Thromboembolism Is Linked to Intraventricular Flow Stasis in a Patient Supported with a Left Ventricle Assist Device

Abstract

A case report is presented of a left ventricular assist device (LVAD) recipient with a pre-existing thrombus that was removed on LVAD implant but quickly reformed and was removed, reformed again, and ultimately embolized, causing death. The thrombus formed proximal to the left ventricular outflow tract, because of the presence and subsequent repair of a calcified left ventricular infarct which had extruded from the septum. This region is vulnerable to flow stasis during LVAD support as predicted by experimental fluid mechanics studies, because of the lack of opening of the aortic valve. The presence of the repair and the altered flow field contributed to blood stasis and thrombus growth in a positive feedback loop. Although LVADs provide tremendous benefits for patients by reducing the symptoms of heart failure, the accompanying changes have some secondary consequences that remain problematic. One of these is an abnormal intraventricular flow field that decreases washout, especially in the region proximal to the left ventricular outflow tract, which is an area of flow stasis.

A clinical method for mapping and quantifying blood stasis in the left ventricle

“…Our results suggest that intraventricular blood stasis in the LVAD-assisted heart can be higher than prior to implanting the device, particularly near the left ventricular outflow tract, a region reported to be thrombogenic during continuous LVAD support (May-Newman et al 2013). Mapping methods as the one proposed herein show an excellent potential to correlate stagnant regions with local and global wall motion abnormalities.…”

“…As a result, a region with high residence time, moderate low kinetic energy and moderate low fluid distortion (moderately high T s ) appears near the LV outflow tract. These factors combined are the hallmark of blood stasis, suggesting a hemodynamic explanation for clinical reports of mural thrombosis in the LV outflow tract of LVAD-implanted patients (May-Newman et al 2013). These in vivo results are in agreement with previous in vitro experiments performed using a cardiac simulator (Wong et al 2014), although it should be noted that the drastic LV volume unloading caused by LVAD implantation was not modeled in the in vitro study.…”

Impact of LVAD Implantation Site on Ventricular Blood Stagnation

“…It has been established experimentally for nearly 100 years that blood stagnation leads to thrombus formation [30]. It is also well-understood in the literature that continuous flow VAD therapy alters physiological blood flow by creating hemodynamically unfavorable stagnant “hot-spots” [18, 31]. In this study, we aimed to identify regions of blood stasis within the LV that could be areas of thrombosis formation under the assumption that stagnant blood promotes thrombotic events associated with chronic complications in VAD patients.…”

“…These parameters are biologically important as they all adversely affect thrombogenicity [17]. More importantly, case reports have demonstrated that areas of stagnation caused by VAD implantation can be fatal [18]. …”

Programmed Speed Reduction Enables Aortic Valve Opening and Increased Pulsatility in the LVAD-Assisted Heart

“…Restoring pulsatility on a periodically rhythmic basis addresses two potential problems with LVAD support: 1) lack of valve opening, which has been associated with AI, and 2) poor blood mixing in the aortic root, which has been associated with thromboembolic events in these patients. 16,17 The control of CF-LVADs has historically ranged from simple fixed speeds (the currently approved operating mode in the HM II) to emulation of complex physiologic responses. The first successful feature developed to augment fixed LVAD speed was suction control.…”