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(Circulation. 2006;114:2113-2121.)
© 2006 American Heart Association, Inc.
Arrhythmia/Electrophysiology |
From the Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Md.
Correspondence to Dr Leslie Tung, Department of Biomedical Engineering, The Johns Hopkins University, 720 Rutland Ave, Baltimore, MD 21205. E-mail ltung{at}jhu.edu
Received November 7, 2005; revision received August 15, 2006; accepted August 18, 2006.
Background Functional reentry in the heart takes the form of spiral waves. Drifting spiral waves can become pinned to anatomic obstacles and thus attain stability and persistence. Lidocaine is an antiarrhythmic agent commonly used to treat ventricular tachycardia clinically. We examined the ability of small obstacles to anchor spiral waves and the effect of lidocaine on their attachment.
Methods and Results Spiral waves were electrically induced in confluent monolayers of cultured, neonatal rat cardiomyocytes. Small, circular anatomic obstacles (0.6 to 2.6 mm in diameter) were situated in the center of the monolayers to provide an anchoring site. Eighty reentry episodes consisting of at least 4 revolutions were studied. In 36 episodes, the spiral wave attached to the obstacle and became stationary and sustained, with a shorter reentry cycle length and higher rate. Spiral waves could attach to obstacles as small as 0.6 mm, with a likelihood for attachment that increased with obstacle size. After attachment, both conduction velocity of the wave-front tip and wavelength near the obstacle adapted from their pre-reentry values and increased linearly with obstacle size. In contrast, reentry cycle length did not correlate significantly with obstacle size. Addition of lidocaine 90 µmol/L depressed conduction velocity, increased reentry cycle length, and caused attached spiral waves to become quasi- attached to the obstacle or terminate.
Conclusions Anchored spiral waves exhibit properties of both unattached spiral waves and anatomic reentry. Their behavior may be representative of functional reentry dynamics in cardiac tissue, particularly in the setting of monomorphic tachyarrhythmias.
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