Platelets and pulmonary arterial hypertension (PAH)

One of the biochemical pathways implicated in PAH is the prostacyclin chain. While prostacyclin is associated with vasodilation and may be provided as treatment, another component of this pathway, thromboxane, promotes vasoconstriction. Thromboxane is secreted mainly by platelets. However, platelets have not been adequately evaluated in PAH Objective: To compare platelet count and volume of PAH patients and controls (normopressoric, submitted to right heart catheterization (RHC) during PAH investigation) Methods: Retrospective analysis of PAH patients and controls of a single PAH center, evaluated for PAH diagnosis between 2008 and 2016. Platelet count and mean platelet volume (MPV) were collected close to baseline RHC Results: Platelet count was available for 243 PAH patients and 79 controls. PAH had a smaller platelet count (203666±90466 vs 246025±126778, p<0,001). 153 PAH patients and 60 controls had the MPV available, no difference was found between groups. When considering PAH with pure vascular disease (IPAH, HIV, veno-occlusive, congenital heart disease) excluding PAH patients that had systemic diseases that could impact in the total platelet count (collagen-tissue and hepatic diseases), PAH (n= 93) had a statistical trend of platelet count smaller than controls (216677±90883, p=0.09). The pure vascular PAH patients had an MPV lower than controls (n=48, 9.8±1.68 vs 10.44±1.25 µm3 p<0.05). Platelet count was a determinant of better survival in pure vascular PAH patients (p<0.05) Conclusion: Platelets are present in less quantity and in smaller sizes in PAH than in controls. Platelet count was a significant determinant of survival in PAH. Platelets biology, metabolites and paracrine function should be better evaluated in PAH