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. 2019 Oct 9;4(7):795–813. doi: 10.1016/j.jacbts.2019.06.004

Table 3.

Effects of Disopyramide on AP and [Ca2+]i

0.2 Hz Baseline Disopyramide % Change p Value
[Ca2+]i, nmol/l
Diastolic Ca 235 ± 44 189 ± 31 −22 ± 8 0.015
Ca2+-transient amplitude 336 ± 53 188 ± 34 −44 ± 15 0.006
Ca2+-transient kinetics, ms
Time to peak 151 ± 15 128 ± 12 −15 ± 8 0.024
90% decay 1,260 ± 99 905 ± 88 −28 ± 8 0.008
Action potentials
MDP, mV −80 ± 3 −80 ± 3. 0 ± 3 >0.05
Amplitude, mV 129.1 ± 3.2 122.2 ± 2.8 −5 ± 1 0.012
Upstroke, V/s 139 ± 18 97 ± 12 −30 ± 9 0.002
APD20, ms 381 ± 44 284 ± 40 −25 ± 9 0.017
APD50, ms 653 ± 63 469 ± 61 −28 ± 7 <0.001

Values are mean ± SEM. The p values were calculated using linear mixed models. Additional data from action potentials and Ca transients were recorded in hypertrophic cardiomyopathy cardiomyocytes stimulated at 0.2 Hz before and during exposure to disopyramide. Data from 28 HCM cardiomyocytes isolated from 8 hypertrophic cardiomyopathy patient samples (ID# 3 to 6, 9, and 11 to 13). Diastolic Ca is the diastolic concentration of Ca during regular stimulation. Ca2+-transient amplitude is the difference between peak systolic Ca and diastolic Ca. Time to peak is the measurement from stimulus to peak. The 90% decay is the time from peak to 90% decay of Ca transients. Upstroke is the upstroke speed of the action potentials.

APD20 (APD50) = action potential duration at 20% (50%) of repolarization; MDP = mean diastolic potential.