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Am J Physiol Heart Circ Physiol 283: H1116-H1122, 2002; doi:10.1152/ajpheart.00927.2001
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Vol. 283, Issue 3, H1116-H1122, September 2002

Increased vulnerability to inducible atrial fibrillation caused by partial cellular uncoupling with heptanol

Toshihiko Ohara, Zhilin Qu, Moon-Hyoung Lee, Keiko Ohara, Chikaya Omichi, William J. Mandel, Peng-Sheng Chen, and Hrayr S. Karagueuzian

Division of Cardiology, Cedars-Sinai Research Institute, Department of Medicine, University of California of Los Angeles School of Medicine, Los Angeles, California 90048

We hypothesized that partial cellular uncoupling produced by low concentrations of heptanol increases the vulnerability to inducible atrial fibrillation (AF). The epicardial surface of 12 isolated-perfused canine left atria was optically mapped before and after 1-50 µM heptanol infusion. At baseline, no sustained (>30 s) AF could be induced in any of the 12 tissues. However, after 2 µM heptanol infusion, sustained AF was induced in 9 of 12 tissues (P < 0.001). Heptanol >5 µM caused loss of 1:1 capture during rapid pacing, causing no AF to be induced. AF was initiated by conduction block across the fiber leading to reentry, which broke up after one to two rotations into two to four independent wavelets that sustained the AF. Heptanol at 2 µM had no effect on the cellular action potential duration restitution or on the maximal velocity rate over time of the upstroke. The effects of heptanol were reversible. We conclude that partial cellular uncoupling by heptanol without changing atrial active membrane properties promotes wavebreak, reentry, and AF during rapid pacing.

optical mapping; reentry


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