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

Vance G Nielsen, David T. Hafner, Evangelina B. Steinbrenner

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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. Smoking patients (n=20, two cigarettes consumed within 90âŠmin, average carboxyhemoglobin concentration of 5%) had plasma collected and normal individual (n=20) plasma was also obtained. Thrombelastographic analyses conducted with addition of tissue-type plasminogen activator revealed that with the exception of the rate of thrombus generation, there was little difference in fibrinolytic kinetics between normal and smoking individuals. Addition of exogenous carbon monoxide resulted in diminished fibrinolytic response to the same extent in both groups. Subanalyses demonstrated that the smoking cohort had both hyperfibrinolytic and hypofibrinolytic patients as defined by confidence interval (5-95%) values generated from normal individuals. Addition of carbon monoxide reduced hyperfibrinolytic parameter values by 80% in smokers, whereas only a 17% decrease in hypofibrinolytic values changed. Our investigation suggests that 'smoker's paradox' involves a marked change in the character of the plasmin-antiplasmin-carbon monoxide interaction. Further investigation will be required to further define the molecular mechanism responsible for the 'smoker's paradox'.

Original languageEnglish (US)
Pages (from-to)381-385
Number of pages5
JournalBlood Coagulation and Fibrinolysis
Volume24
Issue number4
DOIs
StatePublished - Jun 2013

Fingerprint

Antifibrinolytic Agents
Fibrinolysin
Carbon Monoxide
Tobacco
Smoking
Carboxyhemoglobin
Tissue Plasminogen Activator
Tobacco Products
Stents
Reference Values
Thrombosis
Myocardial Infarction
Confidence Intervals
Mortality

Keywords

  • carbon monoxide
  • fibrinolysis
  • smoking
  • thrombelastography

ASJC Scopus subject areas

  • Hematology

Cite this

Can divergent plasmin-antiplasmin-carbon monoxide interactions in young, healthy tobacco smokers explain the 'smoker's paradox'? / Nielsen, Vance G; Hafner, David T.; Steinbrenner, Evangelina B.

In: Blood Coagulation and Fibrinolysis, Vol. 24, No. 4, 06.2013, p. 381-385.

Research output: Contribution to journalArticle

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