Smoking and coronary changes in patients with documented coronary artery disease

  • J. Majewski
  • K. Moczurad
Conference paper


Cigarette smoking is one of the leading risk factors for coronary heart disease. Population-based studies have demonstrated that smokers have a two- to threefold increase in risk for sudden death from cardiac arrest as compared with non-smokers (Kannel & Thomas, 1982). Unstable angina pectoris is a dramatic clinical manifestation of coronary artery disease associated with the risk for developing myocardial infarct, especially among patients with disease involving many vessels (Freeman et al., 1989). The pathophysiological mechanisms underlying unstable angina pectoris are complex and include progression of atherosclerotic lesions, increased platelet aggregation, coronary thrombus formation and increased vasomotor tone (Brown et al., 1984; Kruskal et al., 1987; Haft et al., 1988), all leading to an imbalance between myocardial oxygen demand and supply.


Cigarette Smoking Coronary Stenosis Serum Lipid Profile Myocardial Oxygen Demand Total Cholesterol Concentration 
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  1. Brown, B.G., Bolson, E.L. & Dodge, H.T. (1984) Dynamic mechanisms in human coronary stenosis. Circulation, 70, 917PubMedCrossRefGoogle Scholar
  2. Cabin, H.S. & Roberts W.C. (1982) Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. Quantitative analysis of 2037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients. Am. J. Med., 73, 227PubMedCrossRefGoogle Scholar
  3. Freeman, M.R., Williams, A.E., Chisholm, R.J. & Armstrong, P.W. (1989) Intracoronary thrombus and complex morphology in unstable angina. Relation to timing of angiography and in-hospital cardiac events. Circulation, 80, 17PubMedCrossRefGoogle Scholar
  4. Guize, J. & Ilion, M.C. (1992) Treatment of risk factors of coronary atherosclerosis. Arch. Mal. Coeur. Vais., 85 (Suppl. 11), 1687Google Scholar
  5. Haft, J.I., Haik, B.J., Goldstein, J.E. & Brodyn N.E. (1988) Development of significant coronary artery lesions in areas of minimal disease. A common mechanism for coronary, disease progression. Chest, 94, 731PubMedCrossRefGoogle Scholar
  6. Kannel, W.B. & Thomas, H.E. (1982) Sudden coronary death. The Framingham Study. Ann. N.Y. Acad. Sci., 382, 3PubMedCrossRefGoogle Scholar
  7. Kannel, W.B., D’Agostino, R.B. & Belanger, A.J. (1987) Fibrinogen, cigarette smoking and the risk of cardiovascular disease: Insights from Framingham Study. Am. Heart J., 113, 1006PubMedCrossRefGoogle Scholar
  8. Kruskal, J.B., Commerford, P.J., Franks, J.J., etal. (1987) Fibrin and fibrinogen related antigens in patients with stable and unstable coronary disease. N. Engl. J. Med., 317, 1361Google Scholar
  9. Migas, O.D. (1988) The lipid effects of smoking. Am. Heart J., 115, 272CrossRefGoogle Scholar
  10. Tiwari, A.K., Gode, J.D. & Dubey, G.P. (1989) Effect of cigarette smoking on serum total cholesterol and HDL in normal subjects and coronary heart disease patients. Indian Heart J., 41, 92PubMedGoogle Scholar

Copyright information

© Springer-Verlag London Limited 2000

Authors and Affiliations

  • J. Majewski
    • 1
  • K. Moczurad
    • 1
  1. 1.Institute of Cardiology, Department of Social CardiologyJagiellonian University, Collegium MedicumKrakówPoland

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