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Repetitive responses to ventricular extrastimuli — incidence, mechanism and significance
ABSTRACTS
EFFECT OF AGE ON A'V CONDUCTION IN PATIENTS WITH CHRONIC BIFASCICULAR BLOCK Edwin Palileo, MD; Pablo Denes, MD, FACC; Steven Swiryn, MD; Fernando Amat-y-Leon, MD, FACC; Christopher Wyndham, MD; Delon Wu, MD, FACC; Kenneth Rosen, MD, FACC, University of Illinois, Chicago, Illinois. It has been suggested that advanced age predicts severity of conduction disease in patients (pts) with established chronic bifascicular block (BFB). This hypothesis was tested in 416 prospectively followed (mean follow-up 978 53 days ) pts with BFB. Pts were subdivided into younger group (YG), ages 40 tO 65 years (mean 53 + 1.5) and older group (OG), ages 65 years and over (mean 75 + i,i). The pts were further separated into those with primary conduction disease (PCD) (72 pts), and those with organic heart disease (OHD) (344pts). Electrophysiological findings in the PCD pts were as follows (mean + SEM YG, 28 pts vs OG, 44 pts): P~A (34 + 2.3 vs 35 + 1.7 msec), AH 90 + 5.2 vs i01 0+ 4.2 msec), H---V (51 + 3.3 vs 49 + 1.9 msec)? % with prolo-nged H-V (~ 55•msec)--(32•vs 16%)~ Progression to spontaneous A-V block was seen in 0 YG pts (0%), and 1 OG pt (0.5%). None of these differences were significant. In the OHD group findings were (YG, 180 pts vs OG, 164 ptS)r: P--A (33 + 0.8 VS 3 6 + 0-8 msec), A-H (105 + 2.9 vs 116 ! 4.1 msec), H-V (56 + I.i vs 55 + i.I msec)~ % with prolonged H-V (44% vs 41%~. Progressio--n to SHB was seen in 9 YG pts (5%) and i 0 0 G pts (6%). All differences were insignificant except the increase in A-H in the OG (P< 0.02). In conclusion, with the exception of A-H in OHD group, severity and progression of conduction disease is independent of advanced age in pts with established chronic BFB. Age differences do not appear responsible for d i f f e ~ ent incidences of A-V block in previously reported series of BFB pts.
MECHANISM OF THE REPETITIVEVENTRICULAR RESPONSE IN MAN. H. Lo Greene, M . D . , FACC; A.H. Schaeffer, M.D.; P. Ro Reid, M.D., FACC, Johns Hopkins University School of Medicine, Baltimore, Maryland. This study examined the •mechanism responsible for the repetitive ventricular response (RVR) in man, defined as the production of 2 or more ventricular premature beats in response to a sihgle premature ventricular pacing stimulus during atrial pacing or sinus rhythm. We havepreviously demonstrated that the RVR identifies patients (pts) at risk of ventricular tachycardia or sudden death. Seventy-five pts with RVR were analyzed. Both the surface QRS configuration of the repetitive beats and the presence of conduction system deflections (His bundle or right bundle potentials) were evaluated. Bundle branch reentry a-~ a mechan|sm of RVR wouidbe supported if the surface QRS configuration resembled the beats paced from theright ventricle - a left bundle branch block pattern - and if His bundle or right bundle deflections were present before the repetitive beats. Sixty-nine of the 75 pts had repetitive beats with a different QRS morphology from the beats paced from the right ventricle. In 23 of these 75 pts an additional catheter was positioned to record His bundle or right bundle potentials during ventH~ular premature Stimulation. In 22 Of the 23 pts, there was no His bundle or right bundle potential preceding the repetitive beats. These data support the conclusion that RVR involves reentry which does not include the bundle branches and therefori~ is a different phenomenon than reentry beats seen in normal pts during ventrlcular pacing and ventricular premature stimulation. Reentry in RVR more likely involves diseased myocard~um c~nd may explain the predictive value of RVR for ventHcular tachycardla and sudden death.
