Biomechanical factors in the biology of aortic wall and aortic valve diseases

Abstract

The biomechanical factors that result from the haemodynamic load on the cardiovascular system are a common denominator of several vascular pathologies. Thickening and calcification of the aortic valve will lead to reduced opening and the development of left ventricular outflow obstruction, referred to as aortic valve stenosis. The most common pathology of the aorta is the formation of an aneurysm, morphologically defined as a progressive dilatation of a vessel segment by more than 50% of its normal diameter. The aortic valve is exposed to both haemodynamic forces and structural leaflet deformation as it opens and closes with each heartbeat to assure unidirectional flow from the left ventricle to the aorta. The arterial pressure is translated into tension-dominated mechanical wall stress in the aorta. In addition, stress and strain are related through the aortic stiffness. Furthermore, blood flow over the valvular and vascular endothelial layer induces wall shear stress. Several pathophysiological processes of aortic valve stenosis and aortic aneurysms, such as macromolecule transport, gene expression alterations, cell death pathways, calcification, inflammation, and neoangiogenesis directly depend on biomechanical factors.

Keywords: Abdominal aortic aneurysm; Aortic stenosis; Inflammation; Thoracic aortic aneurysm.

Figure 1.

Basic continuum mechanical definitions. (A) Stress is defined as force per area and can be split into shear and normal stresses, respectively. (B) Definition of strain by relating the deformed to the undeformed configuration. (C) Stress and strains always correspond to a length scale. Left and right images show stress at the macroscopic and microscopic length scale, respectively. The specific length scales are indicated by the scaling bars.

Figure 2.

Haemodynamic differences between a normal (left ) and a stenotic (right ) aortic valve. (A) and (B) shows the velocity and (C) and (D) the vorticity of blood flow based on an axisymmetric CFD simulation. Note the perturbed flow pattern and the jet-like flow in the stenotic valve. (Illustration by J. Biasetti)

Figure 3.

Wall shear stress (dotted arrows) and strain (solid arrows) in the aortic valve during systole (A) and diastole (B and C). During systole, the ventricular side of the valve is subjected to laminar shear stress, whereas on the aortic side the systolic shear stress is mainly oscillatory (A). The bending strain is illustrated with a curved arrow (A). In diastole, axial strain results from the diastolic pressure gradient and tensile strain from the elongation of the valve leaflets (B). At this time, the aortic side is subjected to oscillatory shear as the blood pools into the aortic sinuses, and to laminar shear by the diastolic coronary flow (C). (A) and (B) adapted from ref.

Figure 4.

(A) Circumferential and longitudinal stresses are the dominating principal stresses in the aortic wall. (B) Wall shear stress (WSS) as a consequence of blood flow over the endothelial layer.

Figure 5.

Patterns of calcification of human aortic valve cusps, along the coaptation area (A) and radially from the valve insertion (B). Adapted from ref.