Cigarette smoking is a well-established risk factor in the pathogenesis and progression of IHD, as well as myocardial infarction. 3-13 Smoking increases death from coronary artery disease by 70 percent.3
Furthermore, the excess risk of morbidity and mortality diminishes with cessation of smoking.4-6
Predictably, the benefits of cessation of smoking accrue even in advanced coronary artery disease following percutaneous coronary revascularization.6
Smoking causes norepinephrine and epinephrine release and results in other adrenergically mediated adverse hemodynamic and metabolic events.12
Even passive smoking impairs endothelium-dependent dilatation in healthy young adults.8
Cigarette smoke is a pro-oxidant in pregnant women regardless of antioxidant nutrient intake.9
In human subjects, cigarette smoking raises the pre-smoke nitric oxide-peroxynitrite ratio of 1:0.5 to a post-smoke ration as high 1:9.7
Rat alveolar macrophages challenged by cigarette smoke release nitric oxide and superoxides, which interact with each other to produce peroxynitrite.
Following two to three puffs of smoke, activated phagocytes continue to release nitric oxide and peroxynitrite for up to 30 minutes277 (Deliconstantinos 1994.)
Ethane and pentane are volatile alkanes produced from peroxidation of omega-3 fatty acids, and the breath levels of those compounds are used as indicators of oxidant stress. The breath ethane levels are higher in smokers than in nonsmokers.7 The intake of antioxidants such as vitamin C and E in RDA amounts does not reduce breath ethane levels.
How can the recognized role of tobacco smoking in the pathogenesis of CAD be explained by the hypothesis of AA oxidopathy? Smoking has well-established procoagulant and coronary vasoconstrictive effects.11-13
As discussed earlier, factors directly fan the oxidative coagulative fires within the circulating blood. Cigarette smoke generates an enormous number of free radicals and markedly increases plasma oxidizability.
As indicated earlier, both active and passive smoking impair endothelium-dependent arterial dilatation in healthy adults.8 There is a dose-related inverse relationship between the intensity of passive tobacco smoking and flow-mediated dilatation, indicating direct early arterial damage. Penn et at. reported a dose-dependent size increases of aortic lesions following exposure to 1,2 dimethylbenzene.7
We anticipated and verified by direct microscopic observations, the ability of tobacco smoke to inflict direct plasma and cell membrane injury.
To this purpose, we examined the immediate effects of free radical cascades generated by cigarette smoking on circulating blood in a volunteer who abstained from smoking for a period of 16 hours and then smoked three cigarettes in five minutes.
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