Mechanism of Procainamide-Induced Prevention of Spontaneous Wave Break During Ventricular Fibrillation

Several different patterns of wave break have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. To determine the mechanism by which wave breaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in six isolated swine right ventricles (RV). Among 763 episodes of wave break (0.75 times · s−1· cm−2), optical maps showed three patterns: 80% due to a wave front encountering the refractory wave back of another wave, 11.5% due to wave fronts passing perpendicular to each other, and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in three-dimensional tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-tail interactions and filament break. We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wave break are produced by two fundamental mechanisms: head-tail interaction between waves and filament break.

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Action potential duration restitution and ventricular fibrillation due to rapid focal excitation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00867.2001 ◽

2002 ◽

Vol 282 (5) ◽

pp. H1915-H1923 ◽

Cited By ~ 20

Author(s):

Moshe Swissa ◽

Zhilin Qu ◽

Toshihiko Ohara ◽

Moon-Hyoung Lee ◽

Shien-Fong Lin ◽

...

Keyword(s):

Ventricular Fibrillation ◽

Action Potential ◽

Action Potential Duration ◽

Cardiac Tissue ◽

Diacetyl Monoxime ◽

Focal Excitation ◽

Mean Cycle ◽

Rapid Activation ◽

Action Potential Duration Restitution ◽

Wave Break

The focal source hypothesis of ventricular fibrillation (VF) posits that rapid activation from a focal source, rather than action potential duration (APD) restitution properties, is responsible for the maintenance of VF. We injected aconitine (100 μg) into normal isolated perfused swine right ventricles (RVs) stained with 4-{β-[2-(di- n-butylamino)-6-naphthyl]vinyl}pyridinium (di-4-ANEPPS) for optical mapping studies. Within 97 ± 163 s, aconitine induced ventricular tachycardia (VT) with a mean cycle length 268 ± 37 ms, which accelerated before converting to VF. Drugs that flatten the APD restitution slope, including diacetyl monoxime (10–20 mM, n = 6), bretylium (10–20 μg/ml, n = 3), and verapamil (2–4 μg/ml, n = 3), reversibly converted VF to VT in all cases. In two RVs, VF persisted despite of the excision of the aconitine site. Simulations in two-dimensional cardiac tissue showed that once VF was initiated, it remained sustained even after the “aconitine” site was eliminated. In this model of focal source VF, the VT-to-VF transition occurred due to a wave break outside the aconitine site, and drugs that flattened the APD restitution slope converted VF to VT despite continuous activation from aconitine site.

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