Study: Left Ventricular Assist Device (LVAD) support, despite affording increased survival for patients with advanced systolic heart failure (HF), remains limited by post-implant pump thrombosis. Thrombus formation has been observed to occur at the Left Ventricle (LV) apex-LVAD inflow cannula interface, where altered hemodynamics is characterized by low Wall Shear Stress (WSS), which may trigger an activated prothrombotic phenotype of endothelial cells (ECs) with associated platelet activation, adherence and progressive thrombosis. We present a computational method to compute LV hemodynamics and WSS distribution over consecutive cardiac cycles for both healthy and failing LVs, to evaluate the associated thrombogenic potential. Methods: Patient specific LV geometrical models were reconstructed from 3D TT-ECHO as follows: a) healthy, with ejection volume (EV) of 70 ml; b) failing HF with residual 50% EV (35 ml); c) failing HF with no residual EV + LVAD inflow cannula. Dynamics of the cardiac cycle were simulated in ANSYS Fluent. The LV wall motion was set through mesh motion User Defined Functions, allowing to model contraction and twist during systole, expansion and untwist during diastole (Fig1A) Results: WSS in the apical region was one order of magnitude greater for the healthy LV compared to that of the HF LVs (with/without LVAD, Fig1B), demonstrating that reducing the LV contractility results in reduced WSS. The HF LV + LVAD model revealed a further decrease in WSS (Fig1B). In addition, the presence of the cannula largely altered the LV apex hemodynamics: the velocity magnitude was < 0.1 m/s, revealing the presence of a region of stagnation - i.e. a critical prothrombotic condition. Hemodynamics in the LVAD-implanted LV showed the highest thrombogenic potential, consistent with clinical observations. Our model provides mechanistic insights into the thrombogenic risk of LVAD patients and the significance of the LV apex-LVAD interface as a nidus of thrombosis
Thrombogenic Potential Of Altered Hemodynamics At The Left Ventricular Apex-LVAD Cannula Interface: A Numerical Study
PAPPALARDO, FEDERICO;CONSOLO, FILIPPOUltimo
2017-01-01
Abstract
Study: Left Ventricular Assist Device (LVAD) support, despite affording increased survival for patients with advanced systolic heart failure (HF), remains limited by post-implant pump thrombosis. Thrombus formation has been observed to occur at the Left Ventricle (LV) apex-LVAD inflow cannula interface, where altered hemodynamics is characterized by low Wall Shear Stress (WSS), which may trigger an activated prothrombotic phenotype of endothelial cells (ECs) with associated platelet activation, adherence and progressive thrombosis. We present a computational method to compute LV hemodynamics and WSS distribution over consecutive cardiac cycles for both healthy and failing LVs, to evaluate the associated thrombogenic potential. Methods: Patient specific LV geometrical models were reconstructed from 3D TT-ECHO as follows: a) healthy, with ejection volume (EV) of 70 ml; b) failing HF with residual 50% EV (35 ml); c) failing HF with no residual EV + LVAD inflow cannula. Dynamics of the cardiac cycle were simulated in ANSYS Fluent. The LV wall motion was set through mesh motion User Defined Functions, allowing to model contraction and twist during systole, expansion and untwist during diastole (Fig1A) Results: WSS in the apical region was one order of magnitude greater for the healthy LV compared to that of the HF LVs (with/without LVAD, Fig1B), demonstrating that reducing the LV contractility results in reduced WSS. The HF LV + LVAD model revealed a further decrease in WSS (Fig1B). In addition, the presence of the cannula largely altered the LV apex hemodynamics: the velocity magnitude was < 0.1 m/s, revealing the presence of a region of stagnation - i.e. a critical prothrombotic condition. Hemodynamics in the LVAD-implanted LV showed the highest thrombogenic potential, consistent with clinical observations. Our model provides mechanistic insights into the thrombogenic risk of LVAD patients and the significance of the LV apex-LVAD interface as a nidus of thrombosisI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
