Author + information
- Received December 10, 1985
- Revision received March 3, 1986
- Accepted April 1, 1986
- Published online September 1, 1986.
- Fred Morady, MD, FACC*,1,
- Lorenzo A. DiCarlo Jr., MD1,
- Jeffrey B. Halter, MD1,
- Michael de Buitleir, MB1,
- Ryszard B. Krol, MD1 and
- Jeffrey M. Baerman, MD1
- ↵*Address for reprints:Fred Morady, MD, Division of Cardiology, University of Michigan Hospitals, UH/BIF245/0022, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109-0022.
Adrenergic activation during electrophysiologic study could potentially alter the electrophysiologic properties of the arrhythmia substrate. However, the catecholamine response to ventricular tachycardia induction and termination during electrophysiologic testing has to date not been quantitated. Therefore, in 13 patients undergoing electrophysiologic study, arterial plasma norepinephrine and epinephrine were measured before, during and 1, 3, 5, 10 and 15 minutes after ventricular tachycardia induced by programmed stimulation and terminated by a single 100 J external countershock. Sinus rate and the effective refractory period at the right ventricular apex at a basic drive cycle length of 400 ms were measured after the countershock at the same time intervals used for the catecholamine measurements. The mean ventricular tachycardia cycle length ( ± SD) was 187 ± 30 ms, and the mean duration of ventricular tachycardia was 18 ± 4 seconds.
Plasma norepinephrine and epinephrine increased, respectively, from a baseline of 286 ± 141 and 119 ± 40 pg/ml to 770 ± 330 (169%) and 597 ± 467 pg/ml (402%), (p < 0.01) at 1 minute after the countershock. The mean plasma norepinephrine and epinephrine levels during ventricular tachycardia and at times greater than 1 minute after the shock did not differ significantly from baseline levels. Sinus rate increased from a baseline of 74 ± 13 to 103 ± 26/min (39%) at 1 minute after the shock (p < 0.05) and then returned to baseline. Right ventricular effective refractory period decreased from a baseline of 236 ± 27 to 212 ± 23 ms (−10%) and 226 ± 25 ms (−4%) at 1 and 3 minutes, respectively, after the countershock (p < 0.01), then returned to baseline. In some patients, a 10 to 20 ms decrease in effective refractory period persisted for up to 10 minutes. In an additional six patients without inducible ventricular tachycardia, plasma catecholamine levels did not change during programmed ventricular stimulation.
These data indicate that ventricular tachycardia induction and termination by a 100 J countershock result in a mean threefold increase in plasma norepinephrine level and a fivefold increase in plasma epinephrine level that are short-lived (< 3 minutes). This degree of adrenergic activation may be sufficient to significantly shorten ventricular refractoriness and potentially affect the results of subsequent attempts at programmed stimulation. During an electrophysiologic study, a rest period of 15 minutes after ventricular tachycardia termination by countershock should be adequate to avoid catechol-amine-induced changes in electrophysiologic properties of the arrhythmia substrate.
- Received December 10, 1985.
- Revision received March 3, 1986.
- Accepted April 1, 1986.
- American College of Cardiology Foundation