HEART-RATE-VARIABILITY IN MYOCARDIAL-ISCHEMIA DURING DAILY-LIFE

Citation
K. Sroka et al., HEART-RATE-VARIABILITY IN MYOCARDIAL-ISCHEMIA DURING DAILY-LIFE, Journal of electrocardiology, 30(1), 1997, pp. 45-56
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00220736
Volume
30
Issue
1
Year of publication
1997
Pages
45 - 56
Database
ISI
SICI code
0022-0736(1997)30:1<45:HIMDD>2.0.ZU;2-I
Abstract
The aim of this investigation was to evaluate the role of autonomic ne rvous activity before and during transient ischemic events. Forty-one ischemic episodes detected on Holter recordings were analyzed for hear t rate and heart rate variability (HRV). A time-dependent index of HRV the windowed median successive difference, which is a continuous meas ure of respiratory sinus arrhythmia and therefore a marker of vagal ef ferent activity was used. A small window consisting of five beats, whi ch represented one respiratory cycle, was chosen. This method permitte d continuous assessment of short-term alterations of vagal modulation. With two exceptions, all ischemic episodes were preceded by an acute almost complete suppression of respiratory sinus arrhythmia. During th e entire ischemic episode, HRV stayed at this reduced level, and prece ding the end of the ischemia, it increased again. This suppression of intrinsic heart period variations reflects an almost complete withdraw al of modulated vagal outflow immediately before and during ischemic e pisodes. In 26 cases (63%), Fast Fourier Transformations were carried out when the heart rare was almost constant in two segments around the onset of ischemia. In the other 15 cases we did not perform Fast Four ier Transformations because there was no stationary stage in the data. High-frequency power always decreased drastically at the onset of isc hemia, confirming a significant loss of modulated vagal activity (P < .01). The low frequency/high frequency ratio did not increase, indicat ing that sympathetic activity did not increase significantly at the on set of ischemia in about two-thirds of our cases. The extent to which this suppression of modulated vagal activity reflects a similar suppre ssion of vagal efferent activity is discussed, as well as whether this withdrawal of vagal outflow is cause or consequence of the ischemic e vent. The results suggest that a vagal depression may influence the on set of myocardial ischemia during daily life.