Functional limitation and right ventricular dysfunction at 6-month follow-up in patients with non-massive pulmonary embolism: useful outcomes for testing therapy of acute submassive pulmonary embolism?

Abstract

Acute pulmonary embolism (PE) is a syndrome with a significant annual incidence, potentially associated with an elevated morality rate.1 Patients presenting with acute PE and persistent systemic hypotension, cardiogenic shock, or cardiac arrest are classified as having massive PE; in the absence of haemodynamic instability, PE is defined generically as non-massive. The latter, however, is classified as submassive acute PE in the presence of right ventricular (RV) dysfunction,1 to indicate that patients with normotensive acute PE and RV dysfunction may suddenly need escalation of therapy (vasopressor and/or inotropic support, rescue fibrinolysis, cardiopulmonary resuscitation).2–4 While clinical manifestation of acute PE may vary widely and significantly between patients, acute RV dysfunction is more quantifiable and uniform objective information in PE with relation to the severity of pulmonary vascular impairment.5 RV failure is the prominent cause of death in acute PE. This is further supported by the fact that in the setting of non-massive acute PE, RV dysfunction correlates with brain natriuretic peptide and troponins, which are in turn biomarkers of the severity of RV overload,6 providing additional information for risk stratification of the heterogeneous group of patients with normotensive PE.7–11 However, whether aggressive treatment (i.e. fibrinolysis or catheter-based pulmonary embolectomy) should be employed in acute submassive PE in addition to anticoagulation is controversial.1 In fact, while fibrinolysis or thromboembolectomy are associated with partial recovery of RV dysfunction,12 … *Corresponding author. Tel: +39 081 2543536; fax: +39 081 2543536. E-mail address : vpalmier{at}med.cornell.edu