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.