390
February 1979
The American Journal of CARDIOLOGY
REPETITIVE RESPONSES TO VENTRICULAR EXTRASTIMULI INCIDENCE, MECHANISM AND SIGNIFICANCE Ardeshir Farshidi, MD, FACC; Eric L. Michelson, MD; Allan M. Greenspan, MD; Scott R. Spielman MD; John A. Kastor, MD, FACC; Leonard N. Horowitz •, MD, FACC, Mark E. Josephson, MD, FACC,'University of Pennsylvania, Philadelphia, Pa. Of 400 patients (pts) consecutively studied b y p r o g r a m m e d ventricular stimulation, 238 (59.5%) demonstrated reproducible repetitive ventricular responses (RVR).. Two types of RVR could be identified: i) RVR resulting from bundle branch reentry (BBR) occurred in 53% of all pts without a significant difference~of ina~dence in the presence ( 5 3 ~ o f 289 p t s ) o r absence (54% of iii pts) of organic heart disease; 2) RVR resulting from intraventricular reentry (IVR} occurred in 19.5% of all pts with a significantly higher incidence in pts w i t h ( 2 4 % ) than without (8%) organic heart disease ( p < . 0 0 5 ) . ' I V R occurred reproducibly in 33/39 pts (82%) with recurrent sustained ventricular tachycardia (VT)~and in 29/32 pts (91%) i n w h o m VT was i n d u c i b l e . MoreOver, the mode of initiation and the configuration of IVR frequently resembled that of both spontaneously occurring and inducible VT. I n all 29 pts with both ~VR and inducible VT, IVR occurred in response to extrastimulirat coupling intervals t h a t d i d not initiate VT. Similarly 12/19 pts (63%) with•documented ventricular fibrillation (VF) demonstrated IVR and 9 of these 12 had inducible VF; only 9% of pts without VT or VF however had IVR (p<.001). We conclude that BBR and IVR are different phenomena, both in mechanism and relationship to sustained ventricular tachyarrhythmias. While BBR represents.a physiological response of the His,Purkinje system and i s n o t directly related to ventricula~ arrhythmias, IVR may identify pts who are prone to develop VT or VF. •
OBSERVATIONS ON VENTRICULAR FIBRILLATION IN MAN BY CATHETER RECORDINGS Scott R. Spielman, MD; Allan M. Greenspan, MD; Leonard N. Horowitz, MD, FACC; John A. KaStor, MD, FACC; Mark E. Josephson, MD, FACC, University of Pennsylvania, Philadelphia, Pa. Observations on the mechanism of initiation and termination of ventricular fibrillation (VF) were made using•endoeardial catheter recordings in 15 patients (pts) who developed VF during electrophysiologic studies. Simultaneous electrograms were recorded from multiple ventricufar sites at the onset and offset of VF. In i0 pts VF was initiated:by•double ventricular premature depolarizations during ventricular pacing (8 pts) or sinus rhythm (i pt) ~ In 5 pts VT spontaneously degenerated to VF. In i0 cases acceleration of local ventricular responses was observed before fragmentation and degeneration into continuous fractionated activity•(local fibrillation) occurred in any intracardiac lead. In no pt did all ventricular electrograms degenerate to fibrillation simultaneously. 'The initial site of degeneration was distant from the site of stimulation in 9 cases. QRS morphology became more chaotic as the number of intracardiac elec-• trograms demonstrating fibrillation increased. More organized ECG activity (flutter-fibrillation) was associated with regular activation in Some electrograms and fibrillation in others. In 6 pts VF spontaneously converted to sinus rhythm. In 4 pts termination was preceded by sequential reorganization of local elec~rograms with the reappearance of discrete recordings and a tendency towards increasing interelectrogram intervals. In 2 cases abrupt organization and synchronization of electrograms occurred just prior to termination. These observations are compatible with the multiple wavelet theory of the mainten -• ance of VF•and demonstrate that spontane0us defibrillation may not be uncommon in man.
