**3. Flow dynamics of aortic insufficiency during LVAD support**

For the majority of rotary LVADs, the LVAD inlet is located at the LV apex, and the outlet anastomoses to the ascending aorta, bypassing the AV. Implantation of the LVAD immediately increases systemic blood flow and end-organ perfusion, providing an alternate pathway for blood to flow from the heart to the arterial system, as shown in **Figure 5**. LVAD support unloads the heart, decreasing the magnitude and pulsatility of LV pressure, which can fall below the level needed to open the AV fully during myocardial contraction. With sufficient contraction of the native heart, a fraction of the flow is ejected through the AV, and the heart and LVAD operate in parallel. In this condition, the AV does not open fully, exhibiting a reduced opening area and duration [29]. During periods of high LVAD support, the LV pressure is too small to open the AV, and blood flow occurs entirely through the LVAD, the heart, and the pump operating in series [30]. The AV is continuously closed for this condition and chronically exposed to high transvalvular pressure. For many patients, the level of LVAD support needed to relieve the HF symptoms results in complete and continuous closure of the AV, with all blood exiting the heart through the LVAD.

Adding a rotary LVAD to the native heart reduces the range of pressure and flow experienced in the cardiovascular system, diminishing pulsatility. The last decade of LVAD therapy has revealed several significant complications that worsen with reduced pulsatility, including thrombus formation, AV incompetence, and vascular smooth muscle response [17, 31]. The latter has been tied to arteriovenous malformations and gastrointestinal bleeding [17, 32]. Indices of pulsatility include pulse pressure, normalized flow range, and surplus hemodynamic energy [28, 30], which decrease as LVAD speed increases. When the AV ceases to open, the abnormal flow pattern creates a region of flow stasis adjacent to the AV, which creates a high risk for thromboembolism that could be embolized by a sudden strong contraction of the native heart [33].

Blood flow in the normal healthy heart is unsteady, 3-D and shows a range of different length scales [34]. A typical flow pattern in the LV has been described as consisting of a large diastolic vortex that channels the transit of incoming blood from the mitral valve towards the AV [35]. This vortex contributes to diastolic suction and minimizes kinetic energy losses and cardiac work [36]. The LV vortex has been shown to facilitate the blood mass coming into the normal LV during one beat washing out completely after a few beats [37], which prevents intraventricular blood stagnation [38].

In the LV of a diseased heart, progressive adverse remodeling leads to abnormal flow patterns that may impair pumping efficiency, and therefore affects blood transit within the ventricle. It is believed these abnormal intraventricular flow dynamics may contribute to the progression of certain diseases, leading to a final stage of HF or thrombus formation [39]. In addition, previous studies of flow transport through the heart have correlated dilated cardiomyopathy with increased vortex kinetic energy and decreased flow transport [40]. Models of this pathological condition have identified a high thrombus risk in DCM patients with large regions of blood flow with residence times greater than 2 s that also exhibit low kinetic energy [41]. When AI is present, retrograde flow mixing with the forward flow during diastole contributes to energy loss and increases residence time [41].

Thrombus formation and growth in several locations have been observed clinically, contributing to the high stroke rate in LVAD patients [42]. When AI develops in LVAD patients, the backward flow through the AV may improve pulsatility and flow stasis in

#### **Figure 5.**

*Schematic of flow conditions. A. the normal flow path enters the left ventricle (LV) through the mitral valve and exits through the aortic valve and into the aorta. B. Low LVAD support works with the native heart to produce parallel flow through the LVAD and aortic valve. C. High LVAD support maintains continuous closure of the aortic valve during series flow. D. Aortic insufficiency produces retrograde flow through the aortic valve that can re-enter the LVAD in a regurgitant flow loop.*

#### *Aortic Insufficiency in LVAD Patients DOI: http://dx.doi.org/10.5772/intechopen.106173*

the aortic root, but over time results in reduced systemic flow. In particular, AI results in the formation of a regurgitant flow loop, in which blood from the LVAD flows retrograde through the AV, into the LV, and out through the LVAD again. This loop extends the amount and time-history of shear stress exposure to the blood, increasing hemolysis and thrombogenicity. The pump will also need to run at a higher speed to achieve the original cardiac output, which increases wear on the device. Hemostasis and thromboregulation are already compromised in LVAD patients, and AI adds to this liability.

During LVAD support, LV vortex formation is relatively unaffected, although vortex circulation and kinetic energy increase with LVAD speed, particularly in systole when all flow exits through the LVAD. When AI occurs, the regurgitant jet forms a vortex ring that normally dissipates in the mid-ventricle when no LVAD support is present but collides with the incoming mitral flow, as shown in **Figure 6**. When the LVAD is added, the regurgitant jet is drawn towards the LVAD inflow, impinging on the vortex ring generated by mitral inflow. The oppositely rotating vortices are partially annihilated, dissipating energy in the process. This flow pattern contributes to fluid stasis along the septal wall.

Recent device improvements include an "artificial pulse", based on a rapid LVAD speed change, that produces a small hemodynamic boost. While this artificial pulse provides substantial improvement in pulsatility, it is not synchronized with the native heartbeat and thus offers minimal improvement in the overall flow. The presence of speed modulation does not appear to impact the development of AI, which remains a significant complication of LVADs.
