Electric field perturbations of spiral waves attached to millimeter-size obstacles.

Reentrant spiral waves can become pinned to small anatomical obstacles in the heart and lead to monomorphic ventricular tachycardia that can degenerate into polymorphic tachycardia and ventricular fibrillation. Electric field-induced secondary source stimulation can excite directly at the obstacle, and may provide a means to terminate the pinned wave or inhibit the transition to more complex arrhythmia. We used confluent monolayers of neonatal rat ventricular myocytes to investigate the use of low intensity electric field stimulation to perturb the spiral wave. A hole 2-4 mm in diameter was created in the center to pin the spiral wave. Monolayers were stained with voltage-sensitive dye di-4-ANEPPS and mapped at 253 sites. Spiral waves were initiated that attached to the hole (n = 10 monolayers). Electric field pulses 1-s in duration were delivered with increasing strength (0.5-5 V/cm) until the wave terminated after detaching from the hole. At subdetachment intensities, cycle length increased with field strength, was sustained for the duration of the pulse, and returned to its original value after termination of the pulse. Mechanistically, conduction velocity near the wave tip decreased with field strength in the region of depolarization at the obstacle. In summary, electric fields cause strength-dependent slowing or detachment of pinned spiral waves. Our results suggest a means to decelerate tachycardia that may help to prevent wave degeneration.