title: Pathophysiology of transient myocardial ischemia in acute coronary syndromes. Characterization by continuous ST-segment monitoring.
abstract: BACKGROUND
  Transient ischemia in stable coronary disease peaks in the morning, reflecting increased myocardial oxygen demand and coronary vasomotor tone after walking. In acute coronary syndromes, however, ischemia may result from transient thrombus formation or coronary spasm at the site of a ruptured plaque. We report on the pathophysiological mechanisms underlying transient ischemia in acute coronary syndromes despite optimal therapy, on the basis of analysis of heart rate changes preceding ischemia and its circadian variation.
  
  
  RESULTS
  Two hundred fifty-six patients with unstable angina or non-Q-wave myocardial infarction underwent continuous ST-segment monitoring for 48 hours while receiving maximal medical therapy. All ischemic episodes were characterized by their timing, duration, association with pain, and heart rate changes before the onset of ischemia. During 10,629 hours of monitoring, 44 patients (17.2%) had 176 episodes of transient ischemia. The mean heart rate at onset of ischemia was 68 +/- 12.8 bpm, and > 55% of ischemic episodes were not preceded by a significant increase in heart rate. Ischemic activity had a single nocturnal peak, with 64% of all episodes occurring between 10 PM and 8 AM, this nocturnal preponderance being evident for episodes with or without a preceding increase in heart rate. The characteristics and timing of transient ischemia were similar in unstable angina and non-Q-wave myocardial infarction, but transient ischemia was more frequent (27.3% versus 15.1%; P < .05) and prolonged (median, 20 versus 13.5 minutes; P < .01) in non-Q-wave myocardial infarction.
  
  
  CONCLUSIONS
  In acute coronary syndromes, transient ischemia has a low threshold, occurs predominantly without an increase in myocardial oxygen demand, and is present mainly at night rather than in the morning. These findings in patients receiving maximal medical therapy suggest significant pathophysiological differences underlying transient ischemia compared with stable coronary disease.
authors.affiliation: Department of Cardiology, Royal Brompton Hospital, London, United Kingdom.
authors.forename: D J
authors.initials: DJ
authors.lastname: Patel
authors.forename: C J
authors.initials: CJ
authors.lastname: Knight
authors.forename: D R
authors.initials: DR
authors.lastname: Holdright
authors.forename: D
authors.initials: D
authors.lastname: Mulcahy
authors.forename: D
authors.initials: D
authors.lastname: Clarke
authors.forename: C
authors.initials: C
authors.lastname: Wright
authors.forename: H
authors.initials: H
authors.lastname: Purcell
authors.forename: K M
authors.initials: KM
authors.lastname: Fox
mesh_terms: D000208:Acute Disease; D000789:Angina, Unstable / Q000188:drug therapy / Q000503:physiopathology*; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D002940:Circadian Rhythm; D004359:Drug Therapy, Combination; D015716:Electrocardiography, Ambulatory; D006339:Heart Rate; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D006493:Heparin; D001241:Aspirin