In a clinical study with riociguat applied in pulmonary hypertension secondary to diastolic heart failure, but without increased PVR, there was no change in transpulmonary pressure gradient or pulmonary vascular resistance.28 The explanation for this might be a lower expression of and lower oxidation levels of sGC in the lungs with no primary pathology, abolishing any pulmonary vascular selectivity when the drug is applied intravenously. This evidence concerns the gene SGCB and pulmonary hypertension.