Chest
Volume 136, Issue 1, July 2009, Pages 37-43
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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

https://doi.org/10.1378/chest.08-2784Get rights and content

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.

Section snippets

Patients

All patients undergoing right-heart catheterization at Penn-Presbyterian Medical Center, a large, community-based, academic hospital and regional referral center for pulmonary vascular disease affiliated with the University of Pennsylvania Health System, from January 1, 1998, to December 31, 2007, were included in the study. This study was deemed exempt from review by the University of Pennsylvania Institutional Review Board because it used previously collected, deidentified data.

Patients were

Results

There were 12,744 eligible unique patients who underwent right-heart catheterization at our institution from 1998 to 2007. Of these, 11,523 patients underwent combined catheterizations, and 4,320 patients (37.5%) had PH (Fig 1).

Discussion

This study of a large number of patients undergoing sequential measurement of PCWP and LVEDP suggests that PCWP frequently underestimates LVEDP, that it is poorly calibrated to LVEDP, and that it has a moderate ability to discriminate between patients with normal or elevated LVEDP. Perhaps most importantly, these results suggest that approximately half of all patients who meet the hemodynamic criteria for PAH on the basis of PCWP measurements may, in fact, have elevated left ventricular filling

Conclusions

Some might conclude from our results that LVEDP should be measured routinely among all patients referred for catheterization as part of an evaluation for PH. However, this approach carries increased risks and inconveniences for patients as well as increased costs and resource utilization. We therefore suggest a more conservative approach in routine practice in which clinicians obtain left-heart hemodynamic measurements whenever there are reasons to suspect left-heart disease based on the

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

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

    1

    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.

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