Predicting ventricular tachycardia cycle length after procainamide by assessing cycle length-dependent changes in paced QRS duration.

Abstract

To determine if paced cycle length-dependent changes in the QRS duration correlate with the change in ventricular tachycardia (VT) cycle length after procainamide, we measured the QRS duration during sinus rhythm and during right ventricular pacing before and after procainamide (mean concentration, 9.9 ,ug/ml) in 18 patients with morphologically identical VT induced at both study periods. Pacing was performed at 600 msec or the longest cycle length that allowed for uninterrupted capture and at a cycle length that was within 50 msec of the VT cycle length observed during the control study (mean, 313 ±51 msec). After procainamide, the VT cycle length increased from 285±62 to 368±70 msec (percent change, 30±13%). The QRS duration during sinus rhythm increased from 125+±25 to 145±29 msec (percent change, 16%). The QRS duration at both paced cycle lengths was the same in the baseline state (191±26 msec). However, the change in QRS duration after procainamide at the shorter paced cycle length compared to a 39+±13 msec (18%) increase at the longer paced cycle, p < 0.001. There was a significant correlation between the percent change in QRS duration at the shorter paced cycle length and the percent change in VT cycle length (r=0.84,p <0.001) with the relation expressed by the regression equation: percent change in VT cycle length = -2.8+1.16 x percent change in QRS duration. These findings support the hypothesis that the mechanism for the change in VT cycle length after procainamide is due to a rate-dependent change in conduction. (Circulation 1989;79:39-46

Electrophysiology of Ventricular Tachycardia:

“…The effects of antiarrhythmic agents have been used to sort out the underlying mechanisms. [55][56][57][58][59][60][61][62] Most important was the recognition that triggered activity due to delayed afterdepolarizations most often occurred in response to catecholamines. This was due to enhanced adenyl cyclase activity, which subsequently led to increased intracellular calcium, which then triggered a nonspecific transient inward current carried by sodium.…”

“…The effects of antiarrhythmic agents have been used to sort out the underlying mechanisms 55–62 . Most important was the recognition that triggered activity due to delayed afterdepolarizations most often occurred in response to catecholamines.…”

Electrophysiology of Ventricular Tachycardia:

“…The effects of antiarrhythmic agents were also used to sort out the underlying mechanisms 55–62 . Most importantly was the recognition that triggered activity due to delayed afterdepolarizations most often occurred in response to catecholamines.…”