title: Progressive epicardial coronary blood flow reduction fails to produce ST-segment depression at normal heart rates.
abstract: ST-segment depression is commonly seen in patients with acute coronary syndromes. Most authors have attributed it to transient reductions in coronary blood flow due to nonocclusive thrombus formation on a disrupted atherosclerotic plaque and dynamic focal vasospasm at the site of coronary artery stenosis. However, ST-segment depression was never reproduced in classic animal models of coronary stenosis without the presence of tachycardia. We hypothesized that ST-segment depression occurring during acute coronary syndromes is not entirely explained by changes in epicardial coronary artery resistance and thus evaluated the effect of a slow, progressive epicardial coronary artery occlusion on the ECG and regional myocardial blood flow in anesthetized pigs. Slow, progressive occlusion over 72 min (SD 27) of the left anterior descending coronary artery in 20 anesthetized pigs led to a 90% decrease in coronary blood flow and the development of ST-segment elevation associated with homogeneous and transmural myocardial blood flow reductions, confirmed by microspheres and myocardial contrast echocardiography. ST-segment depression was not observed in any ECG lead before the development of ST-segment elevation. At normal heart rates, progressive epicardial stenosis of a coronary artery results in myocardial ischemia associated with homogeneous, transmural reduction in regional myocardial blood flow and ST-segment elevation, without preceding ST-segment depression. Thus, in coronary syndromes with ST-segment depression and predominant subendocardial ischemia, factors other than mere increases in epicardial coronary resistance must be invoked to explain the heterogeneous parietal distribution of flow and associated ECG changes.
authors.affiliation: Research Center, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada H4J 1C5.
authors.forename: Marilyn
authors.initials: M
authors.lastname: de Chantal
authors.forename: Jean G
authors.initials: JG
authors.lastname: Diodati
authors.forename: James B
authors.initials: JB
authors.lastname: Nasmith
authors.forename: Robert
authors.initials: R
authors.lastname: Amyot
authors.forename: A Robert
authors.initials: AR
authors.lastname: LeBlanc
authors.forename: Erick
authors.initials: E
authors.lastname: Schampaert
authors.forename: Chantal
authors.initials: C
authors.lastname: Pharand
mesh_terms: D000789:Angina, Unstable / Q000503:physiopathology; D000792:Angiography; D000818:Animals; D023921:Coronary Stenosis / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D006339:Heart Rate / Q000502:physiology*; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D009203:Myocardial Infarction / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D010496:Pericardium / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D013552:Swine; D013927:Thrombosis / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology