Circulation, Vol 85, 1271-1278, Copyright © 1992 by American Heart Association
B Avitall, J McKinnie, M Jazayeri, M Akhtar, AJ Anderson and P Tchou
BACKGROUND. Premature stimuli can cause ventricular fibrillation (VF)
during electrophysiological testing. The electrophysiological correlations
associated with the onset of VF were evaluated in 40 patients who had this
rhythm induced during programmed ventricular stimulation. These parameters
were compared with those observed in 51 patients who had inducible
sustained monomorphic ventricular tachycardia (VT) and 45 patients who had
no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS.
Shortest premature coupling intervals for S2, S3, and S4 at induction of
tachycardia or before achieving refractoriness, corresponding conduction
latencies (defined as the time from the premature stimulus to the upstroke
of the depolarization wave front recorded 35 mm away from the stimulation
site), and ventricular activation times (defined as the time from the
premature stimulus to the end of the depolarization wave) were compared.
The mean coupling intervals were longest in the inducible VT patients: 300
+/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively.
In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/-
20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these
coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT
group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194
+/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The
coupling interval of the last premature extrastimulus was above 200 msec in
70% of the patients in whom VF was induced. The largest increases in
latency and activation times were recorded in patients in whom VF was
induced. The cumulative increase in latency, defined as increased
conduction time from baseline, summed for all the premature stimuli was
also the greatest at initiation of VF. In contrast, the smallest increases
in these parameters were noted in the patients with no inducible VT or VF.
Measurements of total activation time yielded similar results as those
recorded for latencies. The most important parameters distinguishing the VT
patient population from the other two groups were the low ejection
fractions and the longer coupling intervals at which VT was induced,
whereas in the VF group, the most important discriminating factor was
cumulative activation time. Sixty-three percent of the inducible VF
patients presented with abnormal hearts (myocardial infarction or
cardiomyopathy), whereas 88% of the inducible VT patients had abnormal
hearts. In contrast, only 25% of the patients in whom no arrhythmia was
induced presented with abnormal hearts. Mean ejection fraction was 32 +/-
15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and
51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus
VT). CONCLUSIONS. The results suggest that 1) initiation of ventricular
tachycardia during programmed ventricular stimulation occurs with minimal
conduction latency; 2) because of the large overlap in coupling intervals
where VF or VT were induced, a single coupling interval cannot be
recommended to adequately separate these groups; and 3) induction of VF was
preceded by increased latency and prolongation of the local activation
time. These parameters should not be allowed to prolong if VF is to be
avoided during programmed stimulation. In addition, 4) the initiation of VF
during electrophysiological studies is often associated with the presence
of structural heart disease; such structural disease may promote conduction
latency and the development of VF.
ARTICLES
Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay
Electrophysiology Laboratory, University of Wisconsin-Milwaukee Clinical Campus, Sinai Samaritan Medical Center 53201.
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