Cigarette smoking and nicotine likely induce cardiac arrhythmia through complex pathophysiological mechanisms including pro-fibrotic effects on myocardial tissue, carbon monoxide, and oxidative stress.
What are the pathophysiological mechanisms by which cigarette smoking induces cardiac arrhythmia?
This review summarizes the pathophysiological mechanisms, including nicotine's pro-fibrotic effects and oxidative stress, by which cigarette smoking may induce cardiac arrhythmias.
Tobacco smoke is the single most important modifiable risk factor for coronary diseases and the leading preventable cause of death in the US. While the effect of cigarette smoking on the progression of atherosclerotic diseases is established and well studied, the role of cigarette smoking on cardiac arrhythmia is less clearly defined. In fact the pathophysiological mechanism of cigarette smoking-induced cardiac arrhythmia is very likely a complex one where the pro-fibrotic effect of nicotine on myocardial tissue with consequent increased susceptibility to catecholamine might play a role. Moreover, other constituents of cigarette smoking, such as carbon monoxide and oxidative stress, are likely to contribute to the generation of arrhythmias. Finally, cigarette smoking may induce coronary artery disease and chronic obstructive pulmonary disease, which also might cause arrhythmia independently. The objective of this paper is to summarize the published studies relating to cardiac arrhythmia induced by cigarette smoking, and to identify a pathophysiological mechanism by which cigarette smoking might induce cardiac arrhythmia.
D’Alessandro et al. (Wed,) conducted a review in Cardiac arrhythmia. Cigarette smoking was evaluated. Cigarette smoking and nicotine likely induce cardiac arrhythmia through complex pathophysiological mechanisms including pro-fibrotic effects on myocardial tissue, carbon monoxide, and oxidative stress.