PECAM1 and chronic obstructive pulmonary disease: Furthermore, COPD patients showed persistent elevated levels in CD31+ EEVs even 12 months after quitting smoking, while in healthy smokers their levels significantly decreased after smoking cessation: these data, together with the previous study, thus confirm that pulmonary endothelial apoptosis likely plays a role in COPD pathogenesis, both at the beginning of this process and in its progression, irrespective of the persistence of the external stimulus (cigarette smoke) [32].