In addition, there was no difference even in patients with side effects, suggesting that this possible increase in adenosine level did not lead to AF susceptibility.. and tissue Doppler imaging. Results Baseline characteristics such as age, sex, heart rate, blood pressure, and laboratory parameters were almost the same in the ticagrelor and clopidogrel groups. The statistical analysis showed no significant difference in P wave dispersion (PWD) between ticagrelor and clopidogrel groups (40.98 12 ms versus 40.06 12 ms, P = 0.304). Subgroups analysis according to ACS types also showed no significant difference in PWD (NSTEMI: 41.16 13.8 ms versus 40.76 13.55 ms, P = 0.799; STEMI: 40.9 12.62 ms versus 39.19 11.18 ms, P = 0.132). In addition, we did not find significant difference in atrial electromechanical delay (EMD) with tissue Doppler imaging (interatrial EMD 24.11 3.06 ms versus 24.46 3.23 ms, P = 0.279). Conclusion In conclusion, we did not find any difference in detailed electrocardiographic and echocardiographic parameters as AF predictors between ticagrelor and clopidogrel groups in patients with ACS. strong class=”kwd-title” Keywords: Acute coronary syndrome, atrial fibrillation, ticagrelor 1. Introduction Acute coronary syndromes (ACS) are one of the major causes of mortality and morbidity worldwide. Current guidelines recommend dual antiplatelet therapy in patients with ACS [1,2]. Ticagrelor, one of the relatively new drugs used in ACS, is usually a reversible and direct-acting oral antagonist of adenosine diphosphate receptor P2Y12, and it was found superior over clopidogrel in the PLATO trial [3]. Although the benefit of ticagrelor has been attributed mostly to its faster, greater, and Phloretin (Dihydronaringenin) more consistent P2Y12 inhibition compared to clopidogrel, continuity of growing benefits of ticagrelor and its effect on reduction of cardiovascular mortality ARF3 in the PLATO trial make it different from Phloretin (Dihydronaringenin) other P2Y12-ADP receptor blockers [3C5]. These differences led to the hypothesis that ticagrelor has pleiotropic properties and nonplatelet directed mechanisms of action. These effects of ticagrelor have been mostly attributed to increased half-life and plasma concentration of adenosine [6,7]. Adenosine is usually a purine nucleoside primarily produced by endothelial cells [8] and it has a number of effects, such as coronary vasodilatation [9], inhibition of platelet aggregation [10], modulation of inflammation [11], reduced ischemia/reperfusion injury [12,13], and reduced atrioventricular conduction [14]. Besides some positive effects, it is also known that adenosine has the potential to cause atrial fibrillation (AF) [15C17]. In addition, there is a case report in the literature suggesting that ticagrelor could cause AF, a possible mechanism of which is usually increased plasma adenosine level [18]. However, there are no studies in the literature investigating the risk of AF in patients treated with ticagrelor. In this study, we aimed to determine whether ticagrelor predisposes to AF in ACS patients by using surrogate electro and echocardiographic parameters. 2. Materials and methods This cross-sectional study was conducted between January 2016 and February 2017 on patients diagnosed with ACS, which consists of ST elevated myocardial infarction (STEMI) and non-ST elevated myocardial infarction (NSTEMI). STEMI is usually defined as having a typical angina that continues 20 min or longer and with STEMI criteria in ECG [2]. Non-ST-elevation myocardial infarction is usually defined as a rise in troponin level (troponin-I 0.06 ng/mL) with common chest pain without STEMI criteria in ECG [1]. The treatment of the patients was arranged in line with the European Society of Cardiology guidelines. Patients were given 180 mg ticagrelor as the Phloretin (Dihydronaringenin) loading dose in the ticagrelor group. Angiotensin converting enzyme inhibitors, beta blockers, and statins were started in all Phloretin (Dihydronaringenin) patients without contraindication within the first 24 h after diagnosis. Patients were treated with percutaneous coronary intervention (stent implantation or balloon angioplasty). Patients who needed coronary bypass surgery were not included in the study. The other exclusion criteria were as follows: atrial infarction diagnostic criteria described by Liu et al. [19], a history of AF, use of antiarrhythmic drug other than beta-blockers, renal dysfunction (creatinine 1.5 mg/dL), severe valvular heart disease, permanent.