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The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing - 12/10/17

Doi : 10.1016/0002-8703(87)90258-4 
Fred Morady, M.D. , a, b, Jeffrey B. Halter, M.D. a, b, Lorenzo A. DiCarlo, M.D. a, b, Jeffrey M. Baerman, M.D. a, b, Michael de Buitleir, M.B. a, b
a Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals Ann Arbor, Mich., USA 
b Division of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals Ann Arbor, Mich., USA 

1Reprint requests: Fred Morady, M.D., Division of Cardiology, University Hospitals, 1500 E. Medical Center Dr., UH-B1 F221-0022, Ann Arbor, MI 48109-0022.

Abstract

Plasma epinephrine and norepinephrine concentrations were measured before, during, and shortly after induced ventricular tachycardia (VT) in 22 selected patients. Sustained, unimorphic VT was induced by programmed ventricular stimulation and terminated after 45 to 384 seconds by overdrive pacing in all patients. In no patient did VT result in loss of consciousness. The baseline plasma catecholamine concentrations did not correlate with the baseline right ventricular effective refractory period, the cycle length of induced VT, or the number of extrastimuli required to induced VT. Induced VT was not associated with a significant increase in the mean plasma epinephrine concentration. In contrast, the plasma norepinephrine concentration increased from a mean baseline level of 317 ± 136 pg/ml (mean ± standard deviation) to 418 ± 220 pg/ml during VT (p = 0.01) and increased further to 569 ± 387 pg/ml shortly after VT (p < 0.01). The plasma norepinephrine concentration shortly after VT correlated with the rate and duration of VT and with the magnitude of decrease in mean blood pressure during VT (p < 0.05 for each). In eight patients the same configuration of VT was induced on two sequential attempts; in five patients the same number of extrastimull were required for the second induction of VT as for the first, whereas in three patients fewer extrastiuli were required. Plasma cateholamine concentrations were not higher in patients requiring fewer extrastimuli to induce the second episode of VT, either shortly after the first episode of VT or shortly after the second episode of VT. In conclusion, plasma catecholamines do not influence baseline ventricular refractoriness, the cycle length of induced VT, or the VT induction technique. Induced VT, which does not require termination by direct-current countershock, is generally associated with little or no increase in plasma epinephrine and a variable increase in plasma norepinephrine concentration, depending on the severity and duration of hypotension during VT. The plasma catecholamine response to VT does not affect a second induction of VT. Therefore, endogenous catecholamines exert little influence on the results of electrophysiologic testing in patients with sustained VT which does not require termination by direct-current countershock.

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© 1987  Pubblicato da Elsevier Masson SAS.
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Vol 113 - N° 2P1

P. 227-233 - febbraio 1987 Ritorno al numero
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