engleski

Smoking as a risk factor for stroke

Smoking as a risky behavior is spread pandemically, with an increasing tendency in developing countries and decreasing tendency in developed countries. The association between smoking and vascular disease is well known and has been demonstrated by many clinical, epidemiologic and experimental studies. Smoking is atherogenic due to the effect of nicotine. Nicotine is a drug that increases the levels of adrenaline and unsaturated fatty acids stimulating VLDL secretion in the liver. Smoking also increases the synthesis of thromboxane A 2 and increases platelet reactivity. Carbon monoxide (CO) is a poisonous gas that can damage endothelial cells and increase endothelium permeability, thus allowing greater lipid infiltration. Smokers have increased plasma levels of factor VII and fibrinogen, which increase their blood viscosity. Inhalation of smoke can cause hemodynamic changes, e.g., increased heart rate, elevated blood pressure, etc. Smokers are at an increased risk of subarachnoid hemorrhage and ischemic stroke, however, no correlation has been demonstrated for intracerebral hemorrhage. Results obtained by noninvasive ultrasonic examination of cerebral circulation have shown the extra- and intracranial circulation impairments to be more common in so-called 'healthy' smokers free from any manifest signs of cerebrovascular disease, and to generally correlate with the duration of smoking and number of cigarettes smoked. Studies have also shown that stroke occurs at a younger age in smokers than in nonsmokers on an average. Finally, smoking habit needs a complex and very dynamic treatment. Every department for the management of smoking disease should practice programs of quitting smoking as an integral mode of treatment.

smoking; stroke

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