Myocardial conduction time and antiarrhythmic drugs

Complete a-v block was induced in anesthetized mongrel dogs by direct electrocoagulation of the a-v node. The ventricles were paced by steady stimulation (S₁) at a rate of 100/min. and by test stimuli (S₂) with varying post S₁ delay. Right ventricular myocardial tension was measured from the S₂ stimulation site by a specially designed miniature strain gage and from a different site by a Walton-Brodie strain gage. A reproducible time lag between the two sites could be measured by comparing the differences in mechanical response to S₂ stimuli. This time difference was called ΔIT. ΔIT varied markedly (from 10-60 msec) when measured at different sites but no linear relationship between ΔIT and the inter-gage distance could be observed. Increasing the S₂ current intensity induced shortening of ΔIT from 37±13 msec (mean±S.D.) at the threshold current to 16±10 msec (mean±S.D.) with 10 mA. A strength-ΔIT curve could be constructed and was found to be remarkably reproducible during the experiment. Quinidine and disopyramide induced upward displacement of the curve, lidocaine did not change it while verapamil lowered the ΔIT values. We suggest that ΔIT can be used as a reliable indicator of myocardial conduction rate. The possible reasoning for this suggestion has been discussed.