title: Changes in Coronary Blood Flow After Acute Myocardial Infarction: Insights From a Patient Study and an Experimental Porcine Model.
abstract: OBJECTIVE
  The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries.
  
  
  BACKGROUND
  An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters.
  
  
  METHODS
  Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11).
  
  
  RESULTS
  In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = -0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p < 0.001) with consistent observations in swine (Δ = -0.9; 1.5 ± 0.4 vs. 2.4 ± 0.9 for after and before AMI, respectively; p = 0.04). An increased baseline and a decreased hyperemic flow contributed to the reduction in CFR in both patients (baseline flow: Δ = +5 and hyperemic flow: Δ = -7 cm/s) and swine (baseline flow: Δ = +8 and hyperemic flow: Δ = -6 cm/s). Similar changes were observed in nonculprit arteries (CFR: 2.8 ± 0.7 vs. 2.0 ± 0.7 for STEMI patients and control subjects; p < 0.001). CFR significantly correlated with infarct size as a percentage of the left ventricle in both patients (r = -0.48; p = 0.001) and swine (r = -0.61; p = 0.047).
  
  
  CONCLUSIONS
  CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction.
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Guus A
authors.initials: GA
authors.lastname: de Waard
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Maurits R
authors.initials: MR
authors.lastname: Hollander
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Paul F A
authors.initials: PF
authors.lastname: Teunissen
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Matthijs F
authors.initials: MF
authors.lastname: Jansen
authors.affiliation: Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
authors.forename: Elise S
authors.initials: ES
authors.lastname: Eerenberg
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Aernout M
authors.initials: AM
authors.lastname: Beek
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Koen M
authors.initials: KM
authors.lastname: Marques
authors.affiliation: Department of Epidemiology and Biostatistics, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
authors.forename: Peter M
authors.initials: PM
authors.lastname: van de Ven
authors.affiliation: Department of Internal Medicine, Division Vascular Pharmacology, Erasmus Medical Center, Rotterdam, the Netherlands.
authors.forename: Ingrid M
authors.initials: IM
authors.lastname: Garrelds
authors.affiliation: Department of Internal Medicine, Division Vascular Pharmacology, Erasmus Medical Center, Rotterdam, the Netherlands.
authors.forename: A H Jan
authors.initials: AH
authors.lastname: Danser
authors.affiliation: Department of Experimental Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands.
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Duncker
authors.affiliation: Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands. Electronic address: n.vanroyen@vumc.nl.
authors.forename: Niels
authors.initials: N
authors.lastname: van Royen
mesh_terms: D000368:Aged; D000818:Animals; D001706:Biopsy; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D017023:Coronary Angiography; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004195:Disease Models, Animal; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D057216:Propensity Score; D000072657:ST Elevation Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy; D013552:Swine; D013997:Time Factors; D016896:Treatment Outcome
keywords: acute myocardial infarction; coronary flow reserve; coronary microcirculation; microcirculatory dysfunction