7 Original article Folia Med. Fac. Med. Univ. Saraeviensis 2018; 53(1): 7-11 foliamedica.mf.unsa.ba Serum aldosterone as a predictor of heart rhythm disorders in acute myocardial infarction Nerma Resić 1 , Mirza Dilić 2 , Azra Durak-Nalbantić 1 , Alen Džubur 1 , Enisa Hodžić 1 , Nina Hadžibegić 1 , Marina Vučiak-Grgurević 1 , Edin Begić 3 1 Clinic of Heart, Blood Vessel and Rheumatic Diseases, Clinical Center University of Sarajevo, Sarajevo, Bosnia and Herzegovina 2 Faculty of Medicine, University of Sarajevo, Sarajevo, Bosnia and Herzegovina 3 Cardiology Department, General Hospital «Prim.dr. Abdulah Nakas», Sarajevo, Bosnia and Herzegovina *Corresponding author Nerma Resic, MD, PhD, Clinic of Heart, Blood Vessel and Rheumatic Diseases, Clinical Center University of Sarajevo, Bolnička 25, Sarajevo, Bosnia and Herzegovina. ORCID ID: https://www.orcid.org: 0000-0002-8499-457X. Email: resicnerma@yahoo.com. Abstract Introduction: In addition to the fastest reperfusion procedure of coronary arteries blood fow, identifcation of patients with increased risk of early and late complications is of the utmost importance in acute myocardial infarction (AMI). Methods: We included total of 207 patients in the acute phase of myocardial infarction, which were divided into two groups, 127 patients without clinical symptoms of heart failure (HF) and 60 patients with HF symptoms. For all patients serum al- dosterone levels were determined 24 hours after acute MI. Results: In the group of decompensated patients, changes in aldosterone level did not show a statistically signifcant efect on paroxysmal supraventricular tachycardia (PSVT) occurrence (p > 0.05), while in the group of compensated patients there is statistically signifcant efect on PSVT occurrence (p =0.004). Changes in aldosterone level in the group of decompensated (p=0,030) and compensated patients (p=0,024), showed statis- tically signifcant infuence on the ventricular tachycardia (VT) occurrence. In the group of compensated patients, changes in aldosterone level showed a statistically signifcant efect on ven- tricular fbrillation (VF) occurrence (p = 0.024). Conclusion: Plasma aldosterone level in patients with acute myocardial infarction has a signifcant infuence on the occur- rence of cardiac rhythm disorders irrespective of the existence of cardiac decompensation. Keywords: aldosterone, myocardial infarction, prediction. © 2018 Folia Medica Facultatis Medicinae Universitatis Saraeviensis. All rights reserved. Introduction Immediately after the onset of myocardial infarction (MI), and in response to the infarct-related coronary artery patency we can expect higher likelihood of he- modynamic changes, neurohumoral activity, includ- ing renin-angiotensin-aldosteron (RAAS) activation, sympathetic nervous system and growth of natriuretic peptide production occurs [1, 2]. Neurohumoral acti- vation in cardiac output in post-infarction period is the pivotal role of aldosterone in the genesis of myocardial and vascular tissue damage [3]. Many organs (heart, blood vessels, β-pancreatic cells, glomerular mesangial cells) have mineralocorticoid receptors (MR) that re- spond to the efects of aldosterone, these efects include the activation of the κB (NF-κB) nucleic factor leading to oxidative stress, infammation, apoptosis and fbrosis [4, 5, 6, 7, 8]. With increase of aldosterone levels in systemic circulation, tissue (local) RAAS is involved in the processes of fbrosis, hypertrophy and blood vessel remodelling, as well as heart and kidney microangiop- athy development, ultimately resulting in damage to these organs [9]. Aldosterone has a number of prov- en adverse efects on the cardiovascular system, where the mechanisms by which some of these efects are achieved are still unresolved and are subject of ongoing studies. It has been considered that aldosterone increas- es sympathetic activity by decreasing the intake of nor- epinephrine into cardiac muscle [10]. It is considered that aldosterone may induce arrhythmia by alteration in electrolyte homeostasis (by combination of Mg2+ and K+ depletion, increased Na+ infux and Na/K pump activity), induction of autonomic dysfunction, potentiation of catecholamine efects, by slowing down the entry of epinephrine into the myocardium, im- pairment of baroreceptor function and potentiation of myocardial fbrosis [11, 12]. It also inhibits the me- tabolism of norepinephrine, which increases the risk of arrhythmias [13]. Aldosterone has been already ob-