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Aging and disease    2016, Vol. 7 Issue (5) : 635-656     DOI: 10.14336/AD.2016.0211
Review Article |
Atrial Fibrillation: The Science behind Its Defiance
Czick Maureen E.1, Shapter Christine L.2, Silverman David I.3
1Department of Anesthesiology,
2Department of Psychiatry, Hartford Hospital/Institute of Living, and
3Echocardiography Laboratory, Hartford Hospital, Hartford, CT 06106, USA.
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Abstract  

Atrial fibrillation (AF) is the most prevalent arrhythmia in the world, due both to its tenacious treatment resistance, and to the tremendous number of risk factors that set the stage for the atria to fibrillate. Cardiopulmonary, behavioral, and psychological risk factors generate electrical and structural alterations of the atria that promote reentry and wavebreak. These culminate in fibrillation once atrial ectopic beats set the arrhythmia process in motion. There is growing evidence that chronic stress can physically alter the emotion centers of the limbic system, changing their input to the hypothalamic-limbic-autonomic network that regulates autonomic outflow. This leads to imbalance of the parasympathetic and sympathetic nervous systems, most often in favor of sympathetic overactivation. Autonomic imbalance acts as a driving force behind the atrial ectopy and reentry that promote AF. Careful study of AF pathophysiology can illuminate the means that enable AF to elude both pharmacological control and surgical cure, by revealing ways in which antiarrhythmic drugs and surgical and ablation procedures may paradoxically promote fibrillation. Understanding AF pathophysiology can also help clarify the mechanisms by which emerging modalities aiming to correct autonomic imbalance, such as renal sympathetic denervation, may offer potential to better control this arrhythmia. Finally, growing evidence supports lifestyle modification approaches as adjuncts to improve AF control.

Keywords atrial fibrillation      pathophysiology      catheter ablation      surgical maze procedure      antiarrhythmic drugs      autonomic imbalance     
Corresponding Authors: Czick Maureen E.   
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These authors contributed equally to this work

Issue Date: 01 October 2016
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Czick Maureen E.
Shapter Christine L.
Silverman David I.
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Czick Maureen E.,Shapter Christine L.,Silverman David I.. Atrial Fibrillation: The Science behind Its Defiance[J]. Aging and disease, 2016, 7(5): 635-656.
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http://www.aginganddisease.org/EN/10.14336/AD.2016.0211     OR     http://www.aginganddisease.org/EN/Y2016/V7/I5/635
Figure 1.  Atrial Action Potential Ion Currents. While the SA cells are depolarizing, the surrounding contractile cells of the atria are at their resting membrane potential of approximately -90mV, due to the IK1 current. Once the SA depolarizes, it promptly passes depolarizing positive ions to the atrial cells through low resistance gap junction channels. These positive ions bring the atrial cells to their own threshold potential, opening voltage-gated sodium channels (INa) in the atrial cell membranes, so that the atrial cells fire their own action potentials. At the peak of the upstroke in the atria, transient outward (Ito) potassium channels open; positively-charged potassium ions exit the cell, beginning the process of repolarization. Their attempt to repolarize the atrial cells is short-lived however, because inward calcium current, conducted through voltage-gated L-type calcium channels (Ica(L)) keeps the cells in a state of depolarization just a bit longer, depicted as a plateau in the middle of the action potential waveform. The SA action potential does not need a calcium-based plateau current because SA cells are not responsible for contracting. Atrial cells, on the other hand, use the electrical depolarization from the action potential as the signal to contract. The “trigger” calcium entry through L-type channels during the plateau acts as a bridge between the electrical depolarization and mechanical contraction. The L-type channels inactivate rapidly, calcium current ceases, and then potassium exit, through multiple channels including the “ultra-rapid”-opening IKur, the “rapid” opening IKr (also called hERG channels) and the “slowly” opening IKs channels, fully repolarizes the cells.
Figure 2.  Sinoatrial Node Depolarization. Under normal conditions, the heart’s electrical rhythm is generated by the cells of the sinoatrial (SA) node. At the beginning of each cardiac cycle the membrane potential of the SA cells is approximately -60 mV, with the interior of the SA cells negatively charged relative to the cell exterior. Unlike contractile cardiac cells, SA cells do not have a stable resting membrane potential, so they remain poised at -60 for just the briefest moment, because “funny channels” (If) promptly spring open, allowing positively charged ions to leak from the extracellular space into the interior of the SA cells. As positive ions enter, the SA cell interiors become progressively less negatively charged (depolarized). The funny channel leak current (soon joined by Ca2+ current through T- and L-type channels, ICa(T), ICa(L)) -- and the change in the membrane potential that results from it -- is represented in the graph of the SA node action potential as the diagonal upslope at the start of action potential waveform, also referred to as “phase 4.” The positive ion influx quickly brings the SA cells toward the “threshold potential,” at approximately -40 mV, at which point voltage-gated calcium channels suddenly open, enabling a sudden massive surge of positive charge entry into the cell. This is the upstroke of the SA action potential, also called “phase 0.” Following the upstroke, there is an exodus of positively-charged potassium ions (IK) which restores the cell interior to its original negatively-charged baseline electrical potential during phase 3 repolarization.
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