• Vance G Nielsen, David T Hafner, and Evangelina B Steinbrenner.
• Department of Anesthesiology, University of Arizona College of Medicine, Tucson, AZ 85724-5114, USA. vgnielsen@E-Mail.arizona.edu
• Blood Coagul. Fibrinolysis. 2013 Jun 1;24(4):405-10.

AbstractVirtually 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. We hypothesized that plasmatic hypercoagulability and formation of carboxyhemefibrinogen (COHF) detected with thrombelastographic methods would be observed after cigarette smoking. Smoking participants (n = 20, two cigarettes consumed within 90 min, average carboxyhemoglobin concentration of 5%) had plasma collected and normal participant (n = 20) plasma was also obtained. Thrombelastographic analyses revealed that plasma obtained from smokers had an 86% greater velocity of clot growth and 65% larger clot strength than normal participant plasma. Forty-five percent of smokers had plasma clot strength that exceeded the 95th percentile of normal participant plasma values; 45% of smoking participants had detectable COHF; and 20% of smoking participants were both hypercoagulable with COHF present. We conclude that smoking induced a hypercoagulable state and COHF formation in an important portion of participants tested. Future investigations of the effects of smoking, plasmatic hypercoagulation and COHF formation are planned in populations with established atherosclerotic/thrombotic disease.

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