title: Circadian variation of ambulatory myocardial ischemia. Triggering by daily activities and evidence for an endogenous circadian component.
abstract: 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 study assesses (1) the effects of exogenous activity triggers at different times of the day and (2) the contribution of an endogenous (ie, activity- and posture-independent) circadian vulnerability for ambulatory ischemia.
  
  
  RESULTS
  Sixty-three stable coronary artery disease patients underwent ambulatory ECG monitoring and completed a structured diary assessing physical and mental 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 activities. During the morning, ischemic versus ischemia-free periods were more likely to occur with high levels of physical activity (P < .001). High physical activity triggered ischemia to a lesser but still significant extent (P < .05) in the afternoon but not in the evening (P = NS). High levels of mental activity triggered ischemia significantly during the morning (P < .04) and evening (P < .04) but not in the afternoon. When a residualized score procedure was used to correct ischemic time for each patient's simultaneously measured activities, for hourly heart rates, or for activity-related heart rate fluctuations, the circadian variation 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) for 2 hours after awakening.
  
  
  CONCLUSIONS
  Exogenous factors (physical and mental activities) are most potent as triggers of ischemia during the morning hours, and the postural change after awakening contributes to the morning increase in ischemia. There is also evidence for an endogenous, activity-independent circadian influence on ischemic susceptibility that is independent of exogenous factors and that sustains the increase in ischemia upon awakening.
authors.affiliation: Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799, USA. krantz@usuhsb.usuhs.mil
authors.forename: D S
authors.initials: DS
authors.lastname: Krantz
authors.forename: W J
authors.initials: WJ
authors.lastname: Kop
authors.forename: F H
authors.initials: FH
authors.lastname: Gabbay
authors.forename: A
authors.initials: A
authors.lastname: Rozanski
authors.forename: M
authors.initials: M
authors.lastname: Barnard
authors.forename: J
authors.initials: J
authors.lastname: Klein
authors.forename: Y
authors.initials: Y
authors.lastname: Pardo
authors.forename: J S
authors.initials: JS
authors.lastname: Gottdiener
mesh_terms: D000203:Activities of Daily Living; D000368:Aged; D002940:Circadian Rhythm; D003289:Convalescence; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009043:Motor Activity / Q000502:physiology*; D009203:Myocardial Infarction / Q000453:epidemiology* / Q000209:etiology / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology; D011996:Records; D014851:Wakefulness / Q000502:physiology