Effect of verapamil on retrograde atrioventricular nodal conduction in the human heart.
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Biomedical subjects
Publications and source records attributed to R Mahmud.
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Patients with DDD pacemakers who have intact retrograde conduction are known to be at risk of developing ventricular and "endless loop" tachycardia. To address this problem, a pacing protocol was designed in which V2A2 conduction was assessed in 16 patients during ventricular pacing alone (standard method) and during paced atrioventricular (AV) sequential drive (AV sequential method); the results were then compared. In eight of 16 patients who had intact retrograde conduction with both methods (group 1), the V2A2 intervals were significantly shorter (by 60 to 340 msec) with the AV sequential method. In the remaining eight patients, who demonstrated V2A2 block with the standard method, no V2A2 block occurred with the AV sequential method. In this study, two sets of AV intervals were programmed to produce collision of the two impulses (atrial and ventricular), either in the AV node or the His-Purkinje system (HPS). The site of V2A2 facilitation was related to the site of impulse collision. These results can be explained by earlier excitation by the atrial impulse (of AV node and/or HPS) during AV sequential pacing. However, in some cases it was evident that antegrade propagation of the atrial impulse was responsible for subsequent facilitation. The data suggest that assessment of retrograde conduction in candidates for DDD pacemakers can be made most accurately by the AV sequential method.
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The concept that refractoriness of the His-Purkinje system (HPS) and ventricular muscle both vary directly with cycle length is based on observations during the use of constant cycle length. During abrupt changes in ventricular cycle length, refractoriness of the ventricular muscle is known to reflect the cumulative durations of preceding cycle lengths. The effect of such changes on retrograde refractoriness of the HPS is not known. In this study refractoriness of ventricular muscle and of the HPS was evaluated in 30 patients with normal intraventricular conduction by the ventricular extrastimulus (V2) technique during constant cycle length (method I) and during abrupt cycle length changes (method II). During method II the cycle length immediately before V2 was identical to the constant cycle length of method I and therefore was designated as the reference cycle length (CLR); however, the cycle length preceding (CLP) CLR was either longer than CLR (method IIA) by 100 to 300 msec in 11 patients or shorter than CLR (method IIB) by 100 to 300 msec in 30 patients. Results showed that compared with method I, method IIA shortened the relative refractory period (RRP) of the HPS from 350 +/- 29 to 344 +/- 29 msec (p less than .04), whereas the effective refractory period (ERP) of the ventricular muscle increased from 225 +/- 21 to 233 +/- 20 msec (p less than .0001). In contrast, compared with method I, method IIB lengthened the RRP of the HPS from 335 +/- 30 to 351 +/- 35 msec (p less than .0001), whereas ERP of the ventricular muscle decreased from 223 +/- 23 to 213 +/- 22 msec (p less than .0001). Similar to the inverse relationship between CLP and RRP of the HPS, ERP of the HPS was prolonged with short CLP (method IIB) compared with long CLP (method IIA). The results indicate a marked divergence between refractoriness of the HPS and of ventricular muscle during abrupt cycle length changes; these results were not previously anticipated. Whereas ventricular muscle responded to cumulative effects of preceding cycle lengths and varied directly with CLP, the HPS appeared to respond to directional and/or dynamic changes in cycle length and varied inversely with CLP. Moreover, in contrast to ventricular muscle, the HPS appeared to be responsive to rate of change in cycle length whereby short-to-long change in cycle length had a greater effect than long-to-short change in cycle length.