Abnormalities in ventricular function following MI.

The authors reply: To the Editor: As stated by Dr. Bete, studies of Purkinje fiber bundles perfused with physiologic salt solution have shown that procaine amide prolongs the action potential duration (APD) and the effective refractory period (ERP), the latter to a greater extent than the former.' We did not discuss the differences Dr. Bete has noted in calculating the AAPD/AERP ratio for our studies because our method for determining the ERP (as outlined in the text) differs somewhat from that used in other investigations. To measure the ERP we delivered a premature stimulus (S2) after each basic drive (S,), not intermittently as is often done. The value we reported for the APD was that at the basic stimulus rate; that for the ERP (with an S2 being delivered after each S) was obtained at a rate twice as fast as the basic drive. Hence, although the method was sensitive to changes in APD and ERP it did not lend itself to the direct determination of the AAPD/AERP which is calculated when both parameters are being measured at the same stimulus rate. Our studies did indicate that at therapeutic plasma procaine amide concentrations there is no significant change in membrane responsiveness and the ERP is only slightly prolonged; while when high concentrations (equivalent to those attained in other studies) are attained membrane responsiveness is depressed and the ERP is more markedly prolonged. We stated that the rather small prolongation of ERP and the lack of effect on membrane responsiveness which occur during maintenance of therapeutic plasma procaine amide concentrations "suggest that altered response to premature impulses may not be as consistent a mechanism for abolition of arrhythmias as are changes in conduction and automaticity." (The latter changes were invariably noted during maintenance of therapeutic concentrations.) I am not certain of the intent of Dr. Bete's comment regarding automaticity and conduction time. We demonstrated that following a single procaine amide injection depression of automaticity occurred well before changes in other parameters including conduction time in the Purkinje fiber bundles. The implication was that tissue concentrations of procaine amide required for suppression of automaticity might be lower than those required for depression of conduction. As a result of these observations we speculated that ventricular arrhythmias which respond rapidly to intravenously administered procaine amide might be due to enhanced automaticity and those which respond more slowly, or require higher concentrations of procaine amide, might be due to abnormal conduction.