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  • In addition evidence of similar resting


    In addition, evidence of similar resting HR׳s before exercise in the patients and in the controls implies similar autonomic activity at rest during the daytime in both groups of subjects. In contrast, previous studies have reported changes in the nocturnal HR of BrS patients [3,28]. The discrepancy of the results may be due to the fact that this study was conducted during the daytime. The abnormal HR in the patients mostly occurs at night [28]. Therefore, differences in resting HR were not shown during the daytime. The other explanation might be related to the severity of the disease in the studied population. The patients in this study were survivors of cardiac arrest who had had an ICD inserted for secondary prevention. Moreover, they were regularly being seen for ICD check-ups at the Queen Sirikit Heart Center of the Northeast, Thailand. The patients in the earlier study had been hospitalized after sudden cardiac arrest for further management. Therefore, the stage of the syndrome may have been different [3]. With respect to this study, an important note, that should be emphasized, is that the ICD implanted in the patients does not control cardiac rhythm. It just stimulates cardiac contraction when there is cardiac arrest. Therefore, the patients in this study had physiological control of the HR. Moreover, there may be a question about the resting HR, which is similar to the controls, although they had been taking anti-arrhythmic drugs. This may be due to the low dose of drugs (e.g., β-blocker for our BrS patients which was 6.25mg carvedilol twice a day). It was surprising that the BrS patients had achieved a smaller HRR than the controls, because they had had a larger increase in vagal activity and a withdrawal of sympathetic activity, which should have increased HRR after the GSK503 of the exercise. This may be due to the patients’ lower peak exercise workload which may have resulted in a lower peak HR than the controls. When the HRR was considered as a proportion of the increase in HR from resting to the maximum level at the termination of exercise and was not different between groups, this was confirmed. In fact, HRR in the BRS patients is still controversial since it was shown to be similar to [29], higher than [30], or lower than [30] the controls. This may be attributed to the electrophysiologic characteristics [30] of the patients. Patients in this study reached their individual because they could not maintain the cycling speed although their HR did not reach 85% of the predicted HRmax. The low in the controls may be explained by the fact that these subjects were very unfit patients and controls who had not been habitual exercisers and who had been unable to exercise at a higher intensity. Middle-aged South Asian individuals have been shown to have lower than their European counterparts [31]. Moreover, the healthy subjects in this study had similar (22±2ml/kg/min) to Thai subjects of the same age as had been reported in a previous study (25.9±3.4ml/kg/min) [32]. In this study BrS patients had lower than the controls. Regarding the inverse relationship between cardio-respiratory fitness and heart failure [7], the impaired cardio-respiratory fitness may be due to imbalanced cardiac sympathovagal and a reduction in K+ concentration induced by the exercise test.
    Funding This research was supported by the Ministry of Science and Technology, Thailand (Grant no. 4/2552). Also, it was partially supported by the Invitation Research Grant from the Faculty of Medicine (Grant no. I55109).
    Conflict of interest
    Introduction Long QT syndrome (LQTS) is characterized by QT intervals longer than 450ms that lead to a torsades de pointes ventricular tachycardia and sudden death. LQTS is attributed to mutations in genes that encode ion channels or their regulatory proteins responsible for the proper repolarization of cardiomyocytes [1–3], and is classified into 13 types based on the mutated genes. LQTS types 1, 2, and 3 account for 90% of LQTS cases [4].