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(Circulation. 2009;120:1248-1254.)
© 2009 American Heart Association, Inc.

Vascular Medicine

Pulmonary Hypertensive Medical Therapy in Chronic Thromboembolic Pulmonary Hypertension Before Pulmonary Thromboendarterectomy

Kurt W. Jensen, MD; Kim M. Kerr, MD; Peter F. Fedullo, MD; Nick Hyong Kim, MD; Victor J. Test, MD; Ori Ben-Yehuda, MD; William R. Auger, MD

From the Division of Pulmonary Critical Care Medicine (K.W.J., K.M.K., P.F.F., N.H.K., V.J.T., W.R.A.) and Division of Cardiology (O.B.-Y.), University of California at San Diego, La Jolla.

Correspondence to Kim M. Kerr, MD, Division of Pulmonary Critical Care Medicine, University of California at San Diego, 9300 Campus Point Dr, La Jolla, CA 92037. E-mail kmkerr{at}ucsd.edu

Received March 24, 2009; accepted July 21, 2009.

Background— The currently recommended treatment for chronic thromboembolic pulmonary hypertension is pulmonary thromboendarterectomy (PTE). No convincing evidence for the use of pulmonary hypertensive medical therapy (PHT) exists in operable candidates. We sought to determine the prevalence of the use of PHT on referral for PTE and the effects on pre-PTE hemodynamics and post-PTE outcomes/hemodynamics.

Methods and Results— We performed a retrospective analysis of chronic thromboembolic pulmonary hypertension patients referred for PTE during 2005–2007. The prevalence of PHT was determined for all patients referred to our institution. Hemodynamic and outcomes analysis involved only those undergoing PTE. Data included baseline demographics, PHT medication(s), dosage, duration of therapy, and time to referral. Hemodynamic data were acquired from the time of diagnosis, the time of referral visit, and after PTE. Outcomes included intensive care unit, hospital, and ventilator days; bleeding and infection rates; incidence of reperfusion lung injury; and in-hospital mortality. The control group (n=244) was compared with the PHT group (n=111); subgroups included monotherapy with bosentan, sildenafil, or epoprostenol and combination therapy. The prevalence of PHT significantly increased from 19.9% in 2005 to 37% in 2007. There was minimal benefit of treatment with PHT on pre-PTE mean pulmonary artery pressure, but its use was associated with a significant delay in time to referral for PTE. Both groups experienced significant improvements in hemodynamic parameters after PTE. The 2 groups did not differ significantly in any post-PTE outcome. Similar results were obtained for each subgroup.

Conclusions— Our results suggest that PHT use has minimal effect on pre-PTE hemodynamics and no effect on post-PTE outcomes/hemodynamics.

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CLINICAL PERSPECTIVE

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Clinical Summaries
Circulation 2009 120: 1165-1167. [Extract] [Full Text]