Comparison of Hemodynamics, Cardiac Electrophysiology and Ventricular Arrhythmia in An Open and a Closed Chest Porcine Model of Acute Myocardial Infarction

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.