Cleveland Family Study

10.1 Background

The endothelium is an important regulator of conduit and resistance artery diameter, platelet aggregation, monocyte adhesion, thrombolysis and vessel growth. Endothelial dysfunction is associated with coronary risk factors, possibly through oxidative stress mechanisms, and is thought to initiate the atherosclerotic process. Endothelium-dependent vasoreactivity can be assessed as conduit or resistance level vasodilation in the coronary and peripheral circulations using endothelium-mediated stimuli such as acetylcholine and flow shear. Endothelial dysfunction is manifest in conduit vessels as reduced vasodilation or paradoxical vasoconstriction (assessed by quantitative coronary arteriography or high-frequency ultrasound) an in resistance vessels as reduced hyperemia (assessed by Doppler guidewire, coronary sinus flow catheter, or venous plethysmography). Although significant correlations have been demonstrated between flow-mediated brachial artery vasodilation and acetylcholine-induced and flow-mediated coronary vasodilation, variations in endothelial function have been observed with different stimuli, parameters, and vascular sites.