Can divergent plasmin-antiplasmin-carbon monoxide interactions in young, healthy tobacco smokers explain the 'smoker's paradox'?

In the setting of acute myocardial infarction, decreases in early/late mortality, reocclusion after thrombolysis, and restenosis rate after percutaneous intervention are lower in smokers - this phenomenon has been designated as the 'smoker's paradox'. These benefits of smoking, however, are abrogated by stent placement. We hypothesized that fibrinolytic vulnerability would change in response to smoking, and that inhaled carbon monoxide may play a role.

Tobacco smoke-induced hypercoagulation in human plasma: role of carbon monoxide.

Virtually every disease state associated with chronic or acute thrombosis has had smoking identified as a risk factor. Further, smoking enhances clot strength as assessed by thrombelastography. Critically, carbon monoxide, a product of cigarette smoking, has been demonstrated to enhance plasmatic coagulation in vitro via modulation of a heme associated with fibrinogen.

Freezing does not decrease carbon monoxide-mediated hypercoagulation and hypofibrinolysis in human plasma.

Carbon monoxide (CO) has been demonstrated to enhance coagulation and attenuate fibrinolysis in vitro and in vivo. Hemostasis is affected by CO interactions with key heme-modulated molecules. We wished to determine whether freezing would affect CO-mediated changes in coagulation/fibrinolysis in plasma in anticipation of collecting samples both within our institution and from collaborating centers.