CIRCADIAN VARIATION OF AMBULATORY MYOCARDIAL-ISCHEMIA - TRIGGERING BYDAILY ACTIVITIES AND EVIDENCE FOR AN ENDOGENOUS CIRCADIAN COMPONENT

Background The morning peak in myocardial ischemia has been related to diurnal variations in physical and mental activities and to postural changes upon awakening. This stud; assesses (1) the effects of exogeno us activity triggers at different times of the day and (2) the contrib ution of an endogenous (ie, activity- and posture-independent) circadi an vulnerability for ambulatory ischemia. Methods and Results Sixty-th ree stable coronary artery disease patients underwent ambulatory ECG m onitoring and completed a structured diary assessing physical and ment al activities. During 2519 hours of observation, a morning increase in ischemia coincided with increases in physical and mental activities, and an evening decrease in ischemia coincided with a decline in activi ties. During the morning, ischemic versus ischemia-free periods were m ore likely to occur with high levels of physical activity (P<.001). Hi gh physical activity triggered ischemia to a lesser but still signific ant extent (P<.05) in the afternoon but not in the evening (P=NS). Hig h levels of mental activity triggered ischemia significantly during th e morning (P<.04) and evening (P<.04) but not in the afternoon, When a residualized score procedure was used to correct ischemic time for ea ch patient's simultaneously measured activities, for hourly heart rate s, or far activity-related heart rate fluctuations, the circadian vari ation in ischemia was still observed (P<.001), with a peak at 6 AM. A significant increase in ischemia occurred immediately after awakening (P<.05). but activity-adjusted increases in morning ischemia persisted (P<.05) fur 2 hours after awakening. Conclusions Exogenous factors (p hysical and mental activities) are most potent as triggers of ischemia during the morning hours, and the postural change after awakening con tributes to tile morning increase in ischemia. There is also evidence for an endogenous, activity-independent circadian influence on ischemi c susceptibility that is independent of exogenous factors and that sus tains the increase in ischemia upon awakening.