Assessment of the Biophysical Mechanical Properties of the Arterial Wall

Arterial Structure

A normal artery consists of three morphologically distinct layers. The intima consists of a single continuous layer of endothelial cells bounded peripherally by a fenestrated sheet of elastic fibers. The media consists entirely of diagonally oriented smooth muscle cells, surrounded by variable amounts of collagen, elastin, and proteoglycans. The adventitia consists predominantly of fibroblasts intermixed with smooth muscle cells loosely arranged between bundles of collagen and proteoglycans. Each structural component has its own characteristic properties. Smooth muscle is the physiologically active element, and by contracting or developing force, it can alter the diameter of the vessel or the tension in the wall. The other components are essentially passive in their mechanical behavior. Elastin, which can be stretched to up to 300% of its length at rest without rupturing, behaves mechanically more closely to a linear elastic material such as rubber than other connective tissue components do. When elastin fibers are stretched and released, they return promptly to their original state. Elastin fibers are important for maintaining normal pulsatile behavior, but they fracture at very low stresses and are probably much less important in determining the overall strength of the vessel wall. Collagen fibers, on the other hand, are much stiffer, but they are much stronger. The proportion of these components varies from artery to artery. In the thoracic aorta, the elastin forms 60% of total fibrous element, and collagen forms 40%. The collagen proportion increases with increasing distance from the heart, reaching 30% elastin and 70% collagen in the extrathoracic vessels. The collagen-to-elastin ratio increases with age, which is one reason why vascular stiffness increases with age. The human thoracic aorta is supplied by vasa vasorum and grows by increasing the number of lamellar units. The abdominal aorta, in comparison, is avascular because it lacks vasa vasorum and grows by increasing the thickness of each lamellar unit. The avascular thickness and the elevated tension per lamellar unit of the abdominal aorta predispose it to atherosclerosis.

The distensibility of a blood vessel depends on the proportions and interconnections of these materials and on the contractile state of the vascular smooth muscle. Elasticity is a material's ability to return to its original shape and dimensions after deformation, the deformation being proportional to the force applied. This proportionality was first described by Hooke in 1676 and is known as Hooke's law. The point at which Hooke's law ceases to apply is known as the elastic limit, and when a solid has been deformed beyond this point, it cannot regain its original form and acquires a permanent distortion. With larger loads still, the yield point is reached when the deformation continues to increase without further load and usually rapidly leads to breakage. In purely elastic bodies, stress (the force per unit area that produces deformation) produces its characteristic strain (the deformation of a stressed object) instantaneously, and strain vanishes immediately on removal of the stress. Some materials, however, require a finite time to reach the state of deformation appropriate to the stress and a similar time to regain their unstressed shape. Blood vessels typically exhibit such behavior, which is called viscoelasticity.

Definition of Vascular Wall Stiffness

Vascular mechanics have been described by using different elastic moduli and assumptions and for different purposes. Several approaches have been described that use clinically available methods for in vivo characterization of the stiffness of the vessel wall. The ability to measure vascular stiffness has been greatly improved by the recent advances in imaging, such as high-frequency ultrasound and CMR.

The relationship between vascular wall deformation (strain) and the pressure exerted on the inner surface of the vascular wall (stress) is commonly used for the measurement of arterial wall biophysical properties (elastic modulus). A plethora of terminology for the description of different elastic moduli, which can be confusing, has been described. The pressure–strain elastic modulus of the arterial wall ( E _p ) described by Peterson and colleagues is commonly used. This elastic modulus that applies to an open-ended vessel in the absence of reflection is defined as E _p = 2Δ P /(Δ V / V ). This is the inverse of the fractional distensibility Δ V / V of the arterial lumen per unit pulse pressure Δ P .

Arterial compliance, C , which is defined as the change in volume Δ V per unit change in pressure Δ P , has been also used in the literature. It has been argued that this definition is appropriate to measurement of ventricular compliance and not to the compliance of an open-ended arterial segment. For the latter, the inverse of Peterson's modulus was suggested 1/ E _p .

The average arterial compliance of a particular vessel pathway can also be determined by measuring the speed of propagation of the pulse in the vessel pathway. The velocity of such waves depends principally on the distensibility of the vessel wall. In real terms, this pulse is measurable by the disturbances in pressure, flow, or vessel diameter that it causes. The propagation of flow waves has not been studied as extensively as that of pressure waves, partly because, unlike flow, accurate methods of pulsatile pressure measurements have been available for a long time and partly because the distinction between flow wave velocity and blood velocity has not always been clearly recognized. Blood velocity means the speed of an average drop of blood, whereas flow wave velocity means the speed with which motion is transmitted. The wave velocity is usually much faster than that of the blood itself. Although CMR is unable to assess pressure changes, alterations in the flow within (or diameter of) a vessel can be measured accurately.

Measurement of Arterial Wall Stiffness

Arterial stiffness, which describes the resistance of arterial wall to deformation, is difficult to measure because of the complex mechanical behavior of arterial wall. As a result, a bewildering number of choices abound. Although smooth muscle tone is not considered, in vitro human arterial compliance has been measured from pressure–volume curves in postmortem arteries. In vivo estimation of arterial wall compliance is more difficult, however, and has been performed by using indirect and invasive techniques, including pulse wave velocity measurements in animals and in humans, the pressure–radius relationship using the Peterson transformer coil in animals, x-ray contrast angiography in humans, and ultrasonography. The contributions of CMR to the assessment of arterial wall mechanics are discussed in the following paragraphs. Other noninvasive measures are forced to rely on the assessment of accessible and often superficial vessels. Under the assumption that central and peripheral arteries behave in a similar fashion, the properties of these arteries are then used as surrogates for those of central arteries. There is, however, considerable heterogeneity between peripheral and central sites. CMR circumvents this problem by allowing the study of central arteries. Its ability to identify anatomic landmarks suggests that reproducibility between studies should be improved, allowing more effective follow-up.