Dynamics of Heart Failure Markers in Patients after Past Myocardial Infarction with the Use of Potassium and Magnesium Salts of Gluconic Acid, Eplerenone and Rivaroxaban

N. V. Savchuk, I. P. Vakaliuk

Abstract


The objective of the research was to increase the efficiency of treatment of patients with chronic heart failure (CHF) and post-infarction cardiosclerosis by adding potassium and magnesium salts of gluconic acid, eplerenone and rivaroxaban to the background therapy taking into account the indices of growth differentiation factor 15 (GDF-15), aldosterone and galectin-3. 

Materials and methods of the research. Emmunoenzymometric determination of the galectin-3, GDF-15 and aldosterone levels concentration in blood serum was conducted to achieve the stated objective. 42 patients with CHF and post-infarction cardiosclerosis after coronary artery stenting in the acute period of myocardial infarction (MI) were examined. The patients were randomized into four groups according to the peculiarities of treatment. Group I included patients with CHF and post-infarction cardiosclerosis treated with the background therapy (BT). Group II consisted of patients with CHF who were treated with BT and addition of potassium and magnesium salts of gluconic acid. Group III included patients with CHF who were prescribed eplerenone secondary to BT. Group IV consisted of patients who were treated with BT and rivaroxaban. 

Results. The proposed treatment regimens were proved to be effective in reduction of GDF-15, aldosterone and galectin-3 indices in 12 months of treatment. Conducted therapy with the use of rivaroxaban secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone on the background of BT. This index constituted (2110.21±107.4) pg/ml before the treatment in these patients and significantly decreased to (1286.75±109.6) pg/ml being significantly before the therapy. The performed treatment with the use of eplerenone secondary to BT was proved to be more effective for normalization of aldosterone and galectin-3 levels in blood serum compared to other studied treatment regimens. The average value of aldosterone changed in the treatment process by 67.24%. Thus, the average level of this index constituted (139.8±7.63) pg/ml before the treatment and was equal to (45.8±5.52) pg/ml at the end of the treatment course. The average value of galectin-3 in patients with CHF and post-infarction cardiosclerosis was noted to be (34.69±1.67) ng/ml before the treatment. It constituted (22.53±0.98) ng/ml after the end of treatment being significantly lower compared to the value before the treatment. The average value of this index changed in the course of twelve-month treatment by 35.05%. Lower risk of sudden cardiac arrest (SCA), acute coronary syndrome (ACS) and stroke was observed in the patients with CHF and post-infarction cardiosclerosis with the use of rivaroxaban secondary to BT.

Conclusions. Thus, the use of rivaroxaban combination therapy secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone. Conducted therapy with the use of eplerenone on the background of BT was more effective for the normalization of galectin-3 and aldosterone levels in the blood compared to other studied treatment regimens.


Keywords


heart failure; growth differentiation factor 15; galectin-3; eplerenone; rivaroxaban

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References


Voronkov LH. The way of patients with chronic heart failure: as long as possible as more comfortable. Sertseva nedostatnist. 2014;1:7–10

Lakomkin SV, Skvortsov AA, Goryunova TV, et al. Galektin-3 - new marker of diagnosis and prognosis of chronic heart failure. Kardiolohiya. 2012;3:45–52

Voronkov LH, Amosova KM, Bahrii AE, et al. Recommendations for the diagnosis and treatment of chronic heart failure. Kyiv: 2012. 106p

Ahmad T, Fiuzat M, Neely B, et al. Biomarkers of Myocardial Stress and Fibrosis as Predictors of Mode of Death in Patients with Chronic Heart Failure. JACC: Heart Failure. 2014;2(3):260–268. DOI: http://doi.org/10.1016/j.jchf.2013.12.004

De Filippi CR, Felker GM. Galectin-3 in heart failure - linking fibrosis, remodelling and progression. Eur. Cardiol. 2010;6:33–36. DOI: http://doi.org/10.15420/ecr.2010.6.2.33

De Filippi CR, Felker GM. Galectin-3 in heart failure linking fibrosis, remodeling, and progressioіn. US. Cardiol. 2010;7(1):67–70. DOI: http://doi.org/10.15420/ecr.2010.6.2.33

Scabbia EV, Scabbia L. The cardio-renal syndrome (CRS). Metabolic Endocrine. 2015;9:1–4. DOI: http://doi.org/10.1016/j.ijcme.2014.10.013

Stahrenberg R, Edelmann F, Mende M. The novel biomarker growth differentiation factor-15 in heart failure with normal ejection fraction. Eur. J. Heart Fail. 2010;12:1309–1316. DOI: http://doi.org/10.1093/eurjhf/hfq151 [PMCid: PMC2990410][PMid: 20837635]

Silva D. Multimarker approach in risk stratification of patients with acute coronary syndromes: towards the ideal stratification. Rev. Port. Cardiol. 2014;33:137–138. DOI: http://doi.org/10.1016/j.repc.2014.02.001 [PMid: 24680557]

Tanai E, Frantz S. Pathophysiology of Heart Failure. Compr. Physiol. 2016;6(1):187–214

ThygesenK, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation. 2012;126:2020–2035. DOI: http://doi.org/10.1161/CIR.0b013e31826e1058 [PMid: 22923432]

Wollert KC, Kempf T. GDF-15 in heart failure: providing insight into end-oegan dysfunction and its recovery? European Heart Journal. 2012;14:1191–1193. DOI: http://doi.org/10.1093/eurjhf/hfs158 [PMid: 23047420]

Wollert KC, Kempf T. Growth differentiation factor-15 in heart failure: an update. Curr. Heart Fail. Rep. 2012;9:337–345. DOI: http://doi.org/10.1007/s11897-012-0113-9 [PMid: 22961192]

Wollert KC, Kempf T, Peter T, et al. Prognostic Value of Growth Differentiation Factor-15 in Patients with Non-ST-Elevation Acute Coronary Syndrome. Circulation. 2007;115:962–971. DOI: http://doi.org/10.1161/CIRCULATIONAHA.106.650846 [PMid: 17283261]

Xu J. GDF15/MIC-1 functions as a protective and anti-hypertrophic factor released from the myocardium in association with SMAD protein activation. Circulation Research. 2006;98(3):342–350. DOI: http://doi.org/10.1161/01.RES.0000202804.84885.d0 [PMid: 16397142]




DOI: http://dx.doi.org/10.21802/acm.2017.1.10

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