
@Article{chd.12696,
AUTHOR = {Jun Oyamada, Chisato Shimizu, Jihoon Kim, Matthew R. Williams, Eileen Png, Martin L. Hibberd, Adriana H. Tremoulet, James C. Perry, Jane C. Burns},
TITLE = {Bifid T waves on the ECG and genetic variation in <i>calcium channel voltage‐dependent beta 2 subunit</i> gene (<i>CACNB2</i>) in acute Kawasaki disease},
JOURNAL = {Structural and Congenital Heart Disease},
VOLUME = {14},
YEAR = {2019},
NUMBER = {2},
PAGES = {213--220},
URL = {http://www.techscience.com/schd/v14n2/38763},
ISSN = {3071-1738},
ABSTRACT = {<b>Background:</b> 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.<br/>
<b>Methods:</b> 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.<br/>
<b>Results:</b> Bifid T waves in limb leads were identified in 24% and 27% of two independ‐
ent cohorts of acute KD subjects. <i>Calcium channel voltage‐dependent beta 2 subunit</i>
gene (<i>CACNB2</i>) (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).<br/>
<b>Conclusion:</b> This genotype/phenotype association study uncovered a variant in 
<i>CACNB2</i> 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.},
DOI = {10.1111/chd.12696}
}



