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1 Depts of Physiology, Cardiology and Intensive Care, Erasme University Hospital Brussels, Brussels, Belgium. 2 Dept of Pneumology, Academic Hospital of the Free University of Amsterdam, Amsterdam, the Netherlands. 3 Dept of Pneumology, Gasthuisberg University Hospital, Leuven, Belgium. 4 Pulmonary and Critical Care Division, UCSD Medical Center, San Diego, CA, USA
CORRESPONDENCE: R. Naeije, Laboratory of Physiology, Erasmus Campus, CP 604, Route de Lennik 808, B-1070, Brussels, Belgium. Fax: 32 25554124. E-mail: rnaeije@ulb.ac.be
Keywords: chronic thromboembolic pulmonary hypertension, effective pulmonary capillary pressure, nitric oxide, pulmonary arterial hypertension, pulmonary vascular resistance, pulmonary veno-occlusive disease
Received: June 24, 2002
Accepted August 19, 2002
Supported by grant number 3.4567.00 from the Fonds de la Recherche Scientifique Médicale, Brussels, Belgium. P. Fesler was a fellow of the Erasmus Foundation, Brussels, Belgium.
The purpose of this study was to determine the site of increased resistance using the arterial occlusion technique in patients with severe pulmonary hypertension.
Pulmonary vascular resistance was partitioned in arterial and venous components based on double exponential fitting analysis of the pulmonary artery pressure decay curve: after balloon occlusion in 36 patients with pulmonary arterial hypertension (PAH); at baseline and during the inhalation of 20 parts per million of nitric oxide (NO); in four patients with chronic thromboembolic pulmonary hypertension; and in two patients with pulmonary veno-occlusive disease.
In the patients with PAH, at baseline, mean pulmonary artery pressure was 56±2 mmHg (mean±se), with an arterial component of resistance of 63±1%. Inhaled NO did not change the partition of resistance. The arterial component of resistance amounted on average to 42% and 77% in the patients with veno-occlusive disease and the patients with thromboembolic pulmonary hypertension, respectively. However, the partitioning of resistance did not discriminate between these three diagnostic categories.
The occlusion technique may help to locate the predominant site of increased resistance in patients with severe pulmonary hypertension, but does not allow for a satisfactory differential diagnosis on an individual basis.
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