The effect of fibrocalcific pathological processes on aortic valve stenosis

08 ביולי 2020, 14:00 - 15:00 
בניין וולפסון 206 
The effect of fibrocalcific pathological processes on aortic valve stenosis


Wednesday, July 08, 2020 at ____
The effect of fibrocalcific pathological processes on aortic valve stenosis:
A gender-specific biomechanical study

Maya Karnibad
Under the supervision of:
Prof. Rami Haj-Ali – School of Mechanical Engineering, Tel Aviv University,
Dr. Mirit Sharabi – Department of Mechanical engineering and mechatronics, Ariel University
Dr. Ashraf Hamdan – Dept. Cardiology, Rabin Medical Center, Faculty of Medicine, Tel Aviv University

Aortic valve (AV) disease is the third most prevalent cardiovascular disorder in the US, and calcific aortic stenosis (AS) is the most common form of valve disease in the western world with a prevalence that affects 2% of the population over 65 years. Most AS cardiovascular research has been gender-blind, ignoring sex-related biological variables. This trend has led to the under-appreciation of sex-differences in cardiovascular disease (CVD) from an etiological, prognostic, diagnostic, and therapeutic perspective.
Among clinical sex differences of CVD, females present pronounced fibrosis and denser connective tissue compared to males who exhibit more calcification for the same AS severity. Therefore, the kinematic of the leaflets is impaired in the female population mainly by fibrocalcific pathological processes: thickening and stiffening, along with relatively smaller calcification volume. In contrast, for males, the leaflets' motion is impaired mainly by calcification deposits.
In this study, we present a computational biomechanical modeling approach that accounts for the fibrocalcific effect on the AS by a parametric study of the total collagen fiber volume and its architecture on the aortic valve area (AVA).  Towards that goal, patient-specific models were generated for three females with stenotic AVs with different volumes of calcium.  The calcium geometries were reconstructed from patient-specific CT scans and represented by embedding volumes in a parametric model of the AV. The patient-specific peak pressure gradient was based on measured Echocardiography (Echo) data.
Two of the female-AVs were selected to perform a parametric fibrocalcific computational study whereby the architecture of the collagen fibers and its variable volumes were examined.  The third female AV-AS case was predominately due to a higher volume of calcification.    The numerical models were validated in their ability to predict the AVA against clinical data obtained from Echo. Computed AVA results compared well with measured AVA data, for the cases of low calcified volume yet higher volume of fibers. The AVA was reduced with increased fiber volumes, as expected. However, the AVA reduction was differently affected by the spatial location of the fiber systems on the leaflets.  The computational results show that, under the same imposed transvalvular pressure, increased fibers with a low calcium volume could actively contribute to AS and reduce the AVA.  The latter fibrocalcific-related AS is shown to be similar to the well-known calcific-only related AS. The proposed computer models confirm that tissue thickening with increased collagen fibers has a crucial role in the fibrocalcific-AS process in female patients.  These models could be used for future diagnostics and the design of valve replacement therapy and treatment.
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