title: Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery.
abstract: BACKGROUND
  Anterior precordial ST-segment depression (APSTD) is common in the setting of inferior myocardial infarction (IMI). The presence of APSTD correlates with increased risk of adverse outcomes in patients with acute IMI as well as more myocardium at risk as assessed by sestamibi, larger infarcts, lower ejection fractions, and more severe wall motion abnormalities in the infarct region. The ECG leads associated with APSTD (V1-V3) are generally thought to represent electrical activity subtended by the anterior myocardium, which is perfused by the left anterior descending artery (LAD). To determine whether APSTD is associated with abnormal blood flow in the uninvolved or non-culprit LAD, we assessed TIMI flow grades and corrected TIMI frame counts (CTFC) in both the culprit and non-culprit arteries of IMI patients.
  
  
  METHODS
  Data were drawn from the TIMI 10B trial of tenecteplase versus front-loaded tissue plasminogen activator in acute MI. Baseline ECGs were obtained within 12 hours of symptom onset, and angiography was performed 90 minutes following thrombolytic administration. A patient was considered to have precordial ST-segment depression if any ST-segment depression was present in any of leads V1-V3.
  
  
  RESULTS
  The majority of IMI's were due to right coronary artery occlusions, both in patients with APSTD (79.6%) and without APSTD (77.9%). In patients in whom the LAD was not the culprit artery but with APSTD were significantly less likely to have TIMI 3 flow at 90 minutes and more likely to have TIMI 2 flow. There was a trend toward slower CTFC in APSTD patients (27.2 +/- 13.4 vs. 22.6 +/- 8.5 frames/sec, p = 0.07).
  
  
  CONCLUSIONS
  Among patients with acute IMI associated with precordial ST-segment depression, flow in the non-culprit left anterior descending artery was slower than that in patients without APSTD. This finding may partially explain the occurrence of APSTD in IMI.
authors: Harvard Clinical Research Institute and Brigham & Women's Hospital, Boston, MA 02215, USA. mgibson@perfuse.org
authors: C Michael
authors: CM
authors: Gibson
authors: Michael
authors: M
authors: Chen
authors: Brad G
authors: BG
authors: Angeja
authors: Sabina A
authors: SA
authors: Murphy
authors: Susan J
authors: SJ
authors: Marble
authors: Hal V
authors: HV
authors: Barron
authors: Christopher P
authors: CP
authors: Cannon
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D023921:Coronary Stenosis / Q000188:drug therapy / Q000503:physiopathology; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D018709:Statistics, Nonparametric; D000077785:Tenecteplase; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use
chemical_list: D010959:Tissue Plasminogen Activator; D000077785:Tenecteplase