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Original Research: PULMONARY HYPERTENSION |

Misclassification of Pulmonary Hypertension Due to Reliance on Pulmonary Capillary Wedge Pressure Rather Than Left Ventricular End-Diastolic Pressure

Scott D. Halpern, MD, PhD; Darren B. Taichman, MD, PhD, FCCP
Author and Funding Information

From the Division of Pulmonary, Allergy and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA.

Correspondence to: Scott D. Halpern, MD, PhD, Center for Clinical Epidemiology and Biostatistics, 724 Blockley Hall, 423 Guardian Dr, Philadelphia, PA 19104-6021; e-mail: scott.halpern@uphs.upenn.edu


This work was supported by an American Thoracic Society Fellows Career Development Award (Dr. Halpern).

Drs. Halpern and Taichman have each received support from Actelion Pharmaceuticals to conduct other research related to pulmonary hypertension. The authors have no other involvement with organizations with a financial interest in the subject matter of this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(1):37-43. doi:10.1378/chest.08-2784
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Background:  Pulmonary arterial hypertension (PAH) is typically distinguished from pulmonary venous hypertension (PVH) by documenting a pulmonary capillary wedge pressure (PCWP) ≤ 15 mm Hg. However, PCWP has uncertain utility in establishing PAH. We sought to determine the calibration, discrimination, and diagnostic accuracy of PCWP, using simultaneously measured left ventricular end-diastolic pressure (LVEDP) as the “gold standard.”

Methods:  We examined hemodynamic data from the 11,523 unique patients undergoing simultaneous right-heart and left-heart catheterization at a large academic center from 1998 to 2007.

Results:  Among 4,320 patients (37.5%) with pulmonary hypertension (PH) [mean pulmonary artery pressure, ≥ 25 mm Hg], hemodynamic data were complete for 3,926 patients (90.9%). Of these, 580 patients (14.8%) met the criteria for PAH with a PCWP ≤ 15 mm Hg, but 310 of these patients (53.5%) had an LVEDP > 15 mm Hg. Such discrepancies remained common among patients with a pulmonary vascular resistance > 3 Wood units and those being catheterized specifically to evaluate PH. PCWP provided moderate discrimination between patients with high vs normal LVEDP (area under the receiver operating characteristic curve, 0.84; 95% confidence interval, 0.81 to 0.86) but was poorly calibrated to LVEDP (Bland-Altman limits of agreement, − 15.2 to 9.5 mm Hg; Hosmer-Lemeshow goodness-of-fit χ2 statistic, 155.4; p < 0.0001).

Conclusions:  Roughly half of the patients presumed to have PAH based on PCWP may be found to have PVH based on LVEDP. Reliance on PCWP may result in the dangerous or cost-ineffective use of pulmonary vasodilators for patients with left-heart disease. Furthermore, without assessing LVEDP, investigators may include patients with left-heart disease in therapeutic trials of PAH drugs, thereby limiting their ability to detect beneficial drug effects.

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