Bifid T waves on the ECG and genetic variation in calcium channel voltage-dependent beta 2 subunit gene (CACNB2) in acute Kawasaki disease

Autor: Oyamada, J, Shimizu, C, Kim, J, Williams, MR, Png, E, Hibberd, ML, Tremoulet, AH, Perry, JC, Burns, JC
Rok vydání: 2019
Předmět:
Zdroj: Congenital heart disease, vol 14, iss 2
Oyamada, J; Shimizu, C; Kim, J; Williams, MR; Png, E; Hibberd, ML; et al.(2018). Bifid T waves on the ECG and genetic variation in calcium channel voltage-dependent beta 2 subunit gene (CACNB2) in acute Kawasaki disease.. Congenital heart disease. doi: 10.1111/chd.12696. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/6d40s7vj
DOI: 10.1111/chd.12696.
Popis: BACKGROUND:We previously described the association of genetic variants in calcium channel genes and susceptibility to Kawasaki disease (KD), an acute, self-limited vasculitis, and the most common cause of acquired cardiac disease in children. Abnormal repolarization of cardiomyocytes and changes in T wave morphology have been reported in KD but have not been studied systematically. METHODS:We analyzed acute and convalescent ECG T wave morphology in two independent cohorts of KD subjects and studied the association between bifid T waves and genetic variants in previously reported genes with SNVs associated with cardiac repolarization. RESULTS:Bifid T waves in limb leads were identified in 24% and 27% of two independent cohorts of acute KD subjects. Calcium channel voltage-dependent beta 2 subunit gene (CACNB2) (rs1409207) showed association with bifid T waves in both cohorts (nominal P = .04 and P = .0003, respectively). This CACNB2 polymorphism also showed association with KD susceptibility in a previously published KD genome wide association study data (nominal P = .009). CONCLUSION:This genotype/phenotype association study uncovered a variant in CACNB2 that may be associated with both KD susceptibility and bifid T waves, a novel signature of altered myocardial repolarization. The present study combined with published reports suggests that genetic variants in calcium channels and intracellular calcium signaling play a prominent role in shaping susceptibility to KD.
Databáze: OpenAIRE