Interventional therapies for pulmonary embolism

Abstract

Pulmonary embolism (PE) is the leading cause of in-hospital death and the third most frequent cause of cardiovascular death. The clinical presentation of PE is variable, and choosing the appropriate treatment for individual patients can be challenging. Traditionally, treatment of PE has involved a choice of anticoagulation, thrombolysis or surgery; however, a range of percutaneous interventional technologies have been developed that are under investigation in patients with intermediate-high-risk or high-risk PE. These interventional technologies include catheter-directed thrombolysis (with or without ultrasound assistance), aspiration thrombectomy and combinations of the aforementioned principles. These interventional treatment options might lead to a more rapid improvement in right ventricular function and pulmonary and/or systemic haemodynamics in particular patients. However, evidence from randomized controlled trials on the safety and efficacy of these interventions compared with conservative therapies is lacking. In this Review, we discuss the underlying pathophysiology of PE, provide assistance with decision-making on patient selection and critically appraise the available clinical evidence on interventional, catheter-based approaches for PE treatment. Finally, we discuss future perspectives and unmet needs.

Fig. 1. Timeline of studies of interventional therapies in PE.

To date, four randomized controlled trials investigating interventional therapies in acute pulmonary embolism (PE) have been published. Five more randomized controlled trials are ongoing. Trials comparing different interventional strategies against standard-of-care and in a head-to-head comparison are particularly needed. CDT, catheter-directed thrombolysis; USCDT, ultrasound-assisted catheter-directed thrombolysis.

Fig. 2. Pathophysiology of PE and concomitant pulmonary hypertension after pulmonary artery obstruction and vasoconstriction.

a, Most commonly, pulmonary embolism (PE) results from proximal deep-vein thrombosis, with the majority of thrombi originating in the lower extremities. Promoted by risk factors, such as active cancer, smoking or obesity, prothrombotic influences outweigh antithrombotic mechanisms. b, Thrombi can obstruct the pulmonary arteries, thereby reducing blood flow and causing the production of vasoactive mediators, such as endothelin 1, serotonin and thromboxane A₂, which themselves further amplify vasoconstriction. The resulting high pulmonary artery pressures can cause cardiac dysfunction and even shock. Downstream effects include hypotension, anaerobic metabolism, respiratory failure and, finally, death.

Fig. 3. Treatment algorithm for PE.

Interventional therapies can be considered in patients with high-risk pulmonary embolism (PE) and contraindications to systemic thrombolysis and in patients with intermediate-risk or low-risk PE if their condition deteriorates despite anticoagulation.

Fig. 4. Large-bore thrombectomy.

Pulmonary angiography of the right and left pulmonary arteries of a patient with acute bilateral intermediate–high-risk pulmonary embolism before (parts a and b) and after (parts c and d) large-bore thrombectomy using the FlowTriever Retrieval/Aspiration System (Inari Medical). Dye defects show intravascular thrombi. The aspirated thrombi from the right and left pulmonary arteries are shown (part e).