Key result
Transitioning from phosphodiesterase-5 inhibitors to riociguat is a potential therapeutic option for pulmonary arterial hypertension, with ongoing assessment in the REPLACE trial.
Why the study?
Does transitioning from a PDE5 inhibitor to riociguat improve clinical outcomes in patients with pulmonary arterial hypertension?
Does transitioning from a PDE5 inhibitor to riociguat improve clinical outcomes in patients with pulmonary arterial hypertension?
This review highlights the mechanistic rationale and ongoing clinical evaluation of transitioning from PDE5 inhibitors to riociguat in patients with pulmonary arterial hypertension.
Endogen nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) deficiency in pulmonary vessels walls plays essential role in pulmonary arterial hypertension (PAH) pathogenesis. Soluble guanylate cyclase stimulator riociguat and phosphodiesterase-5 (PDE5) inhibitor sildenafil increase cGMP content and have proven clinical efficacy in PAH treatment. The potentially beneficial mechanisms of riociguat mechanism of action include endogen NO independence in cGMP synthesis and its independence from other phosphodiesterase isoferments (other than PDE5). Clinical options, safety and effectiveness of iPDE5 - riociguat transition in patients with PAH were for the first time shown in non-controlled study RESPITE and the assessment is continued in randomized placebo-controlled trial REPLACE.
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Shmalts et al. (2018) conducted a review in pulmonary arterial hypertension (PAH). iPDE5 to riociguat transition was evaluated. Transitioning from phosphodiesterase-5 inhibitors to riociguat is a potential therapeutic option for pulmonary arterial hypertension, with ongoing assessment in the REPLACE trial.
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