Cigarette smoking primarily increases the risk of ischaemic heart disease and acute coronary syndromes through thrombogenetic factors rather than a strong atherogenetic effect.
Does cigarette smoking primarily cause ischaemic heart disease through atherogenic or thrombogenic mechanisms?
The cardiovascular risk of chronic smoking is primarily driven by increased thrombogenicity rather than accelerated atherosclerosis.
Cigarette smoking is known to be a strong risk factor for several cardiovascular diseases such as ischaemic heart disease, stroke, intermittent claudication and aortic aneurysm. Atherosclerosis, often with superimposed thrombosis, has been shown to be the underlying disease process in all of these diseases. This fact has led to the assumption that smoking accelerates the atherosclerotic process and thereby promotes premature cardiovascular disease. However, increased occurrence of smoking-mediated thrombosis might also play a causative role. This review therefore considers clinical and experimental evidence regarding the atherogenicity and thrombogenicity of cigarette smoking in the development and occurrence of cardiovascular disease. On the basis of the currently available literature, it is concluded that evidence for the atherogenetic effect of smoking is scarce, and that the effect on the athrosclerotic process in the coronary arteries is only moderate if present at all. On the other hand, both clinical and experimental data strongly support the notion that thrombogenetic factors are responsible for the increased occurrence of ischaemic heart disease, and particularly acute coronary syndromes, among chronic smokers.
Bøttcher et al. (Fri,) conducted a review in Cardiovascular disease (ischaemic heart disease, acute coronary syndromes). Cigarette smoking vs. Non-smoking was evaluated on Atherogenicity and thrombogenicity in cardiovascular disease. Cigarette smoking primarily increases the risk of ischaemic heart disease and acute coronary syndromes through thrombogenetic factors rather than a strong atherogenetic effect.