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Original Articles |
From the Masonic Medical Research Laboratory, Utica, NY (A.B., C.A.), and the Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan (W.S.).
Correspondence to Dr Alexander Burashnikov, Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, New York 13501. E-mail sasha{at}mmrl.edu
Received January 22, 2007; accepted May 30, 2008.
Background— The arrhythmogenic effects of hyperthermia have been highlighted in the Brugada syndrome but remain largely unexplored in other arrhythmic syndromes. The present study examines the effect of hyperthermia on transmural dispersion of action potential duration (TD-APD), early afterdepolarization (EAD) activity, and torsade de pointes (TdP) under long-QT conditions.
Methods and Results— Standard and floating glass microelectrodes were used to record action potentials from epicardial, M cell, and endocardial regions of the arterially perfused left ventricle wedge, from tissue slices isolated from these regions, and from isolated Purkinje fibers. A transmural ECG was simultaneously recorded across the wedge. Under baseline conditions and in the presence of IKs block (chromanol 293B), hyperthermia (39°C to 40°C) abbreviated APD in tissue slices from all 3 regions. In the presence of IKr block (E-4031), hyperthermia prolonged APD and induced or augmented EADs in M cell and Purkinje preparations at pacing cycle lengths
800 ms but abbreviated APD in epicardium and endocardium, resulting in a marked accentuation of TD-APD. Ryanodine prevented the hyperthermia-induced EAD. In perfused wedge preparations, hyperthermia abbreviated APD throughout both in the absence or presence of IKr or IKs block and did not induce EADs or TdP. Combined IKr and IKs block increased TD-APD and induced EADs (4/12) and spontaneous TdP (3/12) at 36°C to 37°C; hyperthermia (39°C to 40°C) further accentuated TD-APD and facilitated the development of EAD activity (9/12) and TdP (6/12).
Conclusions— Our findings suggest that hyperthermia can be associated with an increased arrhythmic risk when the repolarization reserve of the myocardium is compromised.
Key Words: arrhythmias electrophysiology fever long-QT syndrome triggered activity
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