Which effect of cigarette smoking contributes to atherogenesis?

• A. Transient increase in blood pressure
• B. Polycythemia with relative hypoxemia
• C. Increased blood viscosity
• D. Chronic inflammation

Answer: (D)

Chronic inflammation from cigarette smoke drives atherogenesis. The irritants in smoke cause endothelial dysfunction and a sustained proinflammatory state, upregulating adhesion molecules and releasing cytokines that recruit monocytes to the vessel wall. These monocytes transform into macrophages that take up oxidized LDL, becoming foam cells and forming fatty streaks that progress into plaques. Systemic inflammatory signals raise markers like CRP, linking smoking to ongoing plaque development and instability. Other smoking-associated effects, such as temporary blood pressure rises, increased blood viscosity, or polycythemia, can worsen cardiovascular risk but do not explain the core process of plaque formation as directly as chronic inflammation does.