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Original article
Coronary vasomotor function in infarcted and remote myocardium after primary percutaneous coronary intervention
  1. Paul F A Teunissen1,
  2. Stefan A J Timmer1,
  3. Ibrahim Danad1,
  4. Guus A de Waard1,
  5. Peter M van de Ven2,
  6. Pieter G Raijmakers3,
  7. Adriaan A Lammertsma3,
  8. Albert C Van Rossum1,
  9. Niels van Royen1,
  10. Paul Knaapen1
  1. 1Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands
  2. 2Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands
  3. 3Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands
  1. Correspondence to Dr Paul Knaapen, Department of Cardiology, 5F, VU University Medical Center, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands; p.knaapen{at}


Objective In patients with acute myocardial infarction (AMI), coronary vasomotor function is impaired in the myocardial territory supplied by the culprit artery and in remote myocardium supplied by angiographically normal vessels. The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15O]H2O positron emission tomography, after successful percutaneous coronary intervention.

Methods 44 patients with AMI and successful revascularisation by percutaneous coronary intervention were included. Subjects were examined 1 week and 3 months after AMI with [15O]H2O positron emission tomography to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow (MBF) during hyperaemia and rest. Additionally, 45 age-matched and sex-matched subjects underwent similar scanning procedures and served as controls.

Results At baseline, CFR averaged 1.81±0.66 in infarcted myocardium versus 2.51±0.81 in remote myocardium (p<0.01). In comparison, CFR in the control group averaged 4.16±1.45 (p=0.001 vs both). During follow-up, the CFR increased to 2.74±0.85 in infarcted myocardium (p<0.01), and to 2.85±0.70 in remote myocardium (p<0.01). This was predominantly due to an increase in hyperaemic MBF, from 1.62±0.54 mL/min/g to 2.19±0.68 mL/min/g in infarcted myocardium (p<0.001), and 2.17±0.54 mL/min/g to 2.60±0.65 mL/min/g in remote myocardium (p<0.001).

Conclusions CFR in infarcted and remote myocardium is impaired 1 week after AMI. After 3 months vasomotor function partially recovers. However, as compared with control patients, MBF remains impaired in culprit and reference territories in patients with AMI.

Clinical trial registration NTR3164.

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