Atrial-Selective Approaches for the Treatment of Atrial Fibrillation
Joachim R. Ehrlich, MD*,1,*,
Peter Biliczki, MD, PhD*,2,
Stefan H. Hohnloser, MD, FACC*,3 and
Stanley Nattel, MD, FACC ,4
* Division of Cardiology, Section of Electrophysiology, J.W. Goethe-University, Frankfurt, Germany
Research Center, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada.
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Figure 1 Regional Difference in Ionic Current Contribution to APs
Differences in key ion currents between atrial (blue) and ventricular (red) action potentials (APs). Atrial APs have smaller AP amplitude and less negative resting membrane potential. Currents (green) identified above the line illustrating the APs are present in both regions; atrially expressed ionic currents are illustrated below the AP schematic (blue). IKACh = acetylcholine-regulated potassium current; IKur = ultrarapid delayed-rectifier potassium current; INa = sodium current.
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Figure 2 Targets of "Atrial-Selective" Antiarrhythmic Drugs
This figure presents a simplified cell with sarcolemmal membrane and ion currents and transporters that have served as targets for atrial-selective therapy shown. Pharmacologic agents discussed in the paper are presented in boxes, and filled arrows denote inhibition of specific currents. Rotigaptide is a connexin (Cx) activator—as illustrated by the "+" symbol. JTV-519 stabilizes ryanodine-receptor (RyR) and calstabin complexes. DPO = diphenylphosphine oxide; SR = sarcoplasmic reticulum; other abbreviations as in Figure 1.
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