POTENTIAL USEFULNESS OF ANTIPLATELET AGENTS IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

Thrombotic complications of pulmonary circulation might occur in patie nts with chronic obstructive pulmonary disease (COPD) (1-3). It has be en suggested that these thrombotic events could be partly tied to the abnormalities found in platelet function. In fact, in vitro and in viv o platelet activation could actually occur in systemic and pulmonary c irculation as a result of hypoxemia, acidosis or hyperviscosity, all c haracteristic findings of COPD. A shortened platelet half-life, as wel l as increased plasma levels of beta-thromboglobulin (beta-TG) and enh anced platelet aggregation have been reported in patients with COPD (4 -7). Moreover, a decrease in platelet survival time has been correlate d with chronic hypoxemia, thus suggesting an increased platelet consum ption due to in vivo platelet activation (6, 8-10). In 1991, Segall an d 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 v ivo 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 f orced expiratory volume in one second (FEV1).