Why the study?
To review and instruct on the pathophysiology of right ventricular failure in acute massive and submassive pulmonary embolism and CTEPH, providing the rationale for therapeutic intervention by interventional radiologists.
Provides an educational overview of the pathophysiology of right ventricular failure in acute pulmonary embolism and CTEPH to inform therapeutic interventions.
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Enhances clinician awareness of RV failure mechanisms in PE/CTEPH; leaves open optimal management strategies for prospective validation.
Pulmonary embolus (PE) is the third most common cause of cardiovascular death with more than 600,000 cases occurring in the USA per year. About 45% of patients with acute PE will have acute right ventricular failure, and up to 3.8% of patients will develop chronic thromboembolic pulmonary hypertension (CTEPH) with progressive, severe, chronic heart failure. The right ventricle (RV) is constructed to accommodate a low-resistance afterload. Increases in afterload from acute massive and submassive PE and CTEPH may markedly compromise the RV function leading to hemodynamic collapse and death. The purpose of this educational manuscript is to instruct on the pathophysiology of RV failure in massive and submassive PE and CTEPH. It is important to understand the pathophysiology of these diseases as it provides the rationale for therapeutic intervention by the Interventional Radiologist. We review here the pathophysiology of right ventricular (RV) failure in acute massive and submassive PE and CTEPH.
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Bryce et al. (2019) studied this question.
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