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    Coexistence of atrioventricular accessory pathways and drug-induced type 1 Brugada pattern
    (Wiley, 2018) Hasdemir, Can; Juang, Jimmy Jyh-Ming; Kose, Sedat; Kocabas, Umut; Orman, Mehmet N.; Payzin, Serdar; Sahin, Hatice; Celen, Candan; Ozcan, Emin E.; Chen, Ching-Yu Julius; Gunduz, Ramazan; Turan, Oguzhan E.; Senol, Oktay; Burashnikov, Elena; Antzelevitch, Charles
    BackgroundAtrial arrhythmias, particularly atrioventricular nodal reentrant tachycardia, can coexist with drug-induced type 1 Brugada electrocardiogram (ECG) pattern (DI-Type1-BrP). The present study was designed to determine the prevalence of DI-Type1-BrP in patients with atrioventricular accessory pathways (AV-APs) and to investigate the clinical, electrocardiographic, electrophysiologic, and genetic characteristics of these patients. MethodsOne-hundred twenty-four consecutive cases of AV-APs and 84 controls underwent an ajmaline challenge test to unmask DI-Type1-BrP. Genetic screening and analysis was performed in 55 of the cases (19 with and 36 without DI-Type1-BrP). ResultsPatientswith AV-APs were significantly more likely than controls to have a Type1-BrP unmasked (16.1vs 4.8%, P=0.012). At baseline, patients with DI-Type1-BrP had higher prevalence of chest pain, QR/rSr' pattern in V-1 and QRS notching/slurring in V-2 and aVL during preexcitation, rSr' pattern in V-1-V-2, and QRS notching/slurring in aVL during orthodromic atrioventricular reentrant tachycardia (AVRT) compared to patients without DI-Type1-BrP. Abnormal QRS configuration (QRS notching/slurring and/or fragmentation) in V-2 during preexcitation was present in all patients with DI-Type1 BrP. The prevalence of spontaneous preexcited atrial fibrillation (AF) and history of AF were similar (15%vs 18.3%, P=0.726) in patients with and without DI-Type1-BrP, respectively. The prevalence of mutations in Brugada-susceptibility genes was higher (36.8%vs 8.3%, P=0.02) in patients with DI-Type1-BrP compared to patients without DI-Type1-BrP. ConclusionsDI-Type1-BrP is relatively common in patients with AV-APs. We identify 12-lead ECG characteristics during preexcitation and orthodromic AVRT that point to an underlying type1-BrP, portending an increased probability for development of malignant arrhythmias.
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    High prevalence of concealed Brugada syndrome in patients with atrioventricular nodal reentrant tachycardia
    (Elsevier Science Inc, 2015) Hasdemir, Can; Payzin, Serdar; Kocabas, Umut; Sahin, Hatice; Yildirim, Nihal; Alp, Alpay; Aydin, Mehmet; Pfeiffer, Ryan; Burashnikov, Elena; Wu, Yuesheng; Antzelevitch, Charles
    BACKGROUND Atrioventricular nodal reentrant tachycardia (AVNRT) may coexist with Brugada syndrome (BrS). OBJECTIVES The present study was designed to determine the prevalence of drug-induced type 1 Brugada ECG pattern (concealed BrS) in patients presenting with clinical spontaneous AVNRT and to investigate their electrocardiographic, electrophysiological, and genetic characteristics. METHODS Ninety-six consecutive patients without any sign of BrS on baseline electrocardiogram undergoing electrophysiological study and ablation for symptomatic, drug-resistant AVNRT and 66 control subjects underwent an ajmaline challenge to unmask BrS. Genetic screening was performed in 17 patients displaying both AVNRT and BrS. RESULTS A concealed BrS electrocardiogram was uncovered in 26 of 96 patients with AVNRT (27.1%) and in 3 of 66 control subjects (4.5%) (P <= .001). Patients with concealed BrS were predominantly female patients (n = 23 [88.5%] vs n = 44 [62.9%], P = .015), had higher prevalence of chest pain (n = 10 [38.5%] vs n = 13 [18.6%], p = 0.042), migraine headaches (n = 10 [38.5%] vs n = 10 [14.2%], p = 0.008), and drug-induced initiation and/or worsening of duration and/or frequency of AVNRT (n = 4 [15.4%] vs n = 1 [1.4%], p = 0.006) as compared to patients with AVNRT without BrS. Genetic screening identified 19 mutations or rare variants in 13 genes in 13 of 17 patients with both AVNRT and BrS (yield = 76.5%). Ten of these 13 genotype-positive patients (76.9%) harbored genetic variants known or suspected to cause a loss of function of cardiac sodium channel current (SCN5A, SCN10A, SCN1B, GPD1L, PKP2, and HEY2). CONCLUSION Our results suggest that spontaneous AVNRT and concealed BrS co-occur, particularly in female patients, and that genetic variants that reduce sodium channel current may provide a mechanistic link between AVNRT and BrS and predispose to expression of both phenotypes.
