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Updated: Jul 7, 2026
Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Assessing iatrogenic atrial septal defect as a primary unloading strategy in acute myocardial infarction using
Emil Aliev1,2,3,4, Shirel Shtraikh1,2,3,4, Adi Horesh1,2,3,4
1The Heart Institute, Hadassah Medical Center, The Faculty of Medicine, Hebrew University Jerusalem, 9112102, Jerusalem, Israel.
Abstract:
Primary-unloading of the left ventricle in Acute Myocardial Infarction (AMI) may reduce infarct size and resultant heart-failure occurrence. Existing methods, such as percutaneous axial flow pumps, pose cost and complication challenges. Hemodynamic parameters from AMI patients in published cohorts were applied in a real-time cardiovascular computer-model simulating AMI. Hemodynamic changes were tracked after induction of 2.5-12.5 mm Iatrogenic Atrial-Septal Defect (iASD). Subsequently, in-vivo evaluation in swine was performed by inducing AMI using percutaneous-balloon occlusion of the left coronary system. A 7.5 mm iASD was created via transeptal balloon septostomy, repeatedly opened, and occluded, while advanced hemodynamic parameters were monitored. The computer simulation demonstrated a decrease in mean(± SEM) pulmonary capillary wedge pressure (PCWP) of 8.05 ± 0.7 mmHg from a baseline to iASD (21.2 ± 8.3 vs. 13.2 ± 4.2 mmHg, p < 0.001), reaching a maximum reduction of 8.05 ± 1.04at 7.5 mm (13.2 ± 3.9 mmHg). Mean Arterial Pressure (MAP) was reduced from baseline compared to iASD intervention (94.7 ± 14.8 vs. 84.4 ± 13.6 mmHg, p < 0.001) with no difference between iASD sizes. The cardiac output (CO) was reduced by a mean(± SEM) 0.46 ± 0.15 L/min from baseline compared to mean iASD interventions (4.05 ± 1.28 vs. 3.59 ± 1.16 L/min, p = 0.001). In the swine model, 60 measurements were taken. The mean(± SEM) PCWP was increased by 7.23 ± 1.0 from baseline during coronary obstruction (14.72 ± 1.6 vs. 21.95 ± 3.9 mmHg, p < 0.01) and decreased by 4.85 ± 1.1 with the iASD (17.1 ± 2.7 mmHg, p = 0.039). The iASD didn't cause hemodynamic compromise, as there was no reduction in MAP (43.6 ± 13.5 vs. 48.3 ± 12.0 mmHg, p > 0.99) or CO (2.6 ± 0.5 vs. 2.3 ± 0.2 L/min, p > 0.99) compared to coronary obstruction without iASD. In conclusion, iASD unloaded the left ventricle in AMI without causing immediate hemodynamic compromise in this preliminary study. These findings highlight the potential of iASD as a feasible primary-unloading method that warrants further investigation regarding its safety and cost-effectiveness.
