Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction

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Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction. / Lubberding, Anniek Frederike; Sattler, Stefan M; Flethøj, Mette; Tfelt-Hansen, Jacob; Jespersen, Thomas.

I: American Journal of Physiology: Heart and Circulatory Physiology, Bind 318, Nr. 2, 2020, s. H391-H400.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lubberding, AF, Sattler, SM, Flethøj, M, Tfelt-Hansen, J & Jespersen, T 2020, 'Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction', American Journal of Physiology: Heart and Circulatory Physiology, bind 318, nr. 2, s. H391-H400. https://doi.org/10.1152/ajpheart.00406.2019

APA

Lubberding, A. F., Sattler, S. M., Flethøj, M., Tfelt-Hansen, J., & Jespersen, T. (2020). Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction. American Journal of Physiology: Heart and Circulatory Physiology, 318(2), H391-H400. https://doi.org/10.1152/ajpheart.00406.2019

Vancouver

Lubberding AF, Sattler SM, Flethøj M, Tfelt-Hansen J, Jespersen T. Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction. American Journal of Physiology: Heart and Circulatory Physiology. 2020;318(2):H391-H400. https://doi.org/10.1152/ajpheart.00406.2019

Author

Lubberding, Anniek Frederike ; Sattler, Stefan M ; Flethøj, Mette ; Tfelt-Hansen, Jacob ; Jespersen, Thomas. / Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction. I: American Journal of Physiology: Heart and Circulatory Physiology. 2020 ; Bind 318, Nr. 2. s. H391-H400.

Bibtex

@article{72890649a962495b924754f9b8729b08,
title = "Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction",
abstract = "Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open-chest) to minimal-invasive techniques, including balloon occlusion (closed-chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regards to hemodynamics, electrophysiology and arrhythmia development. Forty-two female Danish Landrace pigs (20 open-chest, 22 closed-chest) were anesthetized and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (D -22 mmHg, D -1.5 L/min from baseline, both p<0.001 intra-group). Heart increased with opening of the chest, but increased with balloon placement (p<0.001). AMI-induced ST elevation was lower in the open chest group (p<0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (p=0.005). VF occurred in 7/20 and 12/22 pigs in the open-chest and closed-chest group, respectively (p=0.337), with longer time-to-VF in the open chest group (23.4±1.2 min in open-chest and 17.8±1.4 min in closed-chest; p=0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.",
author = "Lubberding, {Anniek Frederike} and Sattler, {Stefan M} and Mette Fleth{\o}j and Jacob Tfelt-Hansen and Thomas Jespersen",
year = "2020",
doi = "10.1152/ajpheart.00406.2019",
language = "English",
volume = "318",
pages = "H391--H400",
journal = "American Journal of Physiology: Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Comparison of hemodynamics, cardiac electrophysiology and ventricular arrhythmia in an open and a closed chest porcine model of acute myocardial infarction

AU - Lubberding, Anniek Frederike

AU - Sattler, Stefan M

AU - Flethøj, Mette

AU - Tfelt-Hansen, Jacob

AU - Jespersen, Thomas

PY - 2020

Y1 - 2020

N2 - Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open-chest) to minimal-invasive techniques, including balloon occlusion (closed-chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regards to hemodynamics, electrophysiology and arrhythmia development. Forty-two female Danish Landrace pigs (20 open-chest, 22 closed-chest) were anesthetized and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (D -22 mmHg, D -1.5 L/min from baseline, both p<0.001 intra-group). Heart increased with opening of the chest, but increased with balloon placement (p<0.001). AMI-induced ST elevation was lower in the open chest group (p<0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (p=0.005). VF occurred in 7/20 and 12/22 pigs in the open-chest and closed-chest group, respectively (p=0.337), with longer time-to-VF in the open chest group (23.4±1.2 min in open-chest and 17.8±1.4 min in closed-chest; p=0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.

AB - Ventricular fibrillation (VF) during acute myocardial infarction (AMI) is an important contributor to sudden cardiac death. Large animal models are widely used to study AMI-induced arrhythmia, but the mode of AMI induction ranges from thoracotomy and surgical ligation of a coronary vessel (open-chest) to minimal-invasive techniques, including balloon occlusion (closed-chest). How the choice of induction affects arrhythmia development is unclear. The aim of this study was to compare an open-chest and a closed-chest model with regards to hemodynamics, electrophysiology and arrhythmia development. Forty-two female Danish Landrace pigs (20 open-chest, 22 closed-chest) were anesthetized and occlusion of the mid-left anterior descending coronary artery was performed for 60 min. Opening the chest reduced blood pressure and cardiac output (D -22 mmHg, D -1.5 L/min from baseline, both p<0.001 intra-group). Heart increased with opening of the chest, but increased with balloon placement (p<0.001). AMI-induced ST elevation was lower in the open chest group (p<0.001). Premature ventricular contractions occurred in two distinct phases (0-15 and 15-40 min), the latter of which was delayed in the open-chest group (p=0.005). VF occurred in 7/20 and 12/22 pigs in the open-chest and closed-chest group, respectively (p=0.337), with longer time-to-VF in the open chest group (23.4±1.2 min in open-chest and 17.8±1.4 min in closed-chest; p=0.007). In summary, opening the chest altered hemodynamic parameters and delayed the onset of ventricular arrhythmias. Hence, in the search for mechanisms and novel treatments of AMI-induced arrhythmia, caution should be taken when choosing between or comparing the results from these two models.

U2 - 10.1152/ajpheart.00406.2019

DO - 10.1152/ajpheart.00406.2019

M3 - Journal article

C2 - 31922881

VL - 318

SP - H391-H400

JO - American Journal of Physiology: Heart and Circulatory Physiology

JF - American Journal of Physiology: Heart and Circulatory Physiology

SN - 0363-6135

IS - 2

ER -

ID: 234448056