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• Authors' Reply: Smoking and inflammation
  Dimitris Tousoulis
  Published on: 23 November 2015
• Smoking and thrombotic mechanisms
  Graham F. Cope
  Published on: 23 November 2015

• Published on: 23 November 2015

  Authors' Reply: Smoking and inflammation

  • Dimitris Tousoulis, Associate Professor
  • Other Contributors:
    • Charalambos Antoniades and Christodoulos Stefanadis

  Dear Editor

  In a response letter Cope et al. stated that smoking or the amount of tobacco consumed did not influence the biochemical risk factors for coronary artery disease such as cholesterol and HDL, but increased many of the cellular factors which we have reported in the recent review article as contributors to the inflammatory response and to the formation and instability of the atheromatous plaque.[1]...

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  Dear Editor

  In a response letter Cope et al. stated that smoking or the amount of tobacco consumed did not influence the biochemical risk factors for coronary artery disease such as cholesterol and HDL, but increased many of the cellular factors which we have reported in the recent review article as contributors to the inflammatory response and to the formation and instability of the atheromatous plaque.[1] We agree with Dr Cope regarding the possible relationship of smoking with inflammatory process associated with the development of coronary atherosclerosis and acute coronary thrombosis. However, the underlining mechanisms remain obscure.

  Therefore, we have examined whether chronic smoking is associated with increased thrombosis and inflammatory process. We also investigated the role of oxidative stress and the impact of antioxidant vitamins in chronic smokers. We found that smoking is related with abnormalities in thombosis/fibrinolysis system, such as increased levels of von Willebrand factor (vWF), plasminogen activator inhibitor 1 (PAI-1) and increased PAI- 1/tPA ratio. These changes are partly reversible by high-dose antioxidant treatment with vitamins C (2g/day) plus E (800IU/day) for a short period of 4 weeks administration.[2] Furthermore, we have also shown that this combination of antioxidants also decrease the expression of several inflammatory markers such as interleukins 1b and 6, vascular cell adhesion molecule and intercellular adhesion molecule.[3] This beneficial effect of antioxidants reflects the possible role of oxidative stress as a connective link between smoking, inflammatory process and thrombosis/fibrinolysis system. It is widely believed, that oxygen free radicals produced as a result of smoking, lead to both, oxidative inactivation of endothelium-derived nitric oxide and direct oxidative damage of endothelial cells. This phenomenon may increase the release of endothelium-derived components of thrombosis/fibrinolysis system and trigger a generalized vascular inflammatory process, associated with increased risk for atherothrombosis. The findings of Cope et al. and our observations indicate that smoking may indirectly lead to increased risk for coronary atherosclerosis and acute coronary syndromes, by affecting the inflammatory process and thrombosis/fibrinolysis system.

  References

  (1) Tousoulis D, Davies GJ, Stefanadis C, Toutouzas P, Ambrose JA. Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart 2003;89:993-997.

  (2) Antoniades C, Tousoulis D, Tentolouris C, et al. Effects of Antioxidant Vitamins C and E on Endothelial Function and Thrombosis/Fibrinolysis System in Smokers. Thromb/Haemost 2003;85:190-6

  (3) Tousoulis D, Antoniades C, Tentolouris C, et al. Antioxidant Vitamins C and E Administration in Smokers: Effects on Endothelial Function and Adhesion Molecules. Atherosclerosis 2003; in press.

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  Conflict of Interest:
  None declared.

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• Published on: 23 November 2015

  Smoking and thrombotic mechanisms

  • Graham F. Cope, Honorary Senior Research Fellow
  • Other Contributors:
    • Nick Battersby, Medical Student

  Dear Editor

  We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular mechanisms involved in the inflammatory mechanisms and haemostatic factors leading to coronary atherosclerosis. They also describe the role of chronic infection in this process.[1] However, they omit an important factor that is common to the majority of patients su...

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  Dear Editor

  We read the review paper by Tousoulis et al. with great interest. We applaud their thoroughness in describing the molecular and cellular mechanisms involved in the inflammatory mechanisms and haemostatic factors leading to coronary atherosclerosis. They also describe the role of chronic infection in this process.[1] However, they omit an important factor that is common to the majority of patients suffering from this condition – current or previous cigarette smoking.

  We have undertaken an investigation into the relationship between smoking habit, notably quantitative measurement of nicotine intake and factors involved in the formation of the plaque and the inflammatory process. Due to ‘social desirability bias’ associated with smoking patients frequently under-report or deny their smoking habit. It would seem therefore that the greater the clinical impact of smoking the greater the patient guilt enhancing the likelihood of denial.

  To improve the accuracy of information about smoking a 6-minute point -of-care test to detect nicotine metabolites (including cotinine), called SmokeScreen® was developed.[2] The easy to use colorimetric urine test can provide qualitative, semi-quantitative and quantitative measurements of nicotine intake. With this test we undertook an audit of smoking habits of 154 new patients attending a large inner-city hospital cardiology outpatient clinic, comparing the test identification of smoking with self- completed questionnaire of current smoking habit. The results identified 112 (72.7%) as non-smokers, 30 (19.5%) as confessed smokers and 12 (7.8%) as ‘smoking deceivers’. We followed this with another study of the same population (n=85, 33 smokers and 52 never-smokers) to examine the interaction of smoking with risk factors associated coronary artery disease, as assessed by a biochemical screen and a blood count. Interestingly, none of the parameters measured in the biochemical screen, such as cholesterol, HDL and triglycerides; urea and electrolytes and liver function tests were associated with smoking habit or quantitative assessment of nicotine intake. Whereas white blood cell count (WBC) was significantly higher in smokers (p=0.002), in particular neutrophils (p=0.01) and eosinophils (p=0.02). Lymphocytes, monocytes and basophiles were higher but failed to reach significance. Quantitative assessment of nicotine intake of the smokers further revealed a positive correlation with WBC (p<_0.0001 neutrophils="neutrophils" p0.001="p0.001" eosinophils="eosinophils" p0.004="p0.004" and="and" lymphocytes="lymphocytes" p0.02="p0.02" with="with" monocytes="monocytes" approaching="approaching" significance="significance" p="p"/> It would seem from this pilot study that smoking or the amount of tobacco consumed doesn’t influence the biochemical risk factors for coronary artery disease, such as cholesterol and HDL, but does increase many of the cellular factors which Tousoulis et al. identified as contributors to the inflammatory response and to the formation and instability of the atheromatous plaque.[1] We suggest that identification of smokers, feedback from the point-of-care test and subsequent advice on smoking cessation could have a significant impact on reducing many of the risk factors associated with coronary atherosclerosis and lower cardiovascular events and mortality.

  References

  (1) Tousoulis D, Davies G, Stefanadis, Toutouzas P, Ambrose JA. Inflammatory and thrombotic mechanisms in coronary atherosclerosis. Heart 2003;89:993-997.

  (2) Cope GF, Nayyar P, Holder R, Gibbons J, Bunce R. A simple near-patient test for nicotine and its metabolites in urine to assess smoking habit. Clin Chim Acta 1996;256:135-149.

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  Conflict of Interest:
  None declared.

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