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The Mechanism of Pause‐Induced Torsade de Pointes in Long QT Syndrome
Author(s) -
LIU JINQIU,
LAURITA KENNETH R.
Publication year - 2005
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2005.40677.x
Subject(s) - repolarization , medicine , long qt syndrome , cardiology , qt interval , sotalol , ventricular repolarization , torsades de pointes , electrophysiology , atrial fibrillation
Torsade de pointes (TdP), is often preceded by a short‐long cycle length sequence. However, the causal relationship between the pause associated with a short‐long cycle length sequence and TdP is not completely understood. This study tests the hypothesis that a pause enhances both dispersion of repolarization and EAD formation; however, EADs that form where APD is longest will be less likely to initiate TdP. Methods and Results: We used optical mapping to measure transmural action potentials from the canine left ventricular wedge preparation. D‐sotalol and ATX‐II were used to mimic LQT2 and LQT3, respectively. The pause significantly enhanced mean APD (from 356 ± 20 to 381 ± 25 msec in LQT2, P < 0.05; from 609 ± 92 to 675 ± 98 msec in LQT3, P < 0.05) and transmural dispersion (from 35 ± 9 to 46 ± 11 msec in LQT2, P < 0.05; from 121 ± 85 to 171 ± 98 msec in LQT3, P < 0.05) compared to steady state pacing. Under LQT3 condition EADs, EAD‐induced triggered activity, and TdP were more likely to occur following a pause. Interestingly, the triggered beat following a pause always broke through at the region of maximum local repolarization gradient. Conclusion: These data suggest that a pause accentuates transmural repolarization gradients and facilitates the formation of EADs and EAD‐induced triggered activity. In contrast to our hypothesis, the findings of this study support the concept that M‐cells (where APD is longest) can play an important role in both the origination of EAD‐induced triggered activity and unidirectional block associated with TdP.