An interaction between homocyst(e)ine and the endothelium in hypertensive p
atients may promote thrombogenesis and atherogenesis, leading to adverse ca
rdiovascular events. We hypothesized that homocyst(e)ine levels are abnorma
l in patients with essential hypertension, and that this may be related to
an adverse effect on the vascular endothelium. Accordingly, we compared pla
sma levels of homocyst(e)ine and von Willebrand factor (marking endothelial
damage) in 83 patients (43 men; mean age 54 +/- standard deviation 15.9 ye
ars) with essential hypertension (> 160 / 90 mm Hg), with levels in 25 heal
thy normotensive controls (13 men; mean age 56 +/- 11.8 years). Baseline le
vels of the markers and other clinical indices were then related to adverse
cardiovascular events at follow-up.
Plasma homocyst(e)ine (P = .0001) and von Willebrand factor (P = .031) leve
ls were significantly higher in hypertensives compared to controls. After a
mean follow-up of 76 patients for 45 months (range, 1 to 66 months), 17 su
bjects experienced an end point of either cardiovascular death (n = 10) or
adverse cardiovascular event (n = 7). Comparing these 17 with the 59 free o
f an end point, the former were older (P = .0002) and had a longer duration
of known hypertension (P = .018). There was a nonsignificant trend toward
higher median plasma homocyst(e)ine levels in the patients sustaining a vas
cular end point (P = .07).
In this pilot study, we suggest that essential hypertension may be associat
ed with increased plasma homocyst(e)ine levels, but that this amino acid is
unrelated to endothelial damage (von Willebrand factor), clinical indices,
or prognosis. (C) 2001 American Journal of Hypertension, Ltd.