Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Abstract

The understanding of the pathophysiology of atherosclerosis has advanced greatly in the past decade. Cardiovascular risk factors increase the likelihood of an adverse event by having a detrimental effect on the blood vessel wall. Abnormal interactions among cholesterol, inflammatory mediators, platelets and the vascular wall lead to atherogenesis and cardiac events. In an effort to better understand this process, develop surrogate end points for clinical trials and, ultimately, better risk stratify individuals, a variety of measures of arterial function have been studied. These include measures of endothelial health and arterial compliance. The current paper reviews the various techniques available for the study of vascular health. While not yet routinely used for clinical care, these measurements provide important insights into the pathophysiology and treatment of atherosclerosis.

Figures

Figure 1)

Carotid arterial contour. A reflected wave due to increased arterial stiffness generates a systolic wave (Ppk). The difference between this wave and the initial forward-going systolic wave (Pi) is then divided by the pulse pressure (systolic – diastolic pressure [ΔP]) to generate the augmentation index (AIx). AIx = ΔP/pulse pressure (PP). LVET Left ventricular ejection time; Δtp Time to Pi

Figure 2)

Ultrasound image of the brachial artery. At rest, the diameter is 3.52 mm, and between 60 s and 90 s postocclusion, the hyperemic diameter is 3.80 mm. Flow-mediated dilation = 3.80–3.52/3.52 ×100 = 8.0%

Figure 3)

Determination of endothelial function by peripheral artery tonometry. This finger tip plethysmograph measures pulse volume amplitude (PVA) in the index finger of both hands at rest, during a 5 min arm occlusion and then postocclusion. The PVA index is the relative increase in PVA postocclusion in the active finger compared with the control finger. Values greater than approximately 1.4 are normal

Figure 4)

Use of systolic contour to assess endothelial function. The augmentation index (AIx) is measured from a peripheral artery without a generalized transfer function. Measurements are made at rest, in response to the endothelium-dependent stimulus (inhalation of a beta2-agonist) and in response to nitroglycerin (GTN). A fall in AIx with salbutamol is related to nitric oxide release and a decrease in arterial stiffness. Data from reference