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Experimental models of torsade de pointes
L Eckardt1, W Haverkamp, M Borggrefe
1Hospital of the Westfälische Wilhelms-University, Department of Cardiology and Angiology, Münster, Germany. l.eckardt@uni-muenster.de
Cardiovascular Research
|October 9, 1998
Summary
Torsade de pointes, a dangerous heart rhythm, is often caused by QT prolongation. Studies suggest early afterdepolarizations and triggered activity initiate these arrhythmias, with reentry potentially sustaining them.
Area of Science:
- Cardiology
- Electrophysiology
- Molecular Biology
Background:
- Torsade de pointes (TdP) is a life-threatening polymorphic ventricular tachycardia linked to QT prolongation.
- Understanding the ionic mechanisms of delayed repolarization is crucial for TdP research.
Purpose of the Study:
- To review experimental models investigating the mechanisms of Torsade de pointes.
- To synthesize findings on ion channel roles, early afterdepolarizations, and reentry in TdP.
Main Methods:
- In vitro studies on cardiac cells (e.g., M cells) examining ion channel function.
- Development of isolated heart models simulating clinical conditions (bradycardia, hypokalemia).
- In vivo induction of TdP-like arrhythmias in canine and rabbit models using specific drugs and toxins.
Main Results:
- Early afterdepolarizations and triggered activity are implicated in initiating TdP.
- Models using sodium and potassium channel blockers are of particular interest, especially with advances in long QT syndrome genetics.
- Reentry due to refractory period inhomogeneity is a proposed mechanism for sustained TdP.
Conclusions:
- Experimental models provide insights into TdP's ionic basis and arrhythmogenesis.
- Triggered activity is likely the initiating event for TdP, while reentry may perpetuate it.