PURPOSE: Pulmonary Hypertension (PH) is associated with advanced Crhonic Obstructive Pulmonary Disease(COPD) in 20% to 40% of patients. Endothelial disfunction seems to play a relevant role in the pathogenesis and Endothelin(ET)is claimed as a marker of endothelial disfunction. The precise role of ET in the clinical course of COPD under stable state and under relapse is not established. It seems necessary to assess both the changes of PH and ET levels in progressive worsening of COPD stages, the existence of relationship between ET and functional and gas exchange variables and identification of preventive and curative therapy, eg anti-proliferative drugs, administered early in the course of COPD, before pathologic changes take place.
METHODS: We studied 39 patients affected by COPD and PH, 39 patients affected by COPD in different stages but withoutt PH. All patients were submitted to pletismography, EGA, rigth side catetherization. Data were compared to measures obtained in 13 healthy people, performing pulmonary catetherization for other reasons. ET levels were measured by double sandwich immunoassay over peripheral, arterial and mixed venous samples.
RESULTS: Big Endothelin is tenfold increased, as compared to healthy people, in advanced stages of COPD (GOLD stages III e IV)with PH and futhermore under acute relapse. ET is involved in vasospastic response to hypoxia, proliferative response, neuro-endocrine activation and organic remodelling.
CONCLUSION: ET and endothelium are significantly related to pulmonary artery pressure in advanced stages of COPD with PH. Experimental studies and therapeutic trials will evidence the link between endothelin and organic artery changes and assess the existence of the marker of predisposition.
CLINICAL IMPLICATIONS: It is could be useful to administer anti-proliferative drugs, eg bosentan, to COPD predisposed patients to develop PH, at GOLD stages III and IV, as early as possible, before well established PH take place.
DISCLOSURE: Bracciale Pietro, None.