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Original Research: Pulmonary Vascular Disease |

Diastolic Pulmonary Vascular Pressure GradientDiastolic Gradient and Prognosis: A Predictor of Prognosis in “Out-of-Proportion” Pulmonary Hypertension

Christian Gerges; Mario Gerges, MD; Marie B. Lang; Yuhui Zhang, MD; Johannes Jakowitsch, PhD; Peter Probst, MD; Gerald Maurer, MD; Irene M. Lang, MD
Author and Funding Information

From the Department of Internal Medicine II, Division of Cardiology, Vienna General Hospital, Medical University of Vienna, Vienna, Austria.

Correspondence to: Irene Lang, MD, Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria; e-mail: irene.lang@meduniwien.ac.at


Funding/Support: This research was supported by the Austrian fellowship grant Medizinisch-Wissenschaftlicher Fonds des Bürgermeisters der Bundeshauptstadt Wien [Project No. 08080-2009] and by an educational grant from United Therapeutics Corporation.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(3):758-766. doi:10.1378/chest.12-1653
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Background:  Left-sided heart disease (LHD) is the most common cause of pulmonary hypertension (PH). In patients with LHD, elevated left atrial pressure causes a passive increase in pulmonary vascular pressure by hydrostatic transmission. In some patients, an active component caused by pulmonary arterial vasoconstriction and/or vascular remodeling superimposed on left-sided pressure elevation is observed. This “reactive” or “out-of-proportion” PH, defined as PH due to LHD with a transpulmonary gradient (TPG) > 12 mm Hg, confers a worse prognosis. However, TPG is sensitive to changes in cardiac output and left atrial pressure. Therefore, we tested the prognostic value of diastolic pulmonary vascular pressure gradient (DPG) (ie, the difference between invasive diastolic pulmonary artery pressure and mean pulmonary capillary wedge pressure) to better prognosticate death in “out-of-proportion” PH.

Methods:  A large database of consecutive cases was analyzed. One thousand ninety-four of 2,351 complete data sets were from patients with PH due to LHD. For proof of concept, available lung histologies were reviewed.

Results:  In patients with postcapillary PH and a TPG > 12 mm Hg, a worse median survival (78 months) was associated with a DPG ≥ 7 mm Hg compared with a DPG < 7 mm Hg (101 months, P