Michael H. Lehmann

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S1S3 by 66 +/- 17 ms; (2) increased incidence of initiation of sustained VT after the V3 phenomenon resulting from macroreentry within the His-Purkinje system (Re-HPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.

Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia

The relation between the morphologic configuration of QRS complexes during wide QRS tachycardia induced during electrophysiologic studies and sinus rhythm was examined in 18 patients who had preexisting left or right bundle branch block. Representative QRS complexes during sinus rhythm and during tachycardia were isolated from each patient and juxtaposed for comparison. The QRS complexes that constituted each pair were judged by 4 observers as being identical, different or, if the decision was equivocal, similar. Nine patients had supraventricular tachycardia (SVT). In 8 of the 9 patients, all 4 observers found the QRS complexes during sinus rhythm and SVT identical in morphologic configuration. In the other patient, 2 observers found the QRS complexes identical and 2 found them similar. In 12 patients ventricular tachycardia (VT) was induced. In 11 of these 12, all 4 observers found the QRS complexes during VT different from their respective sinus beats. In the other patient, 3 observers found the QRS complexes different, whereas the fourth found them similar. During SVT, the QRS duration was unchanged from the corresponding value during sinus rhythm, whereas in patients with VT, QRS width increased by a mean of 56 +/- 20 ms (p less than 0.001). The results of our study suggest that the electrocardiographic differentiation of wide QRS tachycardia in patients with preexisting bundle branch block can be accomplished easily and accurately by comparing the QRS complexes during tachycardia with those during sinus rhythm: If the complexes are identical, the tachycardia is supraventricular, but if they are different, the arrhythmia is ventricular in origin.

Divergence between refractoriness of His-Purkinje system and ventricular muscle with abrupt changes in cycle length.

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.

Effect of verapamil on retrograde atrioventricular nodal conduction in the human heart

The electrophysiologic effects of intravenous verapamil (0.15 ml/kg) on retrograde atrioventricular (AV) nodal conduction were studied in 17 patients who had no evidence of supraventricular reentrant tachycardia, demonstrable dual AV nodal refractory period curves or accessory pathways. Using the His bundle electrogram, incremental ventricular pacing and the ventricular ex-trastimulus (V2) technique, the ventriculoatrial (VA), retrograde His-Purkinje system (V2H2) and AV nodal conduction (H2A2) times were measured before and after treatment with verapamil. With incremental ventricular pacing during the control period, the cycle length that produced VA block ranged from 260 to 520 ms (mean ± standard deviation 337.0 ± 67.8 ms). After the administration of verapamil, VA conduction was abolished in 2 patients, and in 12 patients the mean ventricular pacing cycle length producing VA block increased from 305.0 ± 35.7 ms during the control period to 413.3 ± 66.8 ms (p The results show that verapamil exerts a depressant effect on retrograde AV nodal conduction in the majority of patients, including those with rapid conduction.

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmacologic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 +/- 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 +/- 9 months was 32% (p less than 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Postextrasystolic alterations in refractoriness of the His-Purkinje system and ventricular myocardium in man.

The changes in refractoriness of the His-Purkinje system (HPS) and ventricular myocardium (VM) that are associated with the occurrence of postextrasystolic beats in man are unknown. Accordingly, using a pacing model of the cycle length changes created by a ventricular extrasystole-postextrasystole sequence, we measured retrograde HPS and VM relative and effective refractory periods (RRP and ERP) in 15 patients with the use of ventricular test extrastimuli during preextrasystolic basic control drive (method I) and after programmed extrasystolic (method II) and postextrasystolic (method III) beats. The basic cycle length (same for all three methods) ranged from 500 to 700 msec (mean 613 +/- 74 msec) and the extrasystolic coupling interval (identical for methods II and III) comprised 68 +/- 4% of the basic cycle length. In method III the postextrasystolic pause was programmed to equal the basic cycle length (i.e., noncompensatory) so that method I could serve as control for method III. RRP-HPS decreased from 331 +/- 37 msec in method I to 245 +/- 37 msec or less during the extrasystolic beat (p less than .001). A less dramatic corresponding shortening of ERP-VM and RRP-VM was observed, i.e., from 245 +/- 21 and 264 +/- 23 msec (method I) to 233 +/- 23 and 251 +/- 22 msec (method II), respectively (p less than .001). With the postextrasystolic beat, however, RRP-HPS increased to exceed the control value of method I by 23 +/- 11 msec (p less than .001). This greater-than-expected RP prolongation was also associated with significantly increased retrograde HPS conduction times (in method III vs method I) at both long and short test stimulus coupling intervals.(ABSTRACT TRUNCATED AT 250 WORDS)