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Implications of ischaemic area at risk and mode of reperfusion in ST-elevation myocardial infarction
  1. Kevin R Bainey1,
  2. Claudio Fresco2,
  3. Yinggan Zheng1,
  4. Sigrun Halvorsen3,
  5. Antonio Carvalho4,
  6. Miodrag Ostojic5,
  7. Patrick Goldstein6,
  8. Anthony H Gershlick7,
  9. Cynthia M Westerhout1,
  10. Frans Van de Werf8,
  11. Paul W Armstrong1
  12. for the STREAM Investigators
  1. 1Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada
  2. 2Department of Cardiothoracic Sciences, Azienda Ospedaliero Universitaria di Udine, Udine, Italy
  3. 3Department of Cardiology, Oslo University Hospital Ulleval, Oslo, Norway
  4. 4Cardiology Division, Department of Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil
  5. 5Medical School, University of Belgrade, Belgrade, Serbia
  6. 6Emergency Department and Service d'aide Medicale Urgente (SAMU), Lille University Hospital, Lille, France
  7. 7Leicester Cardiovascular Biomedical Research Unit, National Institute for Health Research, University Hospitals of Leicester Trust, Leicester, UK
  8. 8Department of Cardiovascular Sciences, University Hospitals Leuven, Leuven, Belgium
  1. Correspondence to Dr Paul W Armstrong, Canadian VIGOUR Centre, University of Alberta, 2-132 Li Ka Shing Centre for Health Research Innovation, Edmonton, Alberta, Canada T6G 2E1; paul.armstrong{at}


Objective Uncertainty exists concerning the relative merits of pharmacological versus mechanical coronary reperfusion in patients presenting early with ST-elevation myocardial infarction (STEMI) with extensive myocardium at risk. Accordingly, we investigated whether the extent of baseline ST-segment shift was related to the response of either reperfusion modality in patients with STEMI presenting within 3 h of symptoms.

Methods We analysed baseline ECGs from 1859 patients enrolled in the STrategic Reperfusion Early After Myocardial Infarction (STREAM) trial. The sum of ST-segment elevation (∑STE) and ST-segment deviation (∑STD) was categorised into quartiles and associations with the primary endpoint (30-day death/shock/congestive heart failure/re-myocardial infarction) for each reperfusion strategy (early fibrinolysis vs primary percutaneous coronary intervention) were explored.

Results Overall, there was a progressive rise in the 30-day primary endpoint according to quartiles of baseline ∑STE (10.3% (0–5 mm), 12.4% (5.5–8.5 mm), 12.1% (9–13.5 mm), 17.6% (>14.0 mm), p=0.008) and ∑STD (9.0% (0–9 mm), 13.5% (9.5–14 mm), 14.7% (14.5–20 mm), 15.3% (>20 mm), p=0.019). Both ∑STE and ∑STD were associated with the primary endpoint (∑STE: p=0.071; ∑STD: p=0.024). However, there was no interaction between quartiles of baseline ∑STE or ∑STD and efficacy of either reperfusion strategy on the 30-day clinical outcomes (∑STE: p (interaction)=0.696; ∑STD: p (interaction)=0.542).

Conclusions These data demonstrate an association between ∑STE or ∑STD on the baseline ECG and clinical events at 30 days following reperfusion therapy in STEMI. More importantly, the response to different reperfusion strategies was not influenced by the extent of jeopardised myocardium.

Trial registration number NCT00623623; Post-results.

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