PMC:6019327 / 85556-86317 JSONTXT

{"project":"2_test","denotations":[{"id":"28506916-20338265-29307432","span":{"begin":200,"end":203},"obj":"20338265"},{"id":"28506916-20338265-29307432","span":{"begin":200,"end":203},"obj":"20338265"},{"id":"T55977","span":{"begin":200,"end":203},"obj":"20338265"},{"id":"T28553","span":{"begin":200,"end":203},"obj":"20338265"},{"id":"T6191","span":{"begin":200,"end":203},"obj":"20338265"},{"id":"T75209","span":{"begin":200,"end":203},"obj":"20338265"}],"text":"Finally, experiments in sheep demonstrated that hypercapnia per se causes profound atrial conduction slowing and increased AF inducibility, which persists following the return of CO2 levels to normal.312 This effect was independent of oxygen levels. Taken together, the results suggest that acute OSA episodes enhance AF vulnerability via a combination of LA dilation and autonomic and electrophysiological changes; however, these abnormalities alone are not enough to significantly enhance AF risk in normal hearts. Repeated nocturnal OSA activates neurohormonal systems that over time produce sustained hypertension and cardiac structural and electrophysiological remodeling. These render the atria susceptible to AF, particularly during an acute OSA episode."}