That hasn't been unequivocably established. For example, a 2016 review article "Cardiovascular Toxicity of Nicotine: Implications for Electronic Cigarette Use"

That hasn't been unequivocably established. For example, a 2016 review article "Cardiovascular Toxicity of Nicotine: Implications for Electronic Cigarette Use" published in Trends in Cardiovascular Medicine (http://sci-hub.cc/10.1016/j.tcm.2016.03.001 http://sci-hub.cc/10.1016/j.tcm.2016.03.001) concluded: > Studies of the pharmacology and toxicology of nicotine in animals and some epidemiologic studies in people support the biological plausibility that nicotine contributes to acute cardiovascular events in smokers with underlying CVD, and exerts pharmacologic effects that could contribute to accelerated atherogenesis. Short-term nicotine use, such as nicotine medication to aid smoking cessation, appears to pose little cardiovascular risk, even to patients with known CVD. Longer term nicotine use, such as in ST users, appears not accelerate atherogenesis, but may contribute to acute cardiovascular events in the presence of CVD. "may contribute to acute cardiovascular events in the presence of CVD" is a far cry from being the sole (or even principle) cause of smoking-related cardiovascular disease.