Cigarette smoking and hyperfibrinogenaemia are both significant risk factor
s for the development of cardiovascular disease. Two studies are described
here which aimed to establish the metabolic mechanism responsible for the r
aised plasma fibrinogen concentration observed in smokers. Chronic smokers
had a significantly elevated absolute rate of fibrinogen synthesis (ASR) co
mpared with non-smokers (22.7 +/- 1.3 mg/kg per day versus 16.0 +/- 1.3 mg/
kg per day; means +/- S.E.M., P < 0.01), with plasma levels of fibrinogen s
ignificantly correlated with fibrinogen synthesis (r = 0.65, P = 0.04). Unl
ike fibrinogen, plasma albumin concentrations were lower in smokers than in
non-smokers (45 <plus/minus> 0.4 versus 47 +/- 0.7 g/l, P < 0.05), but the
re was no difference in rates of albumin synthesis between the two groups.
Two weeks cessation from smoking by previously chronic smokers was associat
ed with a rapid and marked fall in plasma fibrinogen concentration (from 3.
06 <plus/minus> 0.11 g/l to 2.49 +/- 14 g/l, P < 0.001), and a significant
reduction in ASR (a 33% reduction, from 24.1 <plus/minus> 1.7 to 16.1 +/- 1
.0 mg/kg per day, P < 0.001). These studies suggest a primary role for incr
eased synthesis in producing the hyperfibrinogenaemia associated with smoki
ng. Moreover, abstention from smoking for a period of only 2 weeks induces
a significant decrease in the rate of fibrinogen synthesis by the liver, wi
th a concomitant reduction in the plasma fibrinogen concentration.