Ventricular Cross Stimulation in a Dual

Chamber Pacing System: Phenomenon Analysis

ANDREA PUGLISI. RENATO RICCI, PAOLO AZZOLINI,
CARLO PERALDO NEJA, MASSIMO FIORANELLI, GIULIO SPECIALE,
and GERARDO ANGRISANI
From the Department of Cardiology, Fatebenefratelli Hospital, Isola Tiberina, Rome, Italy

PUGLISI A., ET AL.: Ventricular Cross Stimulation in a Dual Chamber Pacing System: Phenomenon
Analysis. Seven cases o/venlricular cross sfimulation from a group of 23 patients implanted with DDD
devices are presented. In two patients the phenomenon was observed at the moment of DDD programming
at nominal values, and in jive other patients it ivas reproduced by increasing (he atrial output voltage up to
ten volts. In all 23 patients cross stimulation disappeared permanently within 24 hours after implantation.
From the onset of cross stimulation to its end. atrial and ventricular threshold voltages were unchanged.
while the atrial and ventricular impedances significantly decreased. These results suggest that an impor-
tant role in the phenomenon occurs by impedance variation al the interface between the pulse generator
and body tissue. (PACE. Vol. 13, August 1990}

cross stimulation, dual chamber pacing .system, impedance

Introduction
Table I.
In a dual chamber pacing system, stimulation
Threshold (volts/msec)
of a cardiac chamber different from the one to
which the stimulus was directed, is defined as Implant Cross End
"cross" stimulation.
The occurrence of venfricular stimulation by pt1
the atrial lead as a consequence of dislocation into A 1/0.5 1/0.5 1/0.5
the right ventricle, near the tricuspid annulus or V 0.5/0.5 0.75/0.4 0.75/0.4
in the coronary sinus has been reported pre- pt2
viously.^^'' Rarely is fhe phenomenon related fo A 1/0.5 0.9/0.5 0.9/0.5
the reversal of leads due fo incorrect connec- V 0.4/0.5 0.75/0.4 0.75/0.4
tions.^ In this study, seven cases of femporary pt3
ventricular cross sfimulafion are reported. In A 0.9/0.5 1/0.5 1/0.5
V 0.4/0.5 0.75/0.3 0.75/0.3
order to analyze this phenomenon, variations of
pt4
bioelectrical parameters were studied. A 1.1/0.5 1.3/0.5 1.3/0.5
V 0.4/0.5 0.75/0.3 0.75/0.4
Materials and Methods pt5
From January 1988 fo lune 1989, 23 Siemens A 1.3/0.5 1.5/0.5 1.5/0.5
(Siemens-Elema. Sfockholm, Sweden) 544 dual V 0.7/0.5 0.75/0.5 0.75/0.5
chamber pacemakers were implanted. Pacesefter pt6
A 1/0.5 1/0.5 1/0.5
V 0.6/0.5 0.75/0.4 0.75/0.4
Address for reprint.s: Andrea Puglisi. Department of Cardiol- pt7
ogy. Fatehenefratelli Hospita], Isola Tiberina. 39, 00186 Rome, A 1.2/0.5 1.3/0.5 1.5/0.5
Ilaly. V 0.4/0.5 0.75/0.4 0.75/0.4
Received October 30, 1989; revision March 6. 1990: accepted
March 7. 1990. pt = patient; A = atrial; V = ventricular.

PACE, Vol. 13 August 1990 993

 PUGLISI, ET AL

1015M ventricular and Pacesetter 1013M leads
(Pacesefter Systems, Sylmar, CA, USA) and Med-
tronic 6957-58 (Medfronic, Inc., Minneapolis, MN,
USA) atrial leads were used. Atrial leads had been
positioned routinely in the right atrial appendage
and, in some cases, in the high anterior wall of the
righf atrium.
Analysis of stimulation parameters, af fhe
fime of lead implantation, was performed with a
Medtronic 5311 pacing system analyzer.
In order to exclude extracardiac stimulation
of surrounding sfructures, fhe afrinm was paced
from the oufpuf threshold value, up fo 10 volts,
both in fhe AAI and DDD modes. For the lead, all
measurements were made 30 minutes after tbe
atrial fixation into afrial myocardium.

Figure 1. Patient 6. DDD mode, rate = 90 ppm, AA (W} = 667 msec, ventricular refractory period
= 325 msec, AV delay = 140 msec, VA ^ 527 msec, blanking period = 38 msec, atrial output = 8.5
volts, magnet off. Paper speed = 50 mm/sec. Full circle = cross stimulation.

994 August 1990 PACE. Vol. 13

 CROSS STIMULATION

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Figure 2A. Patient 3. (A} DDD mode, rate = 70 ppm, AA (Wj = 857 msec, ventricular refraclory
period = 250 msec. AV delay =165 msec, VA = 692 msec, blanking period = 38 msec, atrial output
= 5 volts, magnet off.

