Open Access

ARTICLE

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

by

1 Department of Pediatrics, University of California San Diego School of Medicine, La Jolla, California
2 Division of Biomedical Informatics, Department of Medicine, University of San Diego, La Jolla, California
3 Rady Children’s Hospital San Diego, San Diego, California
4 Genome Institute of Singapore, Singapore

* Corresponding Author: Jane C. Burns, UCSD School of Medicine 9500 Gilman Dr. La Jolla, CA 92093. Email:

Congenital Heart Disease 2019, 14(2), 213-220. https://doi.org/10.1111/chd.12696

Abstract

Background: We previously described the association of genetic variants in calcium channel genes and susceptibility to Kawasaki disease (KD), an acute, self‐limited vas‐ culitis, and the most common cause of acquired cardiac disease in children. Abnormal repolarization of cardiomyocytes and changes in T wave morphology have been re‐ ported in KD but have not been studied systematically.
Methods: We analyzed acute and convalescent ECG T wave morphology in two inde‐ pendent 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 independ‐ ent 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 intra‐ cellular calcium signaling play a prominent role in shaping susceptibility to KD.

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