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Pulmonary capillary endothelial metabolic function in chronic thromboembolic pulmonary hypertension
Author(s) -
ORFANOS S. E.,
HIRSCH A. M.,
GIOVINAZZO M.,
ARMAGANIDIS A.,
CATRAVAS J. D.,
LANGLEBEN D.
Publication year - 2008
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2008.03046.x
Subject(s) - cardiology , medicine , pulmonary hypertension , endothelium , chronic thromboembolic pulmonary hypertension , endocrinology , chemistry
Summary.  Background:  Chronic thromboembolic pulmonary hypertension (CTEPH) causes physical plugging of large pulmonary arteries as well as a distal micro‐vasculopathy. Pulmonary endothelium is an active metabolic tissue in normal humans. The effects of CTEPH on pulmonary endothelial metabolism are unknown. Objectives:  We studied pulmonary capillary endothelium‐bound angiotensin converting enzyme (ACE) activity as an index of endothelial metabolism in patients with CTEPH. Patients/methods:  We measured single‐pass transpulmonary per cent metabolism (%M) and hydrolysis of an ACE synthetic substrate and calculated functional capillary surface area (FCSA), normalized to body surface area (BSA), in 13 patients with CTEPH and 23 controls. Results:  Mean %M for CTEPH (71.6 ± 4.0% SE) was similar to controls (74.7 ± 2.7%). Substrate hydrolysis ( v ) was similar for CTEPH (1.47 ± 0.22) and controls (1.51 ± 0.11). However, FCSA/BSA was reduced ( P  < 0.01) for CTEPH (1530 ± 218 mL min −1 *m −2 ) as compared with controls (2948 ± 245). Conclusions:  The metabolically functional pulmonary capillary bed is reduced in CTEPH. However, because %M and hydrolysis are preserved, this points to a reduction in functional capillary surface area rather than reduced ACE activity on the pulmonary capillary endothelial cell. The reduction in functional capillary surface area may just be a result of decreased capillary recruitment because of upstream vascular plugging by chronic organized thrombus.

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