**18. Embolectomy**

Several interventional techniques including mechanical fragmentation, thrombus aspiration, and direct thrombolytic therapy are currently available for the treatment of acute PE. No clear guidelines can be provided regarding the use of interventional techniques for PE as there are no randomized controlled trials to assess these treatments. ACCP guidelines advise consider‐ ation of these interventions in the setting of massive PE with contraindications to systemic thrombolysis, failed thrombolysis, or likelihood of death before thrombolysis (Kearon 2012). Surgical embolectomy is infrequently required for management of acute PE. There are limited data guiding surgical interventions in this setting. Leacche et al (Leacche 2005) reported surgical outcomes in 47 consecutive patients with acute massive PE treated surgically. Indications for surgery included contraindications to thrombolysis (45%), failed medical treatment (10%) and right ventricular dysfunction (32%). Operative mortality and late mortality were 6% and 12% with the majority (83%) of the late mortality related to metastatic cancer. 86% and 83% of patients were alive 1 and 3 years after surgery, respectively (Leacche 2005). Specific instances when surgical intervention may be indicated are the presence of right atrial thrombus, paradoxical arterial embolism, or closure of a patent foramen ovale (Kearon 2012).

**20. Summary**

**Author details**

Jean M. Elwing1,2\* and Ralph J. Panos1,2

cal Center, Cincinnati, USA

Medicine, Cincinnati, USA

**References**

\*Address all correspondence to: jean.elwing@uc.edu

pects. Blood. 2009 Mar 26;113(13):2878-87.

Acute pulmonary thromboembolism is the third most common acute cardiovascular disease (Giuntini 1995) and is associated with significant morbidity and mortality. Thromboembolic obstruction of the pulmonary vasculature frequently causes dyspnea, hypoxia, and chest pain. In severe cases, PE can cause an acute rise in pulmonary pressures precipitating RV dysfunc‐ tion and hemodynamic instability. The increase in hemodynamic pressures is due to both mechanical obstruction of the pulmonary vascular bed as well as the release of vasoconstricting mediators and derangement of neural regulation of vasomotor tone. Hypotension, RV dysfunction, elevated biomarkers (BNP, troponin I, troponin T) and ECG abnormalities with T-wave inversions are markers of poor prognosis. Rapid evaluation and risk stratification are necessary for effective treatment. Hemodynamically stable PE, i.e. low risk PE, is routinely managed with heparin therapy and clinical monitoring. Hemodynamically unstable PE, i.e. massive PE, is frequently managed with thrombolysis. Optimal management of hemodynam‐ ically stable PE with high risk features, i.e. submassive PE, is unclear at this time. Further study to determine best practice in this group is ongoing. Unfortunately, acute PE has both shortterm and long-term consequences. Additional evaluation and characterization of patients at

Acute Thromboembolic Pulmonary Hypertension

http://dx.doi.org/10.5772/56719

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1 Pulmonary, Critical Care, and Sleep Medicine Division, Cincinnati Veterans Affairs Medi‐

2 Pulmonary, Critical Care, and Sleep Medicine Division, University of Cincinnati College of

[1] Adam SS, Key NS, Greenberg CS. D-dimer antigen: current concepts and future pros‐

[2] Anderson DR, Kahn SR, Rodger MA, Kovacs MJ, Morris T, Hirsch A, Lang E, Stiell I, Kovacs G, Dreyer J, Dennie C, Cartier Y, Barnes D, Burton E, Pleasance S, Skedgel C, O'Rouke K, Wells PS.Computed tomographic pulmonary angiography vs ventila‐ tion-perfusion lung scanning in patients with suspected pulmonary embolism: a

randomized controlled trial. JAMA. 2007 Dec 19;298(23):2743-53.

risk to develop long term complications of pulmonary emboli are needed.
