Yu.A. DYLEVA¹, O.V. GRUZDEVA^1,2, E.G. UCHASOVA¹, V.V. KASHTALAP^1,2

 ¹ Scientific and Research Institute for Complex Problems of Cardiovascular Diseases, 6 Sosnovy boulevard Str., Kemerovo, Russian Federation, 650002

² Kemerovo State Medical University of the Ministry of Health of the Russian Federation, 22a Voroshilova Str., Kemerovo, Russian Federation, 650056

 Dyleva Yu.A. — Ph. D. (medicine), Research Associate of the Laboratory for Research of Homeostasis, tel. +7 (3842) 64-05-53, email: [email protected]

Gruzdeva O.V. — D. Sc. (medicine), Head of the Laboratory for Research of Homeostasis, Associate Professor of the Department of Pathological Physiology, Medical and Clinical Biochemistry, tel. +7 (3842) 64-05-53, email: [email protected]

Uchashova E.G. — Ph. D. (medicine), Senior Research Associate of the Laboratory for Research of Homeostasis, tel. +7 (3842) 64-05-53, email: [email protected]

Kashtalap V.V. — D. Sc. (medicine), Head of the Laboratory of Pathophysiology, Associate Professor of the Department of Cardiology and Cardiovascular Surgery, tel. +7 (3842) 64-31-53, email: [email protected]o.ru

 The work is devoted to assessing the level of ST2 in the dynamics of the hospital period and the study of its relationship with the development of early complications of myocardial infarction (MI).

Material and methods. The study included 88 patients with MI at the age of 59±8,36 years. On the 1st and 12th days of the development of the disease in the serum, the content of ST2 and NT-proBNP was determined using the enzyme immunoassay method. The control group consisted of 30 people. Statistical data processing was performed using the software package STATISTICA 6.1. and SPSS 17.0 for Windows.

Results. The level of ST2 and NT-proBNP in patients with hospital complications of MI was 3,7 and 1,8 times, respectively, higher than the control group on day 1 and higher, compared to the group of patients with a favorable course of MI in 2 and 6,8 times, respectively. By the 12th day, the content of ST2 decreased, and NT-proBNP remained elevated in both study groups. Logistic regression analysis showed a high diagnostic value for determining the level of ST2 (OR 1,7; 95% CI (1,6–2,8) AUC is 0,78, p=0,003) compared to NT-proBNP (OR 1,2; 95% CI (1,1–1,6) AUC is 0,69, p=0,034) in assessing the development of hospital complications of MI. The combined use of these markers increased the diagnostic sensitivity and specificity (OR 1,92; 95% CI (1,7–3,2) AUC is 0,89, p=0,004).

The conclusion. A more sensitive indicator of the course of the hospital period of MI is the level of ST2, compared with NT-proBNP. High diagnostic sensitivity and specificity of the combined use of ST2 and NT-proBNP were revealed.

Key words: stimulating growth factor ST2, N-terminal pro-brain natriuretic peptide (NT-proBNP), myocardial infarction, hospital complications of myocardial infarction, prognosis of myocardial infarction, risk stratification.

 (For citation: Dyleva Yu.A., Gruzdeva O.V., Uchashova E.G., Kashtalap V.V. Stimulating growth factor ST2 – a new marker of risk stratification of hospital complication of myocardial infarction. Practical Medicine. 2018)

