Nicotine may contribute to accelerated atherogenesis by inducing hyperlipidemia, injuring endothelial cells, and/or promoting thrombosis, although the evidence is not conclusive. Nicotine is likely to contribute to acute ischemic events in people who already have coronary heart disease via adverse effects on systemic hemodynamics, by promoting thrombosis, constricting coronary arteries, and/or facilitating arrhythmogenesis. Pharmacodynamic studies suggest that nicotine inhaled in cigarette smoke may have different cardiovascular effects than that absorbed more slowly, as from nicotine gum or transdermally. The safety of chronic nicotine exposure, such as with medicinal use of nicotine, cannot be predicted and requires empiric evaluation.
Copyright © 1991. Published by Elsevier Inc.