutrophil counts on admission, microvascular injury, and left ventricular functional recovery in patients with an anterior wall first acute myocardial infarction treated with primary coronary angioplasty. Am J Cardiol. 2007;100:35–40.
  28. Warnatsch A, Ioannou M, Wang Q, Papayannopoulos V. Inflammation. Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis. Science. 2015;349:316–320.
  29. Ge L, Zhou X, Ji WJ, et al. Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow: Therapeutic potential of DNase-based reperfusion strategy. Am J Physiol Heart Circ Physiol. 2015;308:500–509.
  30. Pytel E, Olszewska-Banaszczyk M, Koter-Michalak M, Broncel M. Increased oxidative stress and decreased membrane fluidity in erythrocytes of CAD patients. Biochem Cell Biol. 2013;91:315–318.
© Wroclaw Medical University