The Heart Valve Society

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Aortic Valve Mechanical, Compositional and Structural Changes with Left-Ventricular Assist Device (LVAD) Implantation
Elizabeth H. Stephens1, Jiho Han1, Emma Trawick1, Elena Dimartino2, Hemanth Akkiraju1, Lewis M. Brown1, K. Jane Grande-Allen3, Jennifer Connell3, Gordana Vunjak-Novakovic1, Hiroo Takayama1.
1Columbia, New York, NY, USA, 2University of Calgary, Calgary, AB, Canada, 3Rice University, Houston, TX, USA.

OBJECTIVE: Aortic regurgitation (AR) is a common complication of left-ventricular assist devices (LVADs) leading to worsening heart failure. LVADs alter aortic valves' (AV) hemodynamic environment, and it is likely that these AVs lack normal mechanical stimulation to maintain valve integrity, leading to AR. However, how AV structure, mechanical properties, and composition change with LVAD support remain unknown. The goal of this study was to use mechanical testing, proteomic analysis and transition electron microscopy to assess for AV changes during LVAD support.
METHODS: AVs were collected from 16 LVAD and 7 non-LVAD patients at time of heart transplant. Biaxial tensile testing was performed using a load-control protocol. Proteins isolated from the AVs were analyzed by shotgun proteomics on a mass spectrometer. Transition electron microscopy was performed using a JEOL JEM-1200 EXII electron microscope. Comparisons between the two groups were made using standard statistical methods.
RESULTS: Demographic data, degree of AR, and AV opening is shown in the Table. Maximum strain in LVAD patients was less than non-LVAD patients (see Table). There was a trend of increasing radial modulus with LVAD duration (0.4, p=0.095). When patients were grouped into non-LVAD, LVAD <1 year duration, and LVAD >1 year duration, there was a trend of decreased circumferential strain (Chart, p=0.063) between the groups. Proteomic mass accuracy was excellent (precursor 4.0 ppm, product 10.0 ppm) with mean sequence coverage of 35.2%. Prominent proteins included numerous collagen chains, galectin 1, biglycan vimentin, metalloproteinase inhibitor 3, serum amyloid P component, actin cytoplasmic 1 and 2, lumican, clusterin, vitronectin, prolargin, elastin, fibromodulin, mimecan, periostin, and decorin. Further studies are underway analyzing differences between groups. Transition electron microscopy analysis is underway.
CONCLUSIONS: AVs in LVAD patients showed decreased maximum strain relative to non-LVAD patients, suggesting increased stiffness. Ongoing studies are assessing for concomitant changes in AV structure and proteomics. Knowledge of the AV compositional, mechanical and structural changes in LVAD patients may provide an opportunity for interventions to prevent and/or reverse this detrimental complication.


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