Guus A de Waard1, Maurits R Hollander1, Paul F A Teunissen1, Matthijs F Jansen1, Elise S Eerenberg2, Aernout M Beek1, Koen M Marques1, Peter M van de Ven3, Ingrid M Garrelds4, A H Jan Danser4, Dirk J Duncker5, Niels van Royen6. 1. Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands. 2. Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands. 3. Department of Epidemiology and Biostatistics, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands. 4. Department of Internal Medicine, Division Vascular Pharmacology, Erasmus Medical Center, Rotterdam, the Netherlands. 5. Department of Experimental Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands. 6. Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands. Electronic address: n.vanroyen@vumc.nl.
Abstract
OBJECTIVES: 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.
OBJECTIVES: 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: Hernán Mejía-Rentería; Nina van der Hoeven; Tim P van de Hoef; Julius Heemelaar; Nicola Ryan; Amir Lerman; Niels van Royen; Javier Escaned Journal: Int J Cardiovasc Imaging Date: 2017-05-13 Impact factor: 2.357
Authors: Nina W van der Hoeven; Gladys N Janssens; Guus A de Waard; Henk Everaars; Christopher J Broyd; Casper W H Beijnink; Peter M van de Ven; Robin Nijveldt; Christopher M Cook; Ricardo Petraco; Tim Ten Cate; Clemens von Birgelen; Javier Escaned; Justin E Davies; Maarten A H van Leeuwen; Niels van Royen Journal: JAMA Cardiol Date: 2019-08-01 Impact factor: 14.676
Authors: Tamás Baranyai; Zoltán Giricz; Zoltán V Varga; Gábor Koncsos; Dominika Lukovic; András Makkos; Márta Sárközy; Noémi Pávó; András Jakab; Csilla Czimbalmos; Hajnalka Vágó; Zoltán Ruzsa; Levente Tóth; Rita Garamvölgyi; Béla Merkely; Rainer Schulz; Mariann Gyöngyösi; Péter Ferdinandy Journal: J Transl Med Date: 2017-04-01 Impact factor: 5.531
Authors: Hernán Mejía-Rentería; Joo Myung Lee; Nina W van der Hoeven; Nieves Gonzalo; Pilar Jiménez-Quevedo; Luis Nombela-Franco; Iván J Núñez-Gil; Pablo Salinas; María Del Trigo; Enrico Cerrato; Niels van Royen; Paul Knaapen; Bon-Kwon Koo; Carlos Macaya; Antonio Fernández-Ortiz; Javier Escaned Journal: J Am Heart Assoc Date: 2019-05-07 Impact factor: 5.501
Authors: Troels Thim; Matthias Götberg; Ole Fröbert; Robin Nijveldt; Niels van Royen; Sergio Bravo Baptista; Sasha Koul; Thomas Kellerth; Hans Erik Bøtker; Christian Juhl Terkelsen; Evald Høj Christiansen; Lars Jakobsen; Steen Dalby Kristensen; Michael Maeng Journal: BMC Res Notes Date: 2020-09-01