Volume 43
EFFECT OF AGE ON A'V CONDUCTION IN PATIENTS WITH CHRONIC BIFASCICULAR BLOCK Edwin Palileo, MD; Pablo Denes, MD, FACC; Steven Swiryn, MD; Fernando Amat-y-Leon, MD, FACC; Christopher Wyndham, MD; Delon Wu, MD, FACC; Kenneth Rosen, MD, FACC, University of Illinois, Chicago, Illinois. It has been suggested that advanced age predicts severity of conduction disease in patients (pts) with established chronic bifascicular block (BFB). This hypothesis was tested in 416 prospectively followed (mean follow-up 978 53 days ) pts with BFB. Pts were subdivided into younger group (YG), ages 40 tO 65 years (mean 53 + 1.5) and older group (OG), ages 65 years and over (mean 75 + i,i). The pts were further separated into those with primary conduction disease (PCD) (72 pts), and those with organic heart disease (OHD) (344pts). Electrophysiological findings in the PCD pts were as follows (mean + SEM YG, 28 pts vs OG, 44 pts): P~A (34 + 2.3 vs 35 + 1.7 msec), AH 90 + 5.2 vs i01 0+ 4.2 msec), H---V (51 + 3.3 vs 49 + 1.9 msec)? % with prolo-nged H-V (~ 55•msec)--(32•vs 16%)~ Progression to spontaneous A-V block was seen in 0 YG pts (0%), and 1 OG pt (0.5%). None of these differences were significant. In the OHD group findings were (YG, 180 pts vs OG, 164 ptS)r: P--A (33 + 0.8 VS 3 6 + 0-8 msec), A-H (105 + 2.9 vs 116 ! 4.1 msec), H-V (56 + I.i vs 55 + i.I msec)~ % with prolonged H-V (44% vs 41%~. Progressio--n to SHB was seen in 9 YG pts (5%) and i 0 0 G pts (6%). All differences were insignificant except the increase in A-H in the OG (P< 0.02). In conclusion, with the exception of A-H in OHD group, severity and progression of conduction disease is independent of advanced age in pts with established chronic BFB. Age differences do not appear responsible for d i f f e ~ ent incidences of A-V block in previously reported series of BFB pts.
MECHANISM OF THE REPETITIVEVENTRICULAR RESPONSE IN MAN. H. Lo Greene, M . D . , FACC; A.H. Schaeffer, M.D.; P. Ro Reid, M.D., FACC, Johns Hopkins University School of Medicine, Baltimore, Maryland. This study examined the •mechanism responsible for the repetitive ventricular response (RVR) in man, defined as the production of 2 or more ventricular premature beats in response to a sihgle premature ventricular pacing stimulus during atrial pacing or sinus rhythm. We havepreviously demonstrated that the RVR identifies patients (pts) at risk of ventricular tachycardia or sudden death. Seventy-five pts with RVR were analyzed. Both the surface QRS configuration of the repetitive beats and the presence of conduction system deflections (His bundle or right bundle potentials) were evaluated. Bundle branch reentry a-~ a mechan|sm of RVR wouidbe supported if the surface QRS configuration resembled the beats paced from theright ventricle - a left bundle branch block pattern - and if His bundle or right bundle deflections were present before the repetitive beats. Sixty-nine of the 75 pts had repetitive beats with a different QRS morphology from the beats paced from the right ventricle. In 23 of these 75 pts an additional catheter was positioned to record His bundle or right bundle potentials during ventH~ular premature Stimulation. In 22 Of the 23 pts, there was no His bundle or right bundle potential preceding the repetitive beats. These data support the conclusion that RVR involves reentry which does not include the bundle branches and therefori~ is a different phenomenon than reentry beats seen in normal pts during ventrlcular pacing and ventricular premature stimulation. Reentry in RVR more likely involves diseased myocard~um c~nd may explain the predictive value of RVR for ventHcular tachycardla and sudden death.
