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

Figures

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  Figure 1. Hemodynamic parameters (MAP and pulse) and respiratory profiles (PaO2/FiO2 ratio and PaCO2) are demonstrated every hour during the 11 days in the ICU for the 49-year-old woman with massive pulmonary embolism. Green arrow indicates the time of systemic thrombolysis. Purple arrow indicates the time of IVC filter implantation. Abbreviations: MAP: middle arterial pressure, PaO2/FiO2 ratio: arterial oxygen partial pressure to fractional inspired oxygen, PaO2: partial pressure of oxygen, PaCO2: partial pressure of arterial carbon dioxide, FiO2: fraction of inspired oxygen, IVC: inferior vena cava.

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  Figure 2. Echocardiography before thrombolysis showed severe right ventricular dysfunction with flattened intraventricular septum (∗) in parasternal short-axis view (a) and thrombus (arrow) in the right atrium in apical four-chamber view (b).

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  Figure 3. CTPA demonstrating a thrombus of 11 centimetre in the inferior vena cava. (a) The thrombus in the IVC before thrombolysis (white arrows); (b) the residual thrombus (white arrow) following thrombolysis and after insertion of the vena cava filter (green arrow). Abbreviations: CTPA: computed tomography pulmonary angiogram, IVC: inferior vena cava.

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  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.