Key result
Chronic atrial fibrillation is associated with cellular electrical remodeling, including increased inward rectifier K+ current and reduced L-type Ca2+ current, which shortens the refractory period.
Why the study?
The ionic and molecular mechanisms underlying atrial electrical remodeling in human atrial fibrillation, including effects of heart failure and beta-blocker therapy, are not fully understood.
Answers are grounded in this paper and cite their sources.
This review highlights the cellular and ionic mechanisms underlying human atrial fibrillation, emphasizing the role of shortened refractory periods and altered ion currents in sustaining the arrhythmia.
Atrial fibrillation (AF) causes substantial morbidity and mortality. It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully understood and may include increased inward rectifier K(+) current and altered Ca(2+) handling. Heart failure, a major cause of AF, may involve arrhythmogenic atrial electrical remodeling, but the pattern is unclear in humans. Beta-blocker therapy prolongs atrial cell refractory period; a potentially antiarrhythmic influence, but the ionic and molecular mechanisms are unclear. The search for drugs to suppress AF without causing ventricular arrhythmias has been aided by basic studies of cellular mechanisms of AF. It remains to be seen whether such drugs will improve patient treatment.
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Workman et al. (2008) conducted a review in Atrial fibrillation. Chronic atrial fibrillation is associated with cellular electrical remodeling, including increased inward rectifier K+ current and reduced L-type Ca2+ current, which shortens the refractory period.
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