REFERENCES

1. Lupon J., de Antonio M., Galan A. et al. Combined use of the novel biomarkers high-sensitivity troponin T and ST2 for heart failure risk stratification vs conventional assessment. Mayo Clin Proc, 2013, no. 88 (3), rr. 234–243. DOI: 10.1016/j.mayocp.2012.09.016.
2. Savic-Radojevic A., Pljesa-Ercegovac M., Matic M. et al. Novel Biomarkers of Heart Failure. Adv Clin Chem, 2017, no. 79, rr. 93–152. DOI: 10.1016/bs.acc.2016.09.002.
3. Braunwald E. Biomarkers in heart failure. New Engl. J. Med, 2008, no. 358, pp. 2148–2159.
4. Pascual-Figal D.A., Januzzi J.L. The biology of ST2: the International ST2 Consensus Panel. Am J Cardiol, 2015, no. 115 (7 Suppl), rr. 3B–7B. DOI: 10.1016/j.amjcard.2015.01.034.
5. Ho J.E., Sritara P., de Filippi C.R. et al. Soluble ST2 testing in the general population. Am J Cardiol, 2015, no. 115 (7 Suppl), rr. 22B–25B. DOI: 10.1016/j.amjcard.2015.01.036.
6. Gravning J., Smedsrud M.K., Omland T. et al. Sensitive troponin assays and N-terminal pro-B-type natriuretic peptide in acute coronary syndrome: prediction of significant coronary lesions and long-term prognosis. Am. Heart J, 2013, no. 165 (5), rr. 716–724. DOI: 10.1016/j.ahj.2013.02.008.
7. Ciccone M.M., Cortese F., Gesualdo M. et al. A Novel Cardiac Bio-Marker: ST2: A Review. Molecules, 2013, no. 18, rr. 15314–15328. DOI: 10.3390/molecules181215314.
8. Maries L., Manitiu I. Diagnostic and prognostic values of B-type natriuretic peptides (BNP) and N-terminal fragment brain natriuretic peptides (NT-pro-BNP). Cardiovasc J Afr, 2013, no. 7, rr. 286–289. DOI: 10.5830/CVJA-2013-055.
9. Chackerian A.A., Oldham E.R., Murphy E.E. et al. IL-1 receptor accessory protein and ST2 comprise the IL-33 receptor complex. J Immunol, 2007, no. 179 (4), rr. 2551–2555.
10. Felker G.M., Fiuzat M., Thompson V. et al. Soluble ST2 in ambulatory patients with heart failure association with functional capacity and long-term qutcomes. Circ Heart Fail, 2013, no. 6, rr. 1172–1179. DOI: 10.1161/CIRCHEARTFAILURE.113.000207.
11. Shimpo M., Morrow D.A., Weinberg E.O. et al. Serum levels of the interleukin-1 receptor family member ST2 predict mortality and clinical outcome in acute myocardial infarction. Circulation, 2004, no. 109, rr. 2186–2190. DOI: 10.1161/01.CIR.0000127958.21003.5A.
12. Skali H., Gerwien R., Meyer T.E. et al. Soluble ST2 and Risk of Arrhythmias, Heart Failure, or Death in Patients with Mildly Symptomatic Heart Failure: Results from MADIT-CRT. J Cardiovasc Transl Res, 2016, no. 5–6, rr. 421–428. DOI: 10.1007/s12265-016-9713-1.
13. Willems S., Sels J.W., Flier S. et al. Temporal changes of soluble ST2 after cardiovascular interventions. Eur J Clin Invest, 2013, no. 43 (2), rr. 113–120. DOI: 10.1111/eci.12022.
14. O’ Donoghue M.L., Morrow D.A., Cannon C.P. et al. Multimarker Risk Stratification in Patients With Acute Myocardial Infarction. J Am Heart Assoc, 2016, no. 5 (5), rr. E002586. DOI: 10.1161/JAHA.115.002586.
15. Maisel A.S., Di Somma S. Do we need another heart failure biomarker: focus on soluble suppression of tumorigenicity 2 (sST2). Eur Heart J, 2016, no. 0, pp. 1-9. DOI: 10.1093/eurheartj/ehw462.
16. Aimo A., Vergaro G., Ripoli A. et al. Meta-analysis of soluble suppression of tumorigenicity-2 and prognosis in acute heart failure. JACC Heart Fail, 2017, №5 (4), rr. 287–296. DOI: 10.1016/j.jchf.2016.12.016.
17. He Q., Wang D., Yang X. et al. Inducible regulation of human brain natriuretic peptide promoter in transgenic mice. Am J Physiol Heart Circ Physiol, 2001, no. 280, rr. 368–376.
18. Mathewkutty S., Sethi S.S., Aneja A. et al. Biomarkers after risk stratification in acute chest pain (from the BRIC Study). Am. J. Cardiol, 2013, no. 111 (4), rr. 493–498. DOI: 10.1016/j.amjcard.2012.10.032.
19. Kakkar R., Lee R.T. The IL-33/ST2 pathway: therapeutic target and novel biomarker. Nat Rev Drug Discov, 2008, no. 7, rr. 827–840. DOI: 10.1038/nrd2660.
20. Sabatine M.S., Morrow D.A., Higgins L.J. et al. Complementary roles for biomarkers of biomechanical strain ST2 and N-terminal prohormone B-type natriuretic peptide in patients with ST-elevation myocardial infarction. Circulation, 2008, no. 117, rr. 1936–1944. DOI: 10.1161/CIRCULATIONAHA.107.728022.
21. Dyleva Yu.A., Gruzdeva O.V., Akbasheva O.E. et al. Physiological and Pathophysiological Role of Stimulating Growth Factor ST2. Klinicheskaya laboratornaya diagnostika, 2017, vol. 62, no. 10, pp. 599–605 (in Russ.).
22. Sanada S., Hakuno D., Higgins L.J. et al. IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system. J. Clin. Invest, 2007, no. 117, rr. 1538–1549. DOI: 10.1172/JCI30634.
23. Mueller T., Jaffe A.S. Soluble ST2-analytical considerations. Am J Cardiol, 2015, no. 115 (7), rr. 8B–21B. DOI: 10.1016/j.amjcard.2015.01.035.