Cellular bases for human atrial fibrillation

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Cellular bases for human atrial fibrillation Antony J. Workman, PhD, Kathleen A. Kane, PhD, Andrew C. Rankin, MD Heart Rhythm Volume 5, Issue 6, Pages S1-S6 (June 2008) DOI: 10.1016/j.hrthm.2008.01.016 Copyright © 2008 Heart Rhythm Society Terms and Conditions

Figure 1 Electrophysiological mechanisms of arrhythmias and their study in human atrial cells. A: Representation of premature APs (*) from AA, EADs, or DADs. B: Premature impulse divides at functional or anatomical obstacle, blocks at tissue with normal (left side), but conducts with short (right) ERP and reenters previously inexcitable zone. λ = wavelength; θ = conduction velocity. C: Original APs stimulated in an atrial cell from a patient in SR or in AF by conditioning pulses (S1) and premature test pulses (S2). ERP (↔) = longest S1-S2 failing to produce S2 response of amplitude >80% of S1. D: Original APs stimulated by a pulse train in the presence of 0.05 μM isoproterenol (ISO), producing CADs (•). The * may represent AA. Panels C and D are based on data in references 2 and 3 with permission from Elsevier. Heart Rhythm 2008 5, S1-S6DOI: (10.1016/j.hrthm.2008.01.016) Copyright © 2008 Heart Rhythm Society Terms and Conditions

Figure 2 Induction of constitutively active acetylcholine-activated K+ current, CA IKACh, in human AF. Single-channel IK1 and CA IKACh currents (A) and mean (±standard error) open probabilities (B), recorded at −120 mV in atrial cells from patients in SR (open symbols) and AF (solid symbols). *P <.05 versus SR. C: Potential signaling mechanism of increased CA IKACh in AF. In SR, IKACh may require channel phosphorylation by calmodulin-dependent PK II (CaMKII), PKG, and PKC.12 In AF, CA IKACh may result from upregulation of PKCϵ.12 Panels A and B are based on data in reference 10 with permission from Lippincott Williams & Wilkins. Heart Rhythm 2008 5, S1-S6DOI: (10.1016/j.hrthm.2008.01.016) Copyright © 2008 Heart Rhythm Society Terms and Conditions

Figure 3 Pharmacological remodeling of human atrial cell electrophysiology by β1-blocker therapy. A: APs and ERP (↔); B: mean (±standard error) APD at 50% and 90% repolarization (APD50 and APD90) and ERP; C: transient outward K+ currents, recorded in single atrial myocytes from patients in SR, treated with a β1-blocker ≥7 days (solid symbols) versus those in SR who were not treated with a β-blocker (open symbols). *P <.05 versus non β-blocker. D: Correlation between atrial cell ERP and patient's atenolol dose/body weight. Heart rate ≤75 bpm. Dashed lines indicate the 95% confidence interval. Panels A and C are based on data in reference 31 with permission from Elsevier. Heart Rhythm 2008 5, S1-S6DOI: (10.1016/j.hrthm.2008.01.016) Copyright © 2008 Heart Rhythm Society Terms and Conditions