Potential usefulness of antiplatelet agents in patients with chronic obstructive pulmonary disease

Thrombotic complications of pulmonary circulation might occur in patients with chronic obstructive pulmonary disease (COPD) (1-3). It has been suggested that these thrombotic events could be partly tied to the abnormalities found in platelet function. In fact, in vitro and in vivo platelet activation could actually occur in systemic and pulmonary circulation as a result of hypoxemia, acidosis or hyperviscosity, all characteristic findings of COPD. A shortened platelet half-life, as well as increased plasma levels of beta-thromboglobulin (beta-TG) and enhanced platelet aggregation have been reported in patients with COPD (4-7). Moreover, a decrease in platelet survival time has been correlated with chronic hypoxemia, thus suggesting an increased platelet consumption due to in vivo platelet activation (6, 8-10). In 1991, Segall and Goetzman (11), in a study carried out on newborn lambs, demonstrated the occurrence of platelet content release in the lung during hypoxia-induced pulmonary hypertension. This observation is in good agreement with the above reported findings of short platelet half-life and in vivo platelet activation in patients with chronic hypoxemia. Moreover, the possibility of platelet content release in the lung during hypoxic conditions may account for impaired respiratory parameters, such as forced expiratory volume in one second (FEV1).