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    Arrhythmogenic Evidence for Epicardial Adipose Tissue: Heart Rate Variability and Turbulence are Influenced by Epicardial Fat Thickness
    (2015) Balcioglu, Akif Serhat; Cicek, Davran; Akinci, Sinan; Eldem, Halil Olcay; Bal, Ugur Abbas; Okyay, Kaan; Muderrisoglu, Haldun; 0000-0002-9635-6313; 0000-0001-6134-8826; 0000-0001-5250-5404; 0000-0002-9446-2518; 25224491; AAC-8036-2020; AAG-8233-2020; AAK-7355-2020; AAD-5564-2021; AAK-4322-2021
    BackgroundEpicardial adipose tissue (EAT) is a local source of various hormones, cytokines, and vasoactive substances affecting the myocardium. EAT contains abundant ganglionic plexi that interact with the autonomic nervous system. Evidence of the association between EAT and arrhythmia is limited, with the exception of atrial fibrillation. This study aimed to investigate the relation between EAT and cardiac autonomic function using heart rate variability (HRV) and heart rate turbulence (HRT) parameters. MethodsAll subjects underwent a 24-hour Holter recording to assess HRV and HRT parameters and a transthoracic echocardiography to measure EAT thickness. Patients were divided into two groups according to the median EAT thickness (3.9 mm). The higher EAT group consisted of 111 patients with a >3.9-mm thickness and the lower EAT group 113 patients with a 3.9-mm EAT thickness. ResultsHRV and HRT parameters were significantly influenced in the higher EAT group. Moreover, we observed significant correlations between EAT thickness and Holter findings (standard deviation of all NN intervals [SDNN]: r = -0.462, P < 0.001; SDNN index: r = -0.349, P < 0.001; standard deviation of the average NN intervals: r = -0.465, P < 0.001; root mean square of successive differences: r = -0.251, P < 0.001; pNN50: r = -0.354, P < 0.001; turbulence onset: r = 0.172, P = 0.010; turbulence slope: r = -0.279, P < 0.001, HRT category: r = 0.169, P = 0.011). In multivariate regression analysis, EAT thickness was independently associated with all measures of HRV and HRT, with the exception of turbulence onset. ConclusionsSympathovagal imbalance, detected by HRV and HRT parameters, is related to EAT thickness. As sympathovagal imbalance is a predictor of arrhythmic events, EAT may play an important arrhythmogenic role not limited to atrial fibrillation.
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    The role of mitochondrial ATP-sensitive potassium channels on cardiovascular effects of thiopental and ketamine in rats
    (2015) Altunkaynak, H.O.; Tecder-Unal, M.; 26435022
    OBJECTIVE: We aimed to investigate whether mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels play any role on cardiovascular effects of thiopental (TP) or ketamine (K) anesthesia in rats. BACKGROUND: mitoK(ATP) channels are the end-effectors of cardioprotection induced by some anesthetics. TP and K are the most frequently used anesthetics with their own cardiovascular effects in experimental studies. To the best of our knowledge, there is no study investigating the cardiovascular effects of TP and K associated with mitoK(ATP) channels. MATERIALS AND METHODS: The experimental groups: TP control, K/Xylazine (X) control, TP+5-hydroxydecanoate (5-HD; mitoK(ATP), channel blocker) and K1X+5-HD. Mean arterial blood pressure (MABP), heart rate (HR) and standard limb lead II ECG were recorded and arrhythmia parameters were evaluated. RESULTS: Blockage of mitoKA(ATP) channels by 5-HD increased MABP and decreased HR in the TP+5-HD and K/X+5-HD groups, respectively. 5-HD caused an increase in ventricular ectopic beat (VEB) incidence. Moreover, VEB incidence was significantly different in TP+5-HD (100 %) than K/X+5-HDgroup (66.6 %) and ventricular tachycardia was only seen in TP+5-HD (incidence was 88.3 %). CONCLUSION: mitoK(ATP) channels play different roles in influencing cardiovascular effects of K/X and TP anesthesia in rats. The differences in hemodynamic parameters and arrhythmia scores of these anesthetics should be considered when they are used in an experimental study associated with mitoK(ATP) channels (Fig. 3, Ref. 35). Text in PDF www.elis.sk.