Aj. Simpson et al., THE EFFECTS OF CHRONIC SMOKING ON THE FIBRINOLYTIC POTENTIAL OF PLASMA AND PLATELETS, British Journal of Haematology, 97(1), 1997, pp. 208-213
We studied tissue-type plasminogen activator (t-PA) and plasminogen ac
tivator inhibitor typ 1 (PAI-1) in healthy individuals divided by smok
ing habit into current smokers, former smokers and non-smokers (who ha
d never smoked). Plasma PAI-1 antigen was significantly higher in smok
ers than in non-smelters with intermediate levels in former smokers. A
similar trend was observed for plasma PAI activity but this did not r
each statistical significance. Platelet PAI-1 and plasma t-PA were not
significantly different when comparing the three groups. After venous
occlusion t-PA rose significantly in all groups; no significant chang
e in plasma PAI-1 was observed. The ratio of t-PA to PAI-1 in plasma w
as similar in non-smokers and former smokers but lower in smelters, su
ggesting that there is at least partial restoration of plasma fibrinol
ytic potential after smoking cessation. Plasma PAI-1 antigen and PAI a
ctivity correlated with estimated pack-years of cigarettes smoked amon
g smokers and former smokers. When all subjects were studied collectiv
ely plasma PAI-1 correlated strongly with plasma t-PA and triglyceride
s; plasma t-PA also correlated strongly with triglycerdes. We conclude
that chronic smoking is associated with impaired fibrinolysis in plas
ma and that this largely reflects elevated plasma PAI-1 in smelters. S
moking does not appear to affect the response to venous occlusion. The
postulated effect of chronic smoking on plasma PAI-1 may be mediated
by the influence of smoking on triglycerides and insulin resistance. S
topping smoking appears to return impaired fibrinolysis towards normal
. Smoking does not quantitatively affect the platelet pool of PAI-I. S
moking habit should be controlled for in clinical analyses of PAI-1 an
d t-PA.