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ST-segment depression resolution predicts infarct size and reperfusion injury in ST-elevation myocardial infarction
  1. Sebastian J Reinstadler1,2,
  2. Anett Baum1,
  3. Karl-Philipp Rommel3,
  4. Charlotte Eitel1,
  5. Steffen Desch1,
  6. Meinhard Mende4,
  7. Bernhard Metzler2,
  8. Janine Poess1,
  9. Holger Thiele1,
  10. Ingo Eitel1
  1. 1Medical Clinic II, Department of Cardiology, Angiology and Intensive Care Medicine, University Heart Center Lübeck, University of Lübeck, Lübeck, Germany
  2. 2Cardiology and Angiology, University Clinic of Internal Medicine III, Medical University of Innsbruck, Innsbruck, Austria
  3. 3Clinic for Internal Medicine/Cardiology, University of Leipzig—Heart Center, Leipzig, Germany
  4. 4Clinical Trial Center Leipzig, University of Leipzig, Leipzig, Germany
  1. Correspondence to Dr Ingo Eitel, Medical Clinic II, Department of Cardiology, Angiology and Intensive Care Medicine, University Heart Center Lübeck, University Lübeck, Ratzeburger Allee 160, Lübeck 23538, Germany; Ingo.Eitel{at}uksh.de

Abstract

Objective ST-elevation myocardial infarction (STEMI) is frequently associated with reciprocal ST-segment depression in contralateral ECG leads. However, the relationship of the resolution of ST-segment depression (STD-R) with myocardial damage is unknown and the potential prognostic value incompletely understood. We sought to evaluate the association between STD-R and markers of myocardial injury as well as to determine the prognostic impact of STD-R in patients with acute reperfused STEMI.

Methods We enrolled 611 patients with STEMI in this multicentre cardiac magnetic resonance (CMR) study. STD-R, defined as either worsened (<0%), incomplete (0–50%) or complete (≥50%), was determined 90 min after primary percutaneous coronary intervention (PCI). Patients underwent CMR in median 3 (2–4) days after infarction. Major adverse cardiac events (MACE) were defined as a composite of death, reinfarction and new congestive heart failure within 12 months after enrolment.

Results Patients with worsened or incomplete STD-R (n=148 (24.2%)) had a significantly larger area at risk (42 (31–50) vs 37 (29–52) vs 34 (24–46) %LV, p=0.001), larger infarct size (20 (13–30) vs 17(10–26) vs 16 (8–24) %LV, p=0.003), larger extent of microvascular obstruction (0.6(0–3.4) vs 0.4 (0–2.4) vs 0.0 (0–1.4) %LV, p=0.003), and a lower LVEF (46 (39–54) vs 48 (40–56) vs 52 (45–58) %, p<0.001). MACE rate (n=37 (6%)) was significantly higher in patients with worsened (n=10 (19%)) or incomplete STD-R (n=7 (7%)) than in patients with complete STD-R (n=20 (4%), p<0.001). In multivariate Cox regression analysis, categorised STD-R emerged as an independent predictor of MACE at 12 months after adjusting for clinical variables (p=0.007).

Conclusions Patients with acute STEMI and worsened or incomplete STD-R after PCI show a more pronounced myocardial as well as microvascular damage as detected by CMR with subsequent independent prognostic information on MACE over a 12-month follow-up period.

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