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Fig. 7 | BMC Cardiovascular Disorders

Fig. 7

From: HiPSC-derived cardiomyocyte to model Brugada syndrome: both asymptomatic and symptomatic mutation carriers reveal increased arrhythmogenicity

Fig. 7

Ca2+ handling abnormalities in hiPSC-CMs. (A) Representative traces of a control CM showing normal regular Ca2+ transients and mutated CMs showing different abnormality types including oscillations (OS), low amplitude peaks (LP), varying amplitude (VA), plateau abnormality (PA) and rise delay (RD). (B) Doughnut charts indicating the abnormality percentage of WT, asymptomatic and symptomatic CMs in baseline and during adrenaline and flecainide perfusion. (C) Bar charts indicating the percentage of each abnormality type of asymptomatic and symptomatic CMs in baseline, and during adrenaline and flecainide perfusion. (D) Bar graph comparisons of standard deviation (SD) of peak duration, rise time 10–90% and instantaneous frequency of WT (n = 155), asymptomatic (n = 143) and symptomatic (n = 219) CMs in baseline. Data are presented as mean ± S.E.M. * or # indicates P < 0.05 and *** P < 0.001. * indicates comparisons with WT CMs and # indicates comparisons with asymptomatic CMs.

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