An important feature of the pathophysiology of COPD patients is represented by the remodelling of pulmonary vasculature. Within this process, a pathogenic element might be the endothelial dysfunction induced by the combined effect of several factors such as: cigarette smoke, inflammatory mediators, hypoxia, mechanical stress, whose contribution differs according to the stage of the disease. The aims of our study were to characterize the structural pulmonary vascular abnormalities present in smokers and patients with mild COPD and to assess their pathophysiological importance. Serial tissue sections from fragments of pulmonary exeresis have been subjected to both morphometric analysis and histochemical examination of muscular pulmonary arteries. Our results have shown a process of arteriolar muscularization and intimal thickening of small muscular arteries in both smokers (intimal index 23.11% +/- 3.04%) and patients with mild COPD (25.62% +/- 3.06%) as compared to controls (17.86% +/- 2.96%). Correlation analysis has demonstrated that intimal thickening is significantly associated with cigarette consumption expressed as packs-years (r = 0.65, p = 0.04) whereas univariate regression has shown a moderate causal relation between the intimal collagen deposits and the degree of vascular thickening (r2=0,53 and p=0,002). In conclusion, cigarette smoking may play a central role within the pathogenesis of vascular abnormalities in patients with mild COPD.