A comparison of flow-mediated dilatation and von Willebrand factor as markers of endothelial cell function in health and in hypertension: relationship to cardiovascular risk and effects of treatment: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial.
Loss of adequate endothelial cell function (associated with various cardiovascular syndromes such as hypertension) is most widely quantified by assessing flow-mediated dilatation (FMD) or measuring plasma markers such as von Willebrand factor (vWF). However, the relationship between these two methods is unclear, as is their relationship to 10-year cardiovascular risk (defined by the Framingham equation) and their response to intensive cardiovascular risk factor management. We tested the hypothesis that there is an inverse relationship between vWF and FMD by measuring both in 132 subjects, of whom 89 were hypertensive (mean blood pressure, 167/91 mmHg) and 43 were healthy normotensive (mean blood pressure, 133/80 mmHg). High-resolution ultrasound assessed endothelium-dependent brachial artery FMD following reactive hyperaemia after occlusion. Plasma vWF was defined by enzyme-linked immunosorbent assay. These measurements were repeated in the patients after 6 months of intensive cardiovascular risk factor management. vWF and FMD correlated significantly (r = -0.517, P < 0.001), and both correlated with 10-year cardiovascular risk using the Framingham equation (vWF, r = 0.48, P < 0.001; FMD, r = -0.624, P < 0.001). Following 6 months intensive cardiovascular risk factor management, plasma vWF was significantly reduced whereas FMD significantly increased (both P < 0.002). We conclude that two fundamentally different methods for assessing endothelial function correlate well with each other, as well as with 10-year cardiovascular risk. Six months of intensive risk factor management is beneficial to the endothelium, as defined by improved vWF and FMD. These methods might therefore be useful indices to identify patients at risk of future cardiovascular events, and may also assist in the understanding of early developments in the pathogenesis of vascular risk in hypertension.
Felmeden
D C
DC
University Department of Medicine, City Hospital, Birmingham, UK.
Blann
A D
AD
Spencer
C G C
CG
Beevers
D G
DG
Lip
G Y H
GY
D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001262:Atenolol / Q000627:therapeutic use; D001916:Brachial Artery / Q000000981:diagnostic imaging; D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology* / Q000503:physiopathology / Q000517:prevention & control; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D018056:Hemorheology; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000188:drug therapy; D006940:Hyperemia / Q000000981:diagnostic imaging / Q000503:physiopathology; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D012306:Risk; D012308:Risk Management; D016896:Treatment Outcome; D014463:Ultrasonography; D014841:von Willebrand Factor / Q000032:analysis*
D000924:Anticholesteremic Agents; D000959:Antihypertensive Agents; D014841:von Willebrand Factor; D017311:Amlodipine; D001262:Atenolol