Circulation, Vol 86, 1495-1500, Copyright © 1992 by American Heart Association
C Rangemark, G Benthin, EF Granstrom, L Persson, S Winell and A Wennmalm
BACKGROUND. Activated platelets have been implicated in both acute thrombus
formation and atherogenesis. Because smoking is a risk factor for
cardiovascular disease in men and women and male smokers have biochemical
evidence of increased platelet activation, we found it of interest to study
whether smoking augments platelet activity in women as well. METHODS AND
RESULTS. Data on smoking habits and a urinary sample were obtained from 125
healthy female nonsmokers and an equal number of smokers, stratified by age
in five groups from 18 to 59 years old. Urinary samples were analyzed with
gas chromatography/mass spectrometry for the 2,3-dinormetabolites of
thromboxane A2 (Tx-M), reflecting platelet activity, and prostacyclin
(PGI-M), representing platelet/vessel wall interaction. Urinary Tx-M in
smokers was higher than in nonsmokers (p < 0.001), increasing with the
number of cigarettes smoked per day and with age. In nonsmokers, there was
no difference in Tx-M between the age groups. Urinary PGI-M in smokers was
higher than that in nonsmokers (p < 0.001) and decreased with age in
nonsmokers but not in smokers. There was no difference in Tx-M between
previous smokers and lifelong nonsmokers. CONCLUSIONS. The elevated Tx- M
in women who smoke cigarettes indicates an increased platelet activity that
is dependent on smoking intensity. In parallel, PGI-M is augmented,
suggesting that platelet/vessel wall interaction is stimulated. Quitting
smoking is an effective means to restore platelet function. We propose that
the observed increase in platelet activity in women who smoke cigarettes
may be related to subsequent development of cardiovascular disease and that
quitting smoking should be considered a high-priority medical target also
in this sex.
ARTICLES
Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age
Department of Clinical Physiology, Gothenburg University, Sweden.
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