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Cellular and ionic basis for T-wave alternans under long-QT conditions
1Masonic Medical Research Laboratory, Utica, NY, USA.
Circulation
|March 23, 1999
Summary
T-wave alternans (TWA) in long-QT syndrome is caused by M-cell alternans and exaggerated repolarization dispersion. Intracellular calcium cycling is critical for maintaining TWA and mechanical alternans.
Area of Science:
- Cardiology
- Electrophysiology
- Molecular Cardiology
Background:
- T-wave alternans (TWA) is an ECG phenomenon linked to long-QT syndromes (LQTS).
- This study investigates the cellular basis of TWA in LQT3 conditions.
Purpose of the Study:
- To examine the cellular and ionic mechanisms of TWA induced by rapid pacing in a canine model of LQT3.
- To elucidate the role of intracellular calcium in TWA.
Main Methods:
- Simultaneous recording of transmembrane action potentials and intramural electrograms.
- Utilized sea anemone toxin (ATX-II) to mimic LQT3 conditions and varied pacing rates.
- Measured isometric tension development and T-wave alternans.
Main Results:
- Rapid pacing induced TWA and mechanical alternans, primarily due to M-cell alternans and increased repolarization dispersion.
- TWA polarity alternations correlated with M-cell repolarization sequence reversal.
- Electrical and mechanical alternans were suppressed by ryanodine and low extracellular calcium, indicating a role for calcium cycling.
Conclusions:
- M-cell action potential duration alternans and exaggerated transmural repolarization dispersion are key drivers of TWA in LQTS.
- Steady-state TWA and mechanical alternans depend on beat-to-beat alternans in intracellular calcium, unlike transient TWA forms.
