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• W2023240247 abstract "Background Cellular replacement strategies using embryonic stem cell-derived cardiomyocytes (ESC-CMs) have been shown to improve left ventricular (LV) ejection fraction and prevent LV remodeling post-myocardial infarction (MI). Nonetheless, the immature electrical phenotypes of ESC-CMs may increase the risk of ventricular tachyarrhythmias (VTs) and sudden death. Objective To investigate whether the forced expression of Kir2.1-encoded inward rectifying K+ channels that are otherwise absent in ESC-CMs would attenuate their proarrhythmic risk after transplantation post-MI. Methods Mouse ESC line stably transduced with a lentivirus (LentV)-based doxycycline (DOX)-inducible system coexpressing the transgenes Kir2.1 and a dsRed (LentV-THM-Kir2.1-GFP/LentV-TR-KRAB-dsRed) was differentiated into ESC-CMs with (DOX+) or without (DOX−) treatment with DOX. Detailed in vitro and in vivo assessments of LV function and cardiac electrophysiology were measured 4 weeks after transplantation. Results ESC-CM DOX+ with atrial and ventricular phenotype exhibited more hyperpolarizing resting membrane potential than did ESC-CM DOX− (P< .05). Transplantations of ESC-CM DOX− and ESC-CM DOX+ both significantly improved LV ejection fraction, LV end-systolic diameter, end-systolic pressure-volume relationship, and positive maximal and negative pressure derivative (P< .05) at 4 weeks compared with the MI group; however, the DOX− group (22 of 40, 55%) had a significantly higher early sudden death rate than the DOX+ group (13 of 40, 32.5%; P = .036). Telemetry monitoring revealed that the DOX− group (6.09%±3.65%) had significantly more episodes of spontaneous VT compared with the DOX+ group (0.92%±0.81%; P< .05). In vivo programmed electrical stimulation at 2 weeks resulted in a significantly higher incidence of inducible VT in the DOX− group (9 of 16, 56.25%) compared with the DOX+ group (3 of 16, 18.75%; P = .031). Conclusions Forced expression of Kir2.1 in ESC-CMs improves their electrical phenotypes and lowers the risk of inducible and spontaneous VT after post-MI transplantation. Cellular replacement strategies using embryonic stem cell-derived cardiomyocytes (ESC-CMs) have been shown to improve left ventricular (LV) ejection fraction and prevent LV remodeling post-myocardial infarction (MI). Nonetheless, the immature electrical phenotypes of ESC-CMs may increase the risk of ventricular tachyarrhythmias (VTs) and sudden death. To investigate whether the forced expression of Kir2.1-encoded inward rectifying K+ channels that are otherwise absent in ESC-CMs would attenuate their proarrhythmic risk after transplantation post-MI. Mouse ESC line stably transduced with a lentivirus (LentV)-based doxycycline (DOX)-inducible system coexpressing the transgenes Kir2.1 and a dsRed (LentV-THM-Kir2.1-GFP/LentV-TR-KRAB-dsRed) was differentiated into ESC-CMs with (DOX+) or without (DOX−) treatment with DOX. Detailed in vitro and in vivo assessments of LV function and cardiac electrophysiology were measured 4 weeks after transplantation. ESC-CM DOX+ with atrial and ventricular phenotype exhibited more hyperpolarizing resting membrane potential than did ESC-CM DOX− (P< .05). Transplantations of ESC-CM DOX− and ESC-CM DOX+ both significantly improved LV ejection fraction, LV end-systolic diameter, end-systolic pressure-volume relationship, and positive maximal and negative pressure derivative (P< .05) at 4 weeks compared with the MI group; however, the DOX− group (22 of 40, 55%) had a significantly higher early sudden death rate than the DOX+ group (13 of 40, 32.5%; P = .036). Telemetry monitoring revealed that the DOX− group (6.09%±3.65%) had significantly more episodes of spontaneous VT compared with the DOX+ group (0.92%±0.81%; P< .05). In vivo programmed electrical stimulation at 2 weeks resulted in a significantly higher incidence of inducible VT in the DOX− group (9 of 16, 56.25%) compared with the DOX+ group (3 of 16, 18.75%; P = .031). Forced expression of Kir2.1 in ESC-CMs improves their electrical phenotypes and lowers the risk of inducible and spontaneous VT after post-MI transplantation." @default.
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• W2023240247 title "Overexpression of Kir2.1 channel in embryonic stem cell-derived cardiomyocytes attenuates posttransplantation proarrhythmic risk in myocardial infarction" @default.
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