Abstract
The progression of calcific aortic valve disease (CAVD) is characterized by extracellular matrix (ECM) remodeling, leading to structural abnormalities and improper valve function. The focus of the present study was to relate aortic valve leaflet axial curvature changes as a function of elastin degradation, which has been associated with CAVD. Circumferential rectangular strips (L × W = 10 × 2.5 mm) of normal and elastin-degraded (via enzymatic digestion) porcine AV leaflets were subjected to cyclic flexure (1 Hz). A significant increase in mean curvature (p < 0.05) was found in elastin-degraded leaflet specimens in comparison to un-degraded controls at both the semi-constrained (50% of maximum flexed state during specimen bending and straightening events) and fully-constrained (maximally-flexed) states. This significance did not occur in all three flexed configurations when measurements were performed using either minimum or maximum curvature. Moreover, the mean curvature increase in the elastin-degraded leaflets was most pronounced at the instance of maximum flexure, compared to un-degraded controls. We conclude that the mean axial curvature metric can detect distinct spatial changes in aortic valve ECM arising from the loss in bulk content and/or structure of elastin, particularly when there is a high degree of tissue bending. Therefore, the instance of maximum leaflet flexure during the cardiac cycle could be targeted for mean curvature measurements and serve as a potential biomarker for elastin degradation in early CAVD remodeling.
Highlights
Calcific aortic valve disease (CAVD) is characterized by pathological remodeling of the aortic valve leaflets, fibrotic tissue formation, and calcified mineral deposition [1]
Elastin degradation in aortic heart valves can serve as an initiating event in CAVD [16]
Matrix components such elastin and collagen are altered during early onset of CAVD [4,15]
Summary
Calcific aortic valve disease (CAVD) is characterized by pathological remodeling of the aortic valve leaflets, fibrotic tissue formation, and calcified mineral deposition [1]. Untreated CAVD leads to valve malfunction typically via narrowing or stenosis of the aortic valve, which substantially augments the workload of the left ventricle This leads to heart failure with current estimates of about 17,000 resulting deaths/year in the United States [7]. Elastin permits sufficient bending and re-coil of the aortic valve leaflets during the systolic and early diastolic phases respectively. This ensures that minimal energy losses are expended for the heart to pump blood to the systemic circulation, and that instantaneously after, the leaflets have efficiently transitioned to the coaptation state.
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