390
February 1979
The American Journal of CARDIOLOGY
REPETITIVE RESPONSES TO VENTRICULAR EXTRASTIMULI INCIDENCE, MECHANISM AND SIGNIFICANCE Ardeshir Farshidi, MD, FACC; Eric L. Michelson, MD; Allan M. Greenspan, MD; Scott R. Spielman MD; John A. Kastor, MD, FACC; Leonard N. Horowitz •, MD, FACC, Mark E. Josephson, MD, FACC,'University of Pennsylvania, Philadelphia, Pa. Of 400 patients (pts) consecutively studied b y p r o g r a m m e d ventricular stimulation, 238 (59.5%) demonstrated reproducible repetitive ventricular responses (RVR).. Two types of RVR could be identified: i) RVR resulting from bundle branch reentry (BBR) occurred in 53% of all pts without a significant difference~of ina~dence in the presence ( 5 3 ~ o f 289 p t s ) o r absence (54% of iii pts) of organic heart disease; 2) RVR resulting from intraventricular reentry (IVR} occurred in 19.5% of all pts with a significantly higher incidence in pts w i t h ( 2 4 % ) than without (8%) organic heart disease ( p < . 0 0 5 ) . ' I V R occurred reproducibly in 33/39 pts (82%) with recurrent sustained ventricular tachycardia (VT)~and in 29/32 pts (91%) i n w h o m VT was i n d u c i b l e . MoreOver, the mode of initiation and the configuration of IVR frequently resembled that of both spontaneously occurring and inducible VT. I n all 29 pts with both ~VR and inducible VT, IVR occurred in response to extrastimulirat coupling intervals t h a t d i d not initiate VT. Similarly 12/19 pts (63%) with•documented ventricular fibrillation (VF) demonstrated IVR and 9 of these 12 had inducible VF; only 9% of pts without VT or VF however had IVR (p<.001). We conclude that BBR and IVR are different phenomena, both in mechanism and relationship to sustained ventricular tachyarrhythmias. While BBR represents.a physiological response of the His,Purkinje system and i s n o t directly related to ventricula~ arrhythmias, IVR may identify pts who are prone to develop VT or VF. •
OBSERVATIONS ON VENTRICULAR FIBRILLATION IN MAN BY CATHETER RECORDINGS Scott R. Spielman, MD; Allan M. Greenspan, MD; Leonard N. Horowitz, MD, FACC; John A. KaStor, MD, FACC; Mark E. Josephson, MD, FACC, University of Pennsylvania, Philadelphia, Pa. Observations on the mechanism of initiation and termination of ventricular fibrillation (VF) were made using•endoeardial catheter recordings in 15 patients (pts) who developed VF during electrophysiologic studies. Simultaneous electrograms were recorded from multiple ventricufar sites at the onset and offset of VF. In i0 pts VF was initiated:by•double ventricular premature depolarizations during ventricular pacing (8 pts) or sinus rhythm (i pt) ~ In 5 pts VT spontaneously degenerated to VF. In i0 cases acceleration of local ventricular responses was observed before fragmentation and degeneration into continuous fractionated activity•(local fibrillation) occurred in any intracardiac lead. In no pt did all ventricular electrograms degenerate to fibrillation simultaneously. 'The initial site of degeneration was distant from the site of stimulation in 9 cases. QRS morphology became more chaotic as the number of intracardiac elec-• trograms demonstrating fibrillation increased. More organized ECG activity (flutter-fibrillation) was associated with regular activation in Some electrograms and fibrillation in others. In 6 pts VF spontaneously converted to sinus rhythm. In 4 pts termination was preceded by sequential reorganization of local elec~rograms with the reappearance of discrete recordings and a tendency towards increasing interelectrogram intervals. In 2 cases abrupt organization and synchronization of electrograms occurred just prior to termination. These observations are compatible with the multiple wavelet theory of the mainten -• ance of VF•and demonstrate that spontane0us defibrillation may not be uncommon in man.
Volume 43