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    High prevalence of concealed Brugada syndrome in patients with atrioventricular nodal reentrant tachycardia
    (Elsevier Science Inc, 2015) Hasdemir, Can; Payzin, Serdar; Kocabas, Umut; Sahin, Hatice; Yildirim, Nihal; Alp, Alpay; Aydin, Mehmet; Pfeiffer, Ryan; Burashnikov, Elena; Wu, Yuesheng; Antzelevitch, Charles
    BACKGROUND Atrioventricular nodal reentrant tachycardia (AVNRT) may coexist with Brugada syndrome (BrS). OBJECTIVES The present study was designed to determine the prevalence of drug-induced type 1 Brugada ECG pattern (concealed BrS) in patients presenting with clinical spontaneous AVNRT and to investigate their electrocardiographic, electrophysiological, and genetic characteristics. METHODS Ninety-six consecutive patients without any sign of BrS on baseline electrocardiogram undergoing electrophysiological study and ablation for symptomatic, drug-resistant AVNRT and 66 control subjects underwent an ajmaline challenge to unmask BrS. Genetic screening was performed in 17 patients displaying both AVNRT and BrS. RESULTS A concealed BrS electrocardiogram was uncovered in 26 of 96 patients with AVNRT (27.1%) and in 3 of 66 control subjects (4.5%) (P <= .001). Patients with concealed BrS were predominantly female patients (n = 23 [88.5%] vs n = 44 [62.9%], P = .015), had higher prevalence of chest pain (n = 10 [38.5%] vs n = 13 [18.6%], p = 0.042), migraine headaches (n = 10 [38.5%] vs n = 10 [14.2%], p = 0.008), and drug-induced initiation and/or worsening of duration and/or frequency of AVNRT (n = 4 [15.4%] vs n = 1 [1.4%], p = 0.006) as compared to patients with AVNRT without BrS. Genetic screening identified 19 mutations or rare variants in 13 genes in 13 of 17 patients with both AVNRT and BrS (yield = 76.5%). Ten of these 13 genotype-positive patients (76.9%) harbored genetic variants known or suspected to cause a loss of function of cardiac sodium channel current (SCN5A, SCN10A, SCN1B, GPD1L, PKP2, and HEY2). CONCLUSION Our results suggest that spontaneous AVNRT and concealed BrS co-occur, particularly in female patients, and that genetic variants that reduce sodium channel current may provide a mechanistic link between AVNRT and BrS and predispose to expression of both phenotypes.
  • Küçük Resim Yok
    Öğe
    High prevalence of concealed Brugada syndrome in patients with atrioventricular nodal reentrant tachycardia
    (Elsevier Science Inc, 2015) Hasdemir, Can; Payzin, Serdar; Kocabas, Umut; Sahin, Hatice; Yildirim, Nihal; Alp, Alpay; Aydin, Mehmet; Pfeiffer, Ryan; Burashnikov, Elena; Wu, Yuesheng; Antzelevitch, Charles
    BACKGROUND Atrioventricular nodal reentrant tachycardia (AVNRT) may coexist with Brugada syndrome (BrS). OBJECTIVES The present study was designed to determine the prevalence of drug-induced type 1 Brugada ECG pattern (concealed BrS) in patients presenting with clinical spontaneous AVNRT and to investigate their electrocardiographic, electrophysiological, and genetic characteristics. METHODS Ninety-six consecutive patients without any sign of BrS on baseline electrocardiogram undergoing electrophysiological study and ablation for symptomatic, drug-resistant AVNRT and 66 control subjects underwent an ajmaline challenge to unmask BrS. Genetic screening was performed in 17 patients displaying both AVNRT and BrS. RESULTS A concealed BrS electrocardiogram was uncovered in 26 of 96 patients with AVNRT (27.1%) and in 3 of 66 control subjects (4.5%) (P <= .001). Patients with concealed BrS were predominantly female patients (n = 23 [88.5%] vs n = 44 [62.9%], P = .015), had higher prevalence of chest pain (n = 10 [38.5%] vs n = 13 [18.6%], p = 0.042), migraine headaches (n = 10 [38.5%] vs n = 10 [14.2%], p = 0.008), and drug-induced initiation and/or worsening of duration and/or frequency of AVNRT (n = 4 [15.4%] vs n = 1 [1.4%], p = 0.006) as compared to patients with AVNRT without BrS. Genetic screening identified 19 mutations or rare variants in 13 genes in 13 of 17 patients with both AVNRT and BrS (yield = 76.5%). Ten of these 13 genotype-positive patients (76.9%) harbored genetic variants known or suspected to cause a loss of function of cardiac sodium channel current (SCN5A, SCN10A, SCN1B, GPD1L, PKP2, and HEY2). CONCLUSION Our results suggest that spontaneous AVNRT and concealed BrS co-occur, particularly in female patients, and that genetic variants that reduce sodium channel current may provide a mechanistic link between AVNRT and BrS and predispose to expression of both phenotypes.