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  • Funding secured by Not applicable Data collection Sheldon

    2019-04-18

    Funding secured by: Not applicable. Data collection: Sheldon M. Singh, MD, Ramanan Kumareswaran, MD.
    Conflict of interest
    Acknowledgments
    Introduction Early repolarization pattern (ERP) is characterized by an elevation greater than 0.1mV of the junction between the end of the QRS complex and the beginning of the ST segment (J point) and notching or slurring of the terminal portion of the QRS complex followed by a positive T wave [1]. The prevalence of ERP is 1–2% in the normal population. The condition is more commonly seen in young individuals, especially those predisposed to vagotonia, and in men. ERP is also frequently observed in athletes, cocaine users, and patients with hypertrophic obstructive cardiomyopathy [2]. The prevalence of ERP is as high as 10% in athletes, especially in high endurance athletes [3]. Over the last decade, evidence has mounted regarding the potential role of ERP in life-threatening arrhythmias and sudden unexplained deaths [4]. Several reports suggested that such arrhythmias are associated with ERP in the inferior or mid- to lateral precordial leads. ERP has recently been associated with vulnerability to ventricular fibrillation in independent case-controlled studies [5]. Clinical interest in ERP has been rekindled because of its similarities to Brugada syndrome (BS) [1]. Several studies attempted to demonstrate an association between ERP and BS, but much remains unknown [6]. BS is highly prevalent in the northeast region of Thailand and in Japan [7–9]. The use of high intercostal leads is a more sensitive method for the detection of the Brugada ECG pattern [7–9]. Little is known about the frequency and predictors of ERP in Asian populations. In addition, the correlation between ERP and Brugada ECG has never been studied in an area endemic for BS. The aim of this acetanilide study was to examine the prevalence and predictors of ERP in young healthy Thai males in northeastern Thailand. The association between ERP and Brugada ECG in Thailand was also studied.
    Materials and methods
    Results During the study period, 322 healthy male volunteers were enrolled. Of those, 40 were excluded due to high blood pressure (n=32), a history of syncope (n=2), an age over 45 years (n=1), premature ventricular contraction (n=2), Wolff–Parkinson White syndrome (n=1), atrial fibrillation (n=1), and complete right bundle branch block (n=1). Of the 282 subjects ultimately included in the analysis, 29 (10.3%) had ERP. Subjects with ERP had a significantly lower body weight and body mass index (BMI), lower systolic blood pressure, lower diastolic blood pressure, a slower heart rate, a shorter QTc duration, and a higher Sokolow–Lyon index than those without ERP (Table 2). All 6 significant factors were included in the multivariate logistic analysis for ERP. Only the Sokolow–Lyon index was an independent factor for ERP, with an adjusted odds ratio of 1.090 (95% confidence interval: 1.027, 1.159), as shown in Table 3. There were 129 subjects who had some J-point elevation. In 100 of these subjects (77.5%), the J-point elevation was <0.1mV. The remaining subjects were those with ERP. These subjects had a significantly lower systolic blood pressure (mean of 108 vs. 114mmHg) and a greater proportion of elevations detected by lateral leads (93.1% vs. 59%) (Table 4). The Brugada ECG pattern was found in 39 (39%) individuals with a J-point elevation <0.1mV in the inferolateral leads and in 11 (37.9%) individuals with ERP (Table 5). Ninety percent of subjects in both groups exhibited a non-type 1 pattern. The Brugada ECG pattern was commonly found in lateral ERP. The associations between the locations and types of Brugada ECG pattern are shown in Table 6. Brugada ECG in ERP subjects mostly occurred in the lateral leads and was defined as non-type 1 (Table 6). After the placement of high intercostal leads in subjects with ERP, the frequency of Brugada ECG increased dramatically in those with and without ERP with particular increases in non-type 1 pattern subjects (Table 5).