Aortic Pulse Wave Velocity: An Independent Marker of Cardiovascular Risk

Michel E. Safar, MD, Olivier Henry, MD, Sylvie Meaume, MD

Disclosures

Am J Geriatr Cardiol. 2002;11(5) 

In This Article

Basic Hemodynamic Concepts

In the absence of widely used noninvasive aortic blood pressure measurements,[3] PWV may be an available method to evaluate the status of central arteries. During systole, the contraction of left ventricular myocardium and the ejection of blood into the ascending aorta acutely dilate the aortic wall and generate a pulse wave that propagates along the arterial tree at a finite speed. This propagation velocity constitutes an index of arterial distensibility and stiffness: the higher the velocity, the higher the rigidity of the vascular wall and the lower the distensibility.[3]

The pressure pulse generated by ventricular ejection is propagated throughout the arterial tree at a speed that is determined by the elastic and geometric properties of the arterial wall and the characteristics (density) of the contained fluid (blood). Since blood is an incompressible fluid and is contained in elastic conduits (arteries), the energy propagation occurs predominantly along the walls of the arteries and not through the incompressible blood. Thus, the properties of the arterial wall, its thickness, and the arterial lumen diameter are the major factors influencing PWV. The relationships between PWV, transmural pressure, wall tension and distensibility have been formalized in many mathematic models. In most of them, the arterial segment studied is considered as a tube either with a thin or a thick vascular wall. Inside this cylindrical tube, there is a positive relationship between the change in pressure and the change in volume (V). The latter is usually expressed per unit length and then evaluated in terms of changes in diameter or radius, considering the length of the tube as constant. In such conditions, PWV may be defined according to the Moens-Korteweg and the Bramwell and Hill equations.[3]

In the Moens-Korteweg equation, it is assumed that: PWV2=E.h/2r.rho, where h is the arterial wall thickness, rho is the internal arterial radius, r is the constant blood density, and E is the elastic modulus of the vessel wall, which is the slope of the stress-strain relationship. For a thin arterial wall, h/r may be considered as constant and PWV is a direct function of the arterial elastic modulus E.

This approximation is given by the Bramwell and Hill formula: PWV2= P.V/ V.rho, in which V/ P represents the slope of the pressure-volume relationship, V the baseline volume in steady state conditions and P.V/ V is the inverse of arterial distensibility. From these equations, it is clear that PWV and E are highly dependent on wall tension, and hence blood pressure level. Any epidemiologic study on the subject should adjust the results to blood pressure level, namely mean arterial pressure, which remains the same in the overall arterial tree.[3]

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