jabbrv-ltwa-all.ldf jabbrv-ltwa-en.ldf Background and Aim: The relationship between SGLT-2 (sodium glucose cotransporter-2) inhibitors and atrial fibrillation (AF) recurrence is under investigation. The aim of this study was to investigate the effect of SGLT-2 inhibitors on AF recurrence in patients diagnosed with diabetes mellitus (DM) who underwent Direct Current Cardioversion (DCCV) in our clinic. Method: Consecutive DCCV was performed until to achieve 120 patients in SR (60 DM patients who used SGLT-2 inhibitors and 60 DM patients who did not use SGLT-2 inhibitors). Patients defined as SGLT-2 inhibitor user group and control group. The two groups were monitored for AF recurrence on the first day, then at one, three, and six months after CV. Result: During the six-months follow-up period, AF recurrence developed in 24 (40%) patients in SGLT-2 inhibitor group and in 35 (58.3%) of the control group, p= 0.04. In univariate analysis, AF duration, SGLT-2 inhibitor, left atrium diameter, and TAPSE value were significant parameters in terms of AF recurrence. In multivariate analysis, AF duration OR: 4.98; 95% CI (2.39-10.38), p< 0,001 and non-use of SGLT-2 inhibitors OR: 0.35; 95% CI (0.13-0.90), were found to be independent predictors for AF recurrence. Conclusion: AF recurrence ratio is significantly lower in patients using SGLT-2 inhibitors, in six-month follow-up period. AF duration was positive and SGLT-2 inhibitor using was negative independent predictors, for AF recurrence in DM patients.

Background: Previous studies have shown that the administration of continuous nitrate significantly affects the activity of hepatic cytochrome-P450. In this pilot study, we assess the impact of intravenous nitrate treatment on the antiplatelet effects of clopidogrel in patients with non-ST-elevation myocardial infarction (non-STEMI). Method: We included 20 non-STEMI patients: 15 in the nitrate group and five in the control group. All patients received a 300 mg acetylsalicylic acid and a 600 mg clopidogrel loading dose. The nitrate group was administered an intravenous glyceryl trinitrate infusion at 10 µg/min for 48 hours. The antiplatelet effect of clopidogrel was evaluated using the platelet-reactivity-unit (PRU) from the Verify-Now P2Y12 assay. Result: The PRU values at baseline and the 30 th, 60 th, 120 th minutes, and 48 th hour were similar between the two groups (p>0.05). However, PRU values at the 4 th and 6 th hours were significantly higher in the nitrate group than in the control group (274.1±53.9 vs. 162.4±39.9; p=0.002 and 272.0±67.0 vs. 185.6±18.1; p=0.03, respectively). Conclusion: The administration of intravenous nitrate treatment to acute coronary syndrome patients delayed the antiplatelet effect of clopidogrel in the early phase. Direct-acting P2Y12 inhibitors may be a more reliable option for patients receiving nitrate treatment to prevent thrombotic complications(NCT06878638).

Objective:The aim of this study is to evaluate the effect of iohexol as a contrast agent on the anticoagulant activity of oral factor Xa inhibitors. Methods:The study included 65 people who underwent contrast computerized tomography (CT). Patients in group 1 were using rivaroxaban (20 patients), patients in group 2 were using apixaban (20 patients), patients in group 3 were using edoxaban (20 patients), and group 4 was the control group (5 volunteers). Iohexol (60ml) was used as a contrast agent. Two tubes were used to collect 2 ml of blood from the patients at 4 hours after the drug dose (rivaroxaban, apixaban, or edoxaban) and 1 hour after the contrast CT (CT was performed 3 hours after the drug was taken). In the control group, at any time and 1 hour after contrast CT, 2 tubes of 2 ml of blood were collected. The anticoagulant properties of rivaroxaban, apixaban, and edoxaban were evaluated using anti-factor Xa levels. Results:The anti-factor Xa level was increased after using the contrast agent in the rivaroxaban group (0.66±0.32U/ml vs. 0.67±0.32U/ml; p=0.01) and the edoxaban group (0.74±0.35 U/ml vs. 0.76±0.36 U/ml; p=0.006). However, there was no significant difference in the apixaban group (0.66±0.33U/ml vs. 0.66±0.32U/ml; p=0.21) and control group (0.02±0.01U/ml vs. 0.03±0.01U/ml; p=0.33). Conclusion:The anticoagulant properties of rivaroxaban and edoxaban tended to increase significantly, but there was no statistically significant difference in the anticoagulant properties of apixaban with contrast agent. The increasing is too small so that these laboratory results need to validate with larger clinical trials(NCT04611386).

Objective:Identification of patients who are nonresponders to cardiac resynchronization therapy (CRT) with the use of simple and objective parameters may be helpful in tailoring treatment. The aim of this study is to investigate whether E/(Ea×Sa) could be a predictor of CRT nonresponders (E=early diastolic transmitral velocity, Ea=early diastolic mitral annular velocity, Sa=systolic mitral annular velocity). Methods:In total, 53 heart failure patients were evaluated for this study, and 33 patients were included according to the study criteria. Before and six months after CRT-D(CRT with a defibrillator) implantation, E, Ea, and Sa were determined at the medial and lateral mitral annular sites, and the average values were obtained. E/(Ea×Sa) was calculated (medial, lateral, average). The patients were followed for six months to monitor their CRT response. A responder was defined as a patient with a reduction in end-systolic volume of <15% and an increase in six-minute walking distance of 50 meters. Results:At a six-month follow-up, 24(72.7%) of the 33 patients responded to CRT. At the six-month follow-up, in the responder group, the E/Ea ratio, lateral mitral, and average E/(Ea×Sa) indices were significantly reduced (p<0.01 for all). The baseline lateral mitral, medial mitral, and average E/(Ea×Sa) indices were significantly lower in the responder group than in the nonresponder group (p≤0.01 for all). The ROC analysis showed that all the E/(Ea×Sa) indices predict the CRT nonresponder patients. The AUC values were 0.89(lateral E/(Ea×Sa)), 0.85(average E/(Ea×Sa)), and 0.77(medial E/(Ea×Sa))(p≤0.01 for all). Conclusion:We found that the E/(Ea×Sa) index is a novel predictor of CRT nonresponder patients.