There is growing evidence that several biochemical constituents of cigarette smoking play a significant role in the development and progression of heart and blood vessel damage, especially atherosclerotic lesions. Some biochemical markers of tobacco smoke may be determined in blood and urine samples. They are also the main responsible factors of cardiovascular harm. Nicotine and its major metabolite, cotinine, carbon monoxide, and thiocyanate seem to be specific markers. Ischaemic heart disease, cardiac arrhythmias, and endothelial dysfunction are the most common evidence of both active and passive smoking exposure. Dosage of cotinine in urine is of easier determination than that of other metabolites in assessing exposure to smoking, although carboxyhaemoglobin levels seem to be a qualitative, but not quantitative factor to estimate either the degree of cardiovascular damage or the level of exposure. Cigarette smoking is addictive because of nicotine, and it is nicotine withdrawal that causes many side effects of quitting smoking as well as the nicotine itself may exacerbate cardiac lesions. Also haematologic changes are a consequence of cigarette smoking exposure. Increased white blood cells, platelet aggregation and adhesiveness, fibrinogen level, and changes in serum lipids characterise the response to smoking. Anatomical and ultrastructural alterations of the heart and blood vessels are also described as a consequence of negative effects of biochemical markers of cigarette smoking. These alterations are known as “Smoke cardiomyopathy” in experimental pathology.
Keywords: cigarette smoking, ischaemic heart disease (ihd), aneurysm (aa), peripheral vascular disease (pvd), biochemical injury, nicotine, cotinine, carbon monoxide, thiocyanate (scn)
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