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(Circulation. 2001;103:1148.)
© 2001 American Heart Association, Inc.

Basic Science Reports

Mechanisms of Resetting Reentrant Circuits in Canine Ventricular Tachycardia

Michael S. Hanna, MD; James Coromilas, MD; Mark E. Josephson, MD; Andrew L. Wit, PhD; Nicholas S. Peters, MD

From the Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pa (M.S.H.); Departments of Medicine (J.C.) and Pharmacology (A.L.W.), College of Physicians and Surgeons, Columbia University, New York, NY; Department of Medicine, Beth Israel Hospital and Thorndike Electrophysiology Laboratory, Harvard Medical School, Boston, Mass (M.E.J.); and Department of Cardiac Electrophysiology, Imperial College School of Medicine and St Mary’s Hospital London, UK (N.S.P.).

Correspondence to Michael S. Hanna, MD, Duncan Building, 301 S 8th St, Philadelphia, PA 19106. E-mail mhanna{at}mail.med.upenn.edu

Background—Resetting has been used to characterize reentrant circuits causing clinical tachycardias.

Methods and Results—To determine the mechanisms of resetting, sustained ventricular tachycardia was induced in dogs with 4-day-old myocardial infarctions by programmed stimulation. Premature stimulation was accomplished from multiple regions within reentrant circuits; resetting curves were constructed and compared with activation maps. Monotonically increasing responses, or a "mixed" response (increasing portion preceded by a flat portion), occurred. All reentrant circuits had a fully excitable gap. Interval-dependent conduction delay and concealed retrograde penetration led to increased resetting response curves.

Conclusions—Multiple mechanisms revealed by mapping cause resetting of reentrant circuits.

Key Words: reentry • resetting • anisotropy • mapping

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