The effect of aortic valve incompetence on the hemodynamics of a continuous flow ventricular assist device in a mock circulation.
There is evidence that the incidence of aortic valve incompetence (AI) and other valvular pathologies may increase as more patients are submitted to longer periods of ventricular assist device (VAD) support. There is a need to better understand the mechanisms associated with the onset of these conditions and other possible complications related to the altered hemodynamics of VAD patients. In this study, the effect of AI on the hemodynamic response of continuous flow VAD (C-VAD) patients was measured in a mock loop over a range of pump speeds and level of native cardiac function. Our results showed that, in the presence of sufficient ventricular function, decreasing the C-VAD speed can allow a transition from series to parallel flow. Our study demonstrated that AI reduces the aortic pressure and flow when system impedance is unchanged. AI produces wasteful recirculation that substantially increases the pump work and decreases systemic perfusion, in particular during series flow conditions coupled with higher C-VAD speeds. The hematologic consequence of this regurgitant flow is a much higher exposure to shear for the blood, increasing the likelihood of hemolysis and thrombosis. While a certain degree of AI can be tolerated by a heart with good cardiac function, the consequences of AI for patients with VADs and poor cardiac function are much greater. Valve dysfunction in VAD patients may be related to structural changes in the tissue induced by altered biomechanics and excessive stress.
Zamarripa Garcia
Mario A
MA
Department of Mechanical Engineering, San Diego State University, San Diego, California 92182-1323, USA.
Enriquez
Luz A
LA
Dembitsky
Walter
W
May-Newman
Karen
K
D001022:Aortic Valve Insufficiency / Q000150:complications / Q000503:physiopathology* / Q000601:surgery*; D001696:Biomechanical Phenomena; D001698:Biomedical Engineering; D006353:Heart-Assist Devices / Q000009:adverse effects; D006439:Hemodynamics; D006461:Hemolysis; D006801:Humans; D066298:In Vitro Techniques; D008955:Models, Cardiovascular; D013927:Thrombosis / Q000209:etiology