Elastic properties and Windkessel function of the human aorta

Abstract

An understanding of the role of the aortic elastic properties indicates their relevance at several sites of cardiovascular function. Acting as an elastic buffering chamber behind the heart (the Windkessel function), the aorta and some of the proximal large vessels store about 50% of the left ventricular stroke volume during systole. In diastole, the elastic forces of the aortic wall forward this 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow. This systolic-diastolic interplay represents the Windkessel function, which has an influence not only on the peripheral circulation but also on the heart, resulting in a reduction of left ventricular afterload and improvement in coronary blood flow and left ventricular relaxation. The elastic resistance (or stiffness), which the aorta sets against its systolic distention, increases with aging, with an increase in blood pressure, and with pathological changes such as atherosclerosis. This increased stiffness leads to an increase in systolic blood pressure and a decrease in diastolic blood pressure at any given mean pressure, an increase in systolic blood velocity, an increase in left ventricular afterload, and a decrease in subendocardial blood supply during diastole, and must be considered a major pathophysiological factor, for example, in systolic hypertension. The elastic properties of the aortic Windkessel can be assessed in vivo in humans in several ways, most easily by measuring the pulse wave velocity along the aorta. The higher this velocity, the higher the elastic resistance, that is, the stiffness. Other methods depend on assessment of the ratio between pulse pressure and aortic volume changes (delata P/delta V), which can be assessed noninvasively by ultrasonic or tomographic methods. All assessments of vessel stiffness have to take into account the direct effect of current blood pressure, and thus judgements about influences of interventions rely on an unchanged blood pressure. Alternatively, to derive the "intrinsic" stiffness of the aortic wall one has to correct for the effect of the blood pressure present. Recently reports about pharmacologic influences on the elastic properties of the aorta have emerged in the literature.(ABSTRACT TRUNCATED AT 400 WORDS)

Compliance and pulse wave velocity assessed by MRI detect early aortic impairment in young patients with mutation of the smooth muscle myosin heavy chain

“…The aortic compliance describes the ease with which the aorta expands during systole (9), and can be defined as the change in crosssectional surface per unit change in pressure (10). The aortic distensibility is the compliance normalized with respect to the minimal surface (11)(12)(13).…”

Correlations between three-dimensional speckle-tracking echocardiography-derived left atrial functional parameters and aortic stiffness in healthy subjects – Results from the MAGYAR-Healthy Study

“…3DSTE has been found to be feasible for non-invasive quantification of LA volumes and functional properties allowing complex evaluation of LA phasic function during cardiac cycle which includes (2, 9) ( Fig. 3): [1] Reservoir function (LA inflow during LA systole), [2] Conduit function (LA passive emptying during LV relaxation and diastasis, when blood transiting from the pulmonary veins to the LV during early diastole), [3] Active contraction or booster pump function (LA active emptying, when LA works like an active contractile chamber that augments LV filling in late diastole). There are several ways for functional assessment of LA including calculation of volumebased and strain parameters by 3DSTE as demonstrated before (4,7,8,11,13,15,18).…”

“…Correlations between LA function and aortic stiffness 201 201 [3] Radial strain (radially directed deformation, strain in the perpendicular direction), [4] 3D strain (strain in the wall thickening direction, combination of radial, circumferential and longitudinal strains), and [5] Area strain (ratio of endocardial area change during the cardiac cycle, percentage change in area). Global and mean segmental peak and pre-atrial contraction LA strain parameters were calculated in each patient.…”

“…[1] maximum LA volume (V max ) defined as the largest LA volume at end-systole just before mitral valve opening, [2] minimum LA volume (V min ) defined as the smallest LA volume at end-diastole before mitral valve closure, [3] LA volume before atrial contraction (V preA ) defined at the last frame before mitral valve reopening or at the time of P wave on ECG at early diastole. Several LA volume-based parameters characterizing each phasis of LA function were calculated from these volumes as demonstrated in Table I.…”

Vascular and neuroendocrine components in altered blood pressure regulation after surgical repair of coarctation of the aorta

“…The PWV is calculated by dividing the distance separating the two sensors (measured with the help of a ribbon meter) by the time corresponding to the period separating the start of the rising phase of the carotid pulse wave and that of the femoral pulse wave, from a simultaneous recording. 13 This calculation is made with the help of a computer program after simultaneous acquisition of the two signals (Complior, Colson, Garges les Gonesse, France).…”