Cardiovascular disease

An estimated 92.1 million US adults have at least 1 type of CVD. By 2030, 43.9% of the US adult population is projected to have some form of CVD 1. Smoking cigarettes is a major risk factor in the development and progression of cardiovascular disease (CVD) such as coronary artery disease, stroke, peripheral arterial disease, congestive heart failure and aortic aneurysms and exerts its detrimental effects via the initiation and progression of atherosclerosis 2-6. Cigarette smoke leads to CVD by numerous mechanisms 7,8: vascular dysfunction, thrombosis, inflammation, oxidative stress, modification of lipid profile, artery spasm.

ATHEROSCLEROSIS is a chronic inflammatory disease in which systemic inflammation underlies the accumulation of plaques in the arterial intima. It is characterized by an excessive accumulation of lipids in the arterial wall, which leads to endothelial dysfunction, the first step towards the early onset of fatty streaks and subsequent plaque formation 9. Plaques are composed of macrophages, dedifferentiated smooth muscle cells and foam cells; they also have a lipid-rich core and a thin fibrous cap that may rupture, causing thrombosis of the narrowed vessels 10. If not properly controlled, atherosclerotic plaques can obstruct the arterial lumen, leading to cardiovascular diseases (CVDs), such as coronary heart disease (CHD), heart attack, stroke, or angina. Cigarette smoke (CS) contains constituents that cross the alveolar barrier into the blood stream, elicit systemic effects, and affect the physiology of the blood vessels and the heart, distal from the lungs. These changes favor and accelerate the appearance of atherosclerotic plaques 6,11,12.

HEART FAILURE affects over 15 million people in Europe 13 and over 6 million people in the United States 1, and is characterized by and clinically defined as the inability of the heart to supply adequate blood perfusion to organs and tissues. Although heart failure is a serious complication of atherosclerosis, other stressors such as diabetes, hypertension, and toxic compounds 14-16 (like cigarette smoke) induce cardiomyopathies, eventually causing heart failure. CS could affect cardiac function and could have an impact on the ultrastructure of cardiomyocytes, enhancing the risk of coronary heart failure 17-21.


  1. Benjamin, E. J. et al. Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association. Circulation (2017)
  2. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. Journal of the American College of Cardiology. 43(10):1731-7 (2004)
  3. He, J. et al. Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study. Archives of internal medicine 161, 996-1002 (2001)
  4. Ockene, I. S. et al. Cigarette smoking, cardiovascular disease, and stroke: a statement for healthcare professionals from the American Heart Association. American Heart Association Task Force on Risk Reduction. Circulation 96, 3243-3247 (1997)
  5. Murray, C. J. et al. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet 349, 1269-1276 (1997)
  6. Messner, B. et al. Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arteriosclerosis, thrombosis, and vascular biology 34, 509-515 (2014)
  7. Flouris, A. D. et al. Biological evidence for the acute health effects of secondhand smoke exposure. American journal of physiology. Lung cellular and molecular physiology 298, L3-L12 (2010)
  8. Barnoya, J. et al. Cardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation 111, 2684-2698 (2005)
  9. Libby, P. et al. Vascular endothelium and atherosclerosis. Handbook of experimental pharmacology, 285-306 (2006)
  10. Lo Sasso, G. et al. The Apoe(-/-) mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction. Journal of translational medicine 14, 146 (2016)
  11. Yanbaeva, D. G. et al. Systemic effects of smoking. Chest 131, 1557-1566 (2007)
  12. Favero, G. et al. Endothelium and its alterations in cardiovascular diseases: life style intervention. BioMed research international 2014, 801896 (2014)
  13. Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). European heart journal. 29(19):2388-442 (2008)
  14. Iacovoni A, De Maria R, Gavazzi A. Alcoholic cardiomyopathy. Journal of cardiovascular medicine. 11(12):884-92.(2010)
  15. Dolci A, Dominici R, Cardinale D, Sandri MT, Panteghini M. Biochemical markers for prediction of chemotherapy-induced cardiotoxicity: systematic review of the literature and recommendations for use. American journal of clinical pathology. 130(5):688-95 (2008)
  16. Dobrin JS, Lebeche D. Diabetic cardiomyopathy: signaling defects and therapeutic approaches. Expert review of cardiovascular therapy. 8(3):373-91 (2010)
  17. Akbarzadeh, M. A. et al. Acute effects of smoking on QT dispersion in healthy males. ARYA atherosclerosis 10, 89-93 (2014)
  18. Zhu, B. Q. et al. Exposure to environmental tobacco smoke increases myocardial infarct size in rats. Circulation 89, 1282-1290 (1994)
  19. Haussmann, H.-J. et al. Chapter 33. Animal models for three major cigarette-smoke-induced diseases. in Inhalation Toxicology, Second Edition 851-873 (CRC Press, 2005)
  20. Al-Arifi, M. N. et al. Impact of cigarette smoke exposure on the expression of cardiac hypertrophic genes, cytochrome P450 enzymes, and oxidative stress markers in rats. The Journal of toxicological sciences 37, 1083-1090 (2012)
  21. Hu, N. et al. Cardiac-specific overexpression of metallothionein rescues against cigarette smoking exposure-induced myocardial contractile and mitochondrial damage. PLoS One 8, e57151 (2013)

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