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  • br Conclusions Wavelet algorithm is

    2019-05-21


    Conclusions Wavelet algorithm is an effective tool for the discrimination of tachycardia. However, it is affected by myopotential interference, which can lead to inappropriate detections. Thus, we should keep this drawback in mind when results reveal a Can-RV coil EGM amplitude of less than 5mV. To reduce inappropriate ICD therapies, it is recommended that we assess the level of physical activity, presence or absence of SVT and slow VT, ICD indication such as primary or secondary prevention, and amplitude of EGM source when the wavelet algorithm is operative. After these assessments, we should determine the programming parameters and tachycardia discrimination algorithms in patients with ICDs.
    Conflict of interest
    Acknowledgments
    Introduction Cardiac arrhythmias are characterized by an irregular heartbeat rhythm, which could be either too slow (<60 beats/min) or too fast (>100 beats/min) [1]. Amiodarone (AMD) (Fig. 1A) is an antiarrhythmic agent widely used to treat cardiac arrhythmias, mainly atrial fibrillation [1]. Despite its pharmacological properties, AMD and its main metabolite N-desethylamiodarone (Fig. 1B) can cause some adverse effects, such as thyroid dysfunction, and hepatic and pulmonary toxicity [2โ€“5]. Pulmonary toxicity occurs in approximately 13% of the patients, who can have an associated mortality rate of 10โ€“23% [2,3]. The mechanism by which AMD causes human toxicity is not well understood, but some studies in mammalian cells [6โ€“8] and an in vivo rat model [9] suggest that oxidative stress and mitochondrial dysfunction may play a role in AMD toxicity. Mitochondria are recognized for their key role not only in ATP biosynthesis, but also in the maintenance of redox metabolism and apoptosis regulation, making this organelle a potential therapeutic target. Disruption of mitochondrial homeostasis is associated with an increase in reactive oxygen species (ROS), mainly in complex I (nicotinamide buy 4EGI-1 dinucleotide/CoQ oxidoreductase) of the mitochondrial electron transport chain. In this complex, the superoxide radical (O2-ยท) is formed from electron escape, leading to decreased electron transport, reduced ATP biosynthesis, and increased oxidative stress [12]. Phenolic compounds are one of the most studied and effective group of bioactive compounds [13]. The flavonoids catechin (CAT) and epicatechin (EPI) (Fig. 2) are among this class of compounds [14]. It has already been demonstrated that CAT can reduce the inhibition of mitochondrial complex I induced by rotenone and N-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium hydrochloride in primary rat mesencephalic cultures [15].
    Materials and methods
    Results
    Discussion Interest in phenolic compounds has grown over the last several decades owing to the recognition of their antioxidant properties and their probable role in the prevention of a number of pathologies associated with oxidative stress [23]. Taking into account the low bioavailability of phenolic compounds [24,25], their biological actions are more likely to be caused by their indirect effects (such as by influencing signaling systems) than their direct antioxidant effects [26]. In fact, researchers have already described how some phenolic compounds such as quercetin, resveratrol, and rutin reduced mitochondrial dysfunction induced by indomethacin in Caco-2 cells [27]. Moreover, our group demonstrated that Plinia cauliflora polyphenolic-rich extract was also able to reduce complex I inhibition and decrease the ATP biosynthesis induced by H2O2 in MRC-5 cells [28]. Although the exact mechanism of AMD toxicity has not been completely elucidated, some studies conducted in mouse liver [6], hamster lung [7], and human hepatocytes cells [8], as well as an in vivo study in a rat model [9] demonstrated that AMD could cause mitochondrial dysfunction. Therefore, our study aimed to assess whether the phenolic compounds CAT and EPI could minimize the mitochondrial dysfunction and oxidative damage induced by AMD in MRC-5 cells.