Intermediate-High Risk Pulmonary Embolism: The Use of Riociguat and Inferior Vena Cava Filter in a Situation of Recurrent Embolism following Insufficient Anticoagulation and Fibrinolytic Therapy

Figure 4

The figure demonstrates a simplified NO-sGC-cGMP pathway. Compromised endogenous NO synthesis and signaling is involved in the pathogenesis of pulmonary hypertension [8, 9]. Both NO and riociguat stimulate sGC which increases the levels of cGMP. This relaxes smooth muscle cells, induces vasodilation, and reduces PVR. Abbreviations: NO: nitric oxide, sGC: soluble guanylate cyclase, cGMP: cyclic guanosine monophosphate, PVR: pulmonary vascular resistance.