Vascular wall function as a risk marker for cardiovascular disease

Abstract

Elevated systolic blood pressure (SBP) and wide pulse pressure (PP) are both important risk markers for cardiovascular disease. They are indicative of a vascular abnormality, most likely located at the endothelial-vascular interface, where the balance between vasodilator and vasoconstriction determines vascular tone, structure and change in blood pressure. This abnormality makes vessel walls vulnerable to degeneration. Reducing blood pressure in patients with endothelial-vascular dysfunction has been found to reduce the rates of cardiovascular events. Preliminary data also suggest that drug therapy has successfully improved endothelial dysfunction. Endothelial release of nitric oxide has little effect on the aorta, but affects the elasticity of thinner-walled branch vessels and arterioles beneficially. Nitric oxide is normally released in response to increased blood flow and this process is often impaired by various disease states. Since blood flow can be measured, endothelial function can be assessed. Arterial compliance can be determined clinically by a technique that combines pulse wave recording and computer analysis of diastolic decay. In certain disease states, compliance seems to be reduced more in smaller vessels, a marker of early stage vascular disease. Screening for arterial elasticity with this tool can identify those patients with early stages of arterial wall disease and prevent further damage. However, further research is needed to determine whether the benefit lies in lowering blood pressure or in the actual effect of the drug in restoring the function of the arterial wall.