Dr KK Aggarwal
Padma Shri and Dr B C Roy National Awardee
President, Heart Care Foundation of India
1. Smoking is associated with high bad LDL cholesterol, high triglycerides and low good HDL cholesterol levels.
2. It can cause insulin resistance.
3. Free radicals in cigarette smoke damage lipids, resulting in the formation of proatherogenic (clot promoting) oxidized LDL cholesterol.
4. A similar effect is seen with acute secondhand smoke exposure.
5. Smoking activates the sympathetic nervous system, producing an increase in heart rate and blood pressure, and cutaneous and coronary vasoconstriction.
6. Smoking enhances the prothrombotic (clot promoting) state via inhibition of tissue plasminogen activator release from the endothelium, elevation in the blood fibrinogen concentration, increased platelet activity (enhanced sympathetic activity), increased expression of tissue factor and in patients with advanced lung disease, elevated blood viscosity due to secondary polycythemia (high red cells count).
7. Smoking can damage the vessel wall leading to impaired prostacyclin (artery dilator) production and enhanced platelet–vessel wall interactions. The end result is reduvtion in the elastic properties of the aorta, resulting in stiffening of and trauma to the wall.
8. Smoking (including passive), impairs endothelium–dependent vasodilatation of normal coronary arteries and reduces coronary (heart artery) flow reserve.
9. Smoking can also potentiate the endothelial dysfunction induced by high cholesterol.
10. This endothelial dysfunction results from oxidative stress with enhanced oxidation of LDL (bad cholestaerol) and from reduced generation of nitric oxide.
11. Concentrations of soluble adhesion molecules are higher in smokers than nonsmokers. Smokers have elevated levels of C–reactive protein and fibrinogen.
12. Smoking contributes to the inflammatory response, a factor in the pathogenesis of atherosclerosis.
13. Smokers have high serum homocysteine levels, which induce vascular injury.