Prolongation of the conduction time of early premature beats: a marker of ventricular action potential duration.

The conduction time of premature ventricular complexes, which are generally quite constant throughout late diastole, abruptly prolongs during repolarization as the refractory period of the ventricle is approached (conduction time breakpoint). The relationship between the conduction time breakpoint and the recovery properties of the ventricle was examined by relating the conduction time of premature ventricular complexes to the effective refractory period and the monophasic action potential derived from the ventricular suction electrode signal. In five anesthetized dogs during ventricular drive (cathode; 2.5 Hz; three times diastolic threshold), effective refractory period and conduction times of premature ventricular complexes were derived from computerized strength-interval curves. The recovery properties of the ventricle were altered by infusion of norepinephrine, calcium, and quinidine and by cooling (29 degrees to 34 degrees C). In these circumstances, the moment of conduction time breakpoint changes correlated well (r = 0.93) with the end of the negative slope of the ventricular suction electrode signal, which suggests that the conduction time breakpoint may be an indirect marker of the ventricular action potential duration. In seven additional dogs the interval between the effective refractory period and the conduction time breakpoint, which defines the relative refractory period, was increased by 5 to 8 minutes of ischemia (coincident with height of ventricular vulnerability) and was reversed by procainamide. Procainamide is known to diminish spontaneous and induced ventricular arrhythmias by reducing the disparity between the effective refractory period and the action potential duration.(ABSTRACT TRUNCATED AT 250 WORDS)