TY - JOUR
T1 - Thoracic Endovascular Aortic RepairAcutely Augments Left Ventricular Biomechanics in An Animal Model
T2 - A Mechanism for Postoperative Heart Failure and Hypertension
AU - Stonko, David P.
AU - Edwards, Joseph
AU - Abdou, Hossam
AU - Treffalls, Rebecca N.
AU - Walker, Patrick
AU - DeMartino, Randall R.
AU - Mendes, Bernardo C.
AU - Hicks, Caitlin W.
AU - Morrison, Jonathan J.
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/11
Y1 - 2023/11
N2 - Background: Thoracic aortic stent grafts are thought to decrease aortic compliance and may contribute to hypertension and heart failure after thoracic endovascular aortic repair (TEVAR). Left ventricular (LV) biomechanics immediately after TEVAR, however, have not been quantified. Pressure-volume (PV) loop analysis provides gold-standard LV functional information. The aim of this study is to use an LV PV loop catheter and analysis to characterize the LV biomechanics before and acutely after TEVAR. Methods: Anesthetized Yorkshire swine (N = 6) were percutaneously instrumented with an LV PV loop catheter. A 20 mm × 10 cm stent graft was deployed distal to the left subclavian via the femoral artery under fluoroscopy. Cardiac biomechanics were assessed before and after TEVAR. As a sensitivity analysis, inferior vena cava occlusion with PV loop assessment was performed pre and post-TEVAR in 1 animal to obtain preload and afterload-independent end-systolic and end-diastolic PV relationships (ESPVR and EDPVR). Results: All animals underwent successful instrumentation and TEVAR. Post-TEVAR, all 6 animals had higher mean LV ESP (106 vs. 118 mm Hg, P = 0.04), with no change in the EDPVR. inferior vena cava occlusion also moved the ESPVR curve upward and leftward, indicating increased LV work per unit time. There was no augmentation of EDPVR following TEVAR (P > 0.05). Postmortem exams in all animals revealed appropriate stent placement and no technical complications. Conclusions: TEVAR was associated with an acute increase in LV end-systolic pressure and shift in the ESPVR, indicating increased ventricular work. This data provides potential mechanistic insights into the development of post-TEVAR hypertension and heart failure. Future stent graft innovation should focus on minimizing the changes in cardiac physiology.
AB - Background: Thoracic aortic stent grafts are thought to decrease aortic compliance and may contribute to hypertension and heart failure after thoracic endovascular aortic repair (TEVAR). Left ventricular (LV) biomechanics immediately after TEVAR, however, have not been quantified. Pressure-volume (PV) loop analysis provides gold-standard LV functional information. The aim of this study is to use an LV PV loop catheter and analysis to characterize the LV biomechanics before and acutely after TEVAR. Methods: Anesthetized Yorkshire swine (N = 6) were percutaneously instrumented with an LV PV loop catheter. A 20 mm × 10 cm stent graft was deployed distal to the left subclavian via the femoral artery under fluoroscopy. Cardiac biomechanics were assessed before and after TEVAR. As a sensitivity analysis, inferior vena cava occlusion with PV loop assessment was performed pre and post-TEVAR in 1 animal to obtain preload and afterload-independent end-systolic and end-diastolic PV relationships (ESPVR and EDPVR). Results: All animals underwent successful instrumentation and TEVAR. Post-TEVAR, all 6 animals had higher mean LV ESP (106 vs. 118 mm Hg, P = 0.04), with no change in the EDPVR. inferior vena cava occlusion also moved the ESPVR curve upward and leftward, indicating increased LV work per unit time. There was no augmentation of EDPVR following TEVAR (P > 0.05). Postmortem exams in all animals revealed appropriate stent placement and no technical complications. Conclusions: TEVAR was associated with an acute increase in LV end-systolic pressure and shift in the ESPVR, indicating increased ventricular work. This data provides potential mechanistic insights into the development of post-TEVAR hypertension and heart failure. Future stent graft innovation should focus on minimizing the changes in cardiac physiology.
UR - http://www.scopus.com/inward/record.url?scp=85158095459&partnerID=8YFLogxK
U2 - 10.1016/j.avsg.2023.04.007
DO - 10.1016/j.avsg.2023.04.007
M3 - Article
C2 - 37068623
AN - SCOPUS:85158095459
SN - 0890-5096
VL - 97
SP - 18
EP - 26
JO - Annals of Vascular Surgery
JF - Annals of Vascular Surgery
ER -