In two patients, cross stimulation of the ven- Results

tricle from fhe atrial lead was observed af the
moment of fhe DDD programming, immediately There were seven patients, aged 68 fo 79
after implant af nominal values. In five patients, years (four males and three females]. Three had
fhe phenomenon was reproduced by increasing sick sinus syndrome and atriovenfricular block;
fhe atrial oufpuf voltage in tho DDD mode. two trifascicular block; one sick sinus syndrome;
From tbe onsef of cross stimulation fo its end and one afrioventricular block. Three had idio-
fhe following procedures were performed, using a pathic heart disease; two hypertensive heart dis-
Paceseffer System Inc. Model 380 programmer ease: and fwo chronic ischemic hearf disease. In
wifh function pack 385B: deferminafion of atrial two patients, the venfricular cross stimulation
and venfricular stimulation threshold voltage; was observed at the moment of DDD program-
atrial sfimulafion af increasing voltage, from ming at nominal value, The minimum afrial out-
threshold value up fo 10 volfs, in the DDD mode; put volfage needed to induce the phenomenon
measurement of afrial and venfricular pacing im- was 3 and 4 volts, respectively.
pedance and current at an oufpuf of 5 volfs and af In fhe remaining five pafienfs. cross sfimula-
a pulse duration of 0.5 msec. tion was induced by increasing fhe outpuf voltage

PACE. Vol. 13 August 1990 995

 PUGLISI, ET AL

Figure 2B. Afrial output - 6 volts. Paper speed = 50 mm/sec.

to a mean value of 7.4 ± 1.1 volts (range 6 to 8.5
volts). In all patients, during cross stimulation, the
QRS complex was paced from the atrial stimulus,
and after the programmed AV delay tbe ventricu-
lar stimulus appeared (Figs. 1 and 2). The ventric-
ular stimulus was ineffective as it fell into the
refractory period ofthe ventricular myocardium.
Tbe QRS morphology caused by the atrial stimu-
lus and ventricular stimulation were identical.
During cross stimulation, the ventricular
stimulus was absent in four patients because of a
cross-talk phenomenon; consequently, tbe pacing
rate increased: as the pacing cycle length was
equal to the programmed VA interval plus the
blanking period (Figs. 3A, 3B, 4A). By increasing
the blanking period from 38 to 50 msec, and leav-
ing the atrial output unchanged, only cross stimu-
lation was present [Figs. 3C, 4B).
None of the seven patients showed cross
stimulation 24 hours after implant or during later
follow-up.
From the onset of cross stimulation to its end,
tbe following variations of bioelectrical parame-
ters were observed: atrial and ventricular thresb-

996 August 1990 PACE, Vol. 13

 CROSS STIMULATION

Figure 3A. Patient 4. (A) DDD mode, rale = 90 ppm, AA (W) = 667 msec, venlricuJar refractory
period = 250 msec, AV delay = 165 msec, VA = 502 msec, blanking period = 38 msec, alrial oufpul
= 7 volts, magnet off.

old voltage were unchanged; mean atrial imped-
ance decreased from 606 ± 83 to 529 ± 89 ohms (P
< 0.01): mean ventricular impedance decreased
from 705 ± 144 to 527 ± 85 ohms (P < 0.01); mean
atrial current increased from 7.4 ± 1.4 to 8.4 ± 1.2
mA (P < 0.01); mean ventricular current in-
creased from 6,4 ± 1 to 8.5 ± .6 mA {P < 0.01).
Table I lists atrial and ventricular threshold
values. Variation of atrial and ventricular imped-
ance and current are shown in Tables II and III.
Discussion
In the majority of cases reported, ventricular
stimulation by an atrial lead was attributed to
lead dislocation.^'^'^ When this occurred, the phe-
nomenon was permanent and the morphology of
the paced QRS was clearly different from that in-
duced by the ventricular stimulus. In such cases,
chest X ray shows the malposition.
In our patients, diagnosis of dislocation could
be excluded for the following reasons; the QRS
morphology during cross phenomenon was iden-
tical to that recorded in the VVI mode; by pro-
gramming the unit to the AAI mode at nominal
values, normal atrial pacing occurred; chest X
rays taken after pacemaker implantation showed
that both atrial and ventricular leads were in good
position; in all cases the phenomenon disap-
peared spontaneously within 24 hours, and no
cross stimulation was observed during foIIow-up.^
Others have pointed out the possibility of
cross stimulation when the lead positioned in the
right atrial appendage is very close to the right
ventricular outflow tract,^ in which case suffi-

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 PUGLISI. ET AL

Figure 3B. Atriai output = 8.5 vo/Is. Pacing cycle length = 550 msec. (VA + blanking -I- 10 ms.

