Two types of ventricular fibrillation in isolated rabbit hearts: importance of excitability and action potential duration restitution.
BACKGROUND
The combined effects of excitability and action potential duration (APD) restitution on wavefront dynamics remain unclear.


RESULTS
We used optical mapping techniques to study Langendorff-perfused rabbit hearts. In protocol IA (n=10), D600 at increasing concentrations was infused during ventricular fibrillation (VF). With concentration increased to 0.5 mg/L, fast VF (dominant frequency, 19.1+/-1.8 Hz) was consistently converted to ventricular tachycardia (VT). However, increasing D600 further to 2.5 or 5.0 mg/L converted VT to slow VF (11.9+/-2.3 Hz, P=0.0011). In an additional 4 hearts (protocol IB), tetrodotoxin converted a preexisting VT to slow VF (11.0+/-1.4 Hz). Optical maps show wandering wavelets in fast VF, organized reentry in VT, and spatiotemporal periodicity in slow VF. In protocol II, we determined APD and conduction time(-1) (CT(-1)) restitutions during D600 infusion. CT(-1) was used as an estimate of excitability. At 0.1 mg/L, APD and CT(-1) restitutions were steep and flat, respectively. APD restitution became flattened when D600 increased to 0.5 mg/L, converting fast VF to VT. Further increasing D600 to 2.5 or 5.0 mg/L steepened CT(-1) restitution and widened the range of S(1) pacing cycle lengths over which CT(-1) decreased, converting VT to slow VF.


CONCLUSIONS
Two types of VF exist in isolated rabbit hearts. Fast (type I) VF is associated with a steep APD restitution, a flat CT(-1) restitution, and wandering wavelets. Slow (type II) VF is associated with a flat APD restitution, a steep CT(-1) restitution, and spatiotemporal periodicity. Both excitability and APD restitution are important in VF maintenance.
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D018780:Body Surface Potential Mapping; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002304:Cardiac Pacing, Artificial; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography / Q000187:drug effects / Q000379:methods; D004567:Electrodes, Implanted; D022062:Electrophysiologic Techniques, Cardiac; D005456:Fluorescent Dyes; D005583:Fourier Analysis; D005711:Gallopamil / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D008027:Light; D055095:Optics and Photonics; D011726:Pyridinium Compounds; D011817:Rabbits; D026941:Sodium Channel Blockers / Q000494:pharmacology; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000145:classification* / Q000188:drug therapy / Q000503:physiopathology*
D002121:Calcium Channel Blockers; D005456:Fluorescent Dyes; D011726:Pyridinium Compounds; D026941:Sodium Channel Blockers; D005711:Gallopamil; D013779:Tetrodotoxin; C050019:1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium betaine