Smoking and cardiovascular function

Compared to non-smokers, chronic smokers are at increased risk of developing atherosclerotic vascular disease, myocardial infarction, unstable angina and sudden death. The acute systemic hemodynamic response to smoking includes an increase in the heart rate, arterial pressure, cardiac output and myocardial contractility. These acute effects are primarily mediated by activation of the sympathetic nervous system. In patients with heart disease, smoking may cause a deterioration in cardiac performance. In the coronary circulation, smoking induces coronary vasoconstriction which can be prevented by alpha-adrenergic blockade, nitrates and calcium channel blockers. Non-selective beta-adrenergic blockade potentiates both the systemic and coronary vasoconstrictor effect of smoking. Other adverse effects of smoking on the cardiovascular system include a reduction in high-density lipoprotein (HDL) cholesterol, an increase in platelet reactivity and an increase in fibrinogen concentrations. These effects on systemic and coronary hemodynamics, lipid metabolism and hemostasis may contribute to the long-term adverse consequences of smoking.