ciently high pacing energy can be transmitted to
the ventricle, causing depolarization. This could
also be ruled out in our patients because of the
paced QRS morphology, and at implantation,
using a PSA. temporary stimulation was routinely
carried out in AAI and DDD modes with output
up to 10 volts, without observing the cross stimu-
lation phenomenon.
Cross stimulation in these instances de-
pended on a pacemaker circuit defect or on modi-
fications of hioelectrical parameters between the
pulse generator case and body surface. Normal
intracircuit resistances are very high. The possi-
bility of transferring sufficient energy from the
atrial to the ventricular circuit to produce a stim-
ulation is very low and, if present, should either
regress according to stimulation threshold varia-
tions, or persist. In all patients cross stimulation
disappeared permanently within 24 hours after
implantation, and no atrial and ventricular
threshold differences were noticed from the im-
plantation to the end of the phenomenon (Table i).
Therefore a circuit defect was very unlikely. Si-
multaneously with the end of cross stimulation,
atrial and ventricular impedances decreased sig-
nificantly (Tables II and III).
As stimulation thresholds were unchanged,
impedance reduction is related to a better pace-
maker/subcutaneous tissue contact that there-
fore played a role in the cause of the cross stimu-

998 August 1990 PACE. Vol. 13

 CROSS STIMULATION

Figure 3C. Blanking period = 50 msec. Pacing cycle Jenglh = 667 msec. Paper speed = 50
mm/sec.

lation.° Levine et aP described cross stimulation
in DDD pacing system when the pacer was out of
the pocket with both atrial and ventricular leads
connected. In this case because of the high imped-
ance, a small amount of current flowed between
the implanted atrial and ventricular electrode
when atrial or ventricular outputs are delivered,
resulting in atrial and/or ventricular anodal stim-
ulation.
In the clinical setting, a similar condition
could be observed if the impedance at case-body
tissue level significantly increases. The Siemens
544 pacemaker is derived from the model 285
Genesis electronically and mechanically identical
to Pacesetter model 285. The only differences
(confirmed hy the manufacturer) are in labeling
on the can and the coating applied to the can. The
window of the can is considerably smaller on the
544 as compared to the 285; postoperatively this
may not allow a good contact with the body tissue
and produce high impedance.
In this case, atrial stimulation will produce a
"small" current flow from the atrial to the ven-
tricular electrode becoming clinically significant
in the presence of very low ventricular thresholds
and/or high atrial output voltage, resulting in
cross stimulation.
The phenomenon is temporary probably be-
cause of the following mechanisms: impedance
decrease at the generator-subcutaneous tissue in-

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 PUGLISI, ET AL

Figure 4. Patient 2. {A} DDD mode, rate = 65 ppm, AA fW)

= 923 msec, ventricular refractory period - 250 msec. AV
delay = 140 msec, VA = 783 msec. Wanking period = 38 msec,
atrial output - 5 volts, magnet off. Pacing cycle length = 830
msec. (VA + blanking + 9 msec.) fB) blanking period = 50
msec. Pacing cycle length = 923 msec. Paper speed; 25 mm/

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Table II. Table III.

Impedance (ohms) Current (mA)

Implant Cross End Implant Cross End

pt1 pt1
A 667 617 579 A 1.5 7.7 8.4
V 1000 739 577 V 0.6 6.6 8.4
pt2 pt2
A 440 473 352 A 2.3 4.6 6.1
V 444 437 372 V 0.9 4.9 5.6
pt3 pt3
A 483 707 617 A 3.1 7.5 8.4
V 500 813 551 V 0.7 6.5 9.5
pt4 pt4
A 526 609 537 A 2.1 7.4 8.4
V 500 705 522 V 0.7 6.4 8.6
pt5 pt5
A 376 532 478 A 3.1 9.4 10.4
V 650 674 462 V 0.9 7.7 10.8
pt6 pt6
A 474 608 569 A 1.9 8.1 8.6
V 625 668 620 V 0.8 7.4 7.9
pt7 pt7
A 538 697 571 A 2.6 7.1 8.6
V 800 897 587 V 0.5 5.5 8.4

A = atrial; V = ventricular. A = atrial; V = ventricular.

terface; increase of ventricular stimulation Acknowledgment: We gratefully acknowledge Mr. Rivetti

threshold; impedance increase at lead-tissue in- (Siemens-Italy) and Mr. I.. Sfilznick (Pacesetter Systems, CA,
terface. USA) for technical assistance.

References
1. Nathan AW, Camm AI. Douhle ventricular pacing
in a patient with a DDD universal pacemaker.
PACE 1984; 7:432-435.
2. Stark S, Fashidi A, Hager WD, et al. Unusual pre-
sentation of DDD pacemaker system malfunction.
PACE 1985; 8:255-259.
3. Levine PA, Rihanek BD, Sanders R, et al. CTORS
stimulation: The unexpected stimulation of the
unpaced chamber. PACE 1985; 8:600-606.
4. Barold SS, Falkoff MD, Ong LS, fit al. Function and
electrocardiography of DVI pacing system. In SS
Barold (ed.): Modern Cardiac Pacing. Mount Kisco,
New York, Futura Publishing Co., Inc., 1985, pp.
625-644.
Bognolo DA. Clinical application of A-V sequential
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