SGCB and pulmonary arterial hypertension: Nitric oxide and prostacyclin are important negative regulators ofplatelet activation, adhesion, and aggregation and reduced levels areconsistently observed in PAH.78 It is biologically plausible that reduced bioavailability ofnitric oxide and prostacyclin in the pulmonary circulation could leadto excess local platelet activation and drive disease progression.11 Evidence suggests that the phosphodiesterase type 5 inhibitor sildenafil79 and the sGC stimulator riociguat78 restore nitric oxide-mediated inhibition of plateletaggregation.