Angerlike behavioral state potentiates myocardial ischemia-induced T-wave alternans in canines

Citation
Ja. Kovach et al., Angerlike behavioral state potentiates myocardial ischemia-induced T-wave alternans in canines, J AM COL C, 37(6), 2001, pp. 1719-1725
Citations number
47
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
37
Issue
6
Year of publication
2001
Pages
1719 - 1725
Database
ISI
SICI code
0735-1097(200105)37:6<1719:ABSPMI>2.0.ZU;2-9
Abstract
OBJECTIVES The main goal of this study was to determine whether induction o f an angerlike state can result in significant levels of T-wave alternans, a marker of electrical instability, in the normal and ischemic heart. BACKGROUND Outbursts of anger have been implicated in the occurrence of myo cardial infarction and sudden cardiac death, but the pathophysiologic mecha nisms remain unknown. METHODS A standardized behavioral challenge of eliciting an angerlike state was conducted before and during a 3-min period of coronary artery occlusio n in six canines. RESULTS Precordial T-wave alternans increased from 0.04 +/- 0.02 at baselin e to 1.40 +/- 0.32 mV x ms (p < 0.05) during the angerlike response. When t he angerlike state and myocardial ischemia were superimposed, the augmentat ion in T-wave alternans magnitude (to 3.27 +/- 0.61 mV x ms, p < 0.05) exce eded their additive effects, increasing by 130% over the angerlike state al one ir < 0.05) and by 390% over occlusion alone (p < 0.05). Adrenergic infl uences were reduced by the beta(1)-adrenergic receptor blocking agent metop rolol (1.5 mg/kg, intravenous), which diminished T-wave alternans magnitude (p < 0.0004 for all) during the angerlike response (from 1.40 +/- 0.32 to 0.80 +/- 0.17 mV x ms) and during the combined intervention (from 3.27 +/- 0.61 to 1.23 +/- 0.13 mV x ms). In five additional normal anesthetized cani nes, atrial pacing at 180 beats/min did not increase T-wave alternans magni tude monitored from lead II electrocardiogram. CONCLUSIONS Provocation of an angerlike state results in T-wave alternans i n the normal heart and potentiates the magnitude of ischemia-induced T-wave alternans. Elevation in heart rate during arousal does not appear to be th e main factor in the development of alternans in the normal heart but may b e an important component during myocardial ischemia. Enhanced adrenergic ac tivity appears to mediate the effects in both the normal and ischemic heart s. T-wave alternans may constitute a useful electrophysiologic measure for clinical use in conjunction with behavioral stress testing or ambulatory mo nitoring. (I Am Coil Cardiol 2001;37:1719-25) (C) 2001 by the American Coll ege of Cardiology.