Cigarette smoking (CS) is a major health hazard particularly for the cardiovascular system and cancer. The mechanisms involved in CS-related cardiovascular dysfunction have been largely debated. CS increases inflammation, thrombosis, and oxidation of low-density lipoproteins. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction. Cardiac myocytes, as well as and other long-lived postmitotic cells show dramatic smoke-related alterations that mainly affect the mitochondria and lysosomal compartment. Mitochondria are primary sites of reactive oxygen species formation that cause progressive damage to mitochondrial DNA and proteins in parallel to intralysosomal lipofuscin accumulation. There is amassing evidence that various mechanisms may contribute to accumulation of damaged mitochondria following initial oxidative injury. Such mechanisms may include clonal expansion of defective mitochondria, decreased propensity of altered mitochondria to become autophagocytosed, suppressed autophagy because of heavy lipofuscin loading of lysosomes and decreased efficiency of specific proteases involved into mitochondrial degradation. A possible interplay between microtubule plasticity and oxidative stress also exists in cardiomyocytes, so this could represent another potential mechanism by which smoking induces/accelerates atherosclerosis.
The definition of smoking as the inhalation of the smoke of burned tobacco that may occur occasionally or habitually as a consequence of a physical addiction to some chemicals, primarily nicotine, cannot be fully accepted today since several clinical, biological, metabolic, epidemiologic, statistic and socio-economic factors which play a basic role in determining individual damage due to smoking are missing in this assessment. The analysis of findings shows undoubtedly that several constituents of cigarette smoking play a strong role in the development and progression of cardiovascular damage, primarily atherosclerotic lesions. Nicotine and its metabolites, carbon monoxide and thiocyanate seem to be the most specific markers of damage that, in the time, becomes irreversible. Cigarette smoking is addictive because of nicotine and nicotine withdrawal causes many side effects of quitting smoking as well as nicotine itself usually increases cardiovascular risk. Therefore, what is smoking? Smoking must be defined as a chemical toxicosis which is able to cause detrimental effects either of acute or chronic type on different structures of the body being some of these like cardiovascular system, respiratory system and epithelial glands target organs. Smoking also causes physical addiction, primarily due to nicotine, that adversely influences smoking cessation. From these observations there is evidence that a large number of socio-economic and epidemiologic implications arise in smokers and that requires the necessity of specific structures which may help to face up the problem.
Epidemiological surveys demonstrate undoubtedly that cardiovascular disorders caused or associated with hypertension are at a high risk of non-fatal or fatal events and occurring with a great rate. Ischaemic heart disease with effort angina and myocardial infarction, often unrecognized myocardial infarction, stroke and transient ischaemic attack may be observed more frequently than other cardiovascular disorders in hypertensive patients. Large-scale trials do not support the hypothesis that effective benefits are reached by current non-pharmacological or pharmacological prevention which need enormous costs to public health. Lowering blood pressure is the main target to reach in an attempt to reduce cardiovascular complications in hypertensive patients. Therefore, the costs-benefit ratio, which estimates public health costs, needs yet marked improvement since the public health expenses are heaviest with results that do not support the economic effort. Statistically, quantitative measures to modify the current regimen need to better evaluate both public health costs and reached benefits.
Macroeconomic variables primarily related to the health care system are the result of two key factors. On the one hand, the results obtained for preserving the health of individuals improving, also, the quality of life and, on the other hand, the costs to be supported in order to reach these results. There is evidence that a balance between these two parameters must be obtained in an era of limited economic resources and, therefore, measures, which can achieve these variables, are under study. Cost-effectiveness ratio is the most economic factor analyzed still lending to define the relationship between costs and disease. With regard to cardiovascular risk, budgets not always in line with established expectations are under exam. Quantitative measures related to cost-effectiveness ratio as the estimate-score system, which sets specific scores for the symptoms of the disease, are studied to improve the budget that regulates costs and results on public health including cardiovascular risk characterized by a high frequency of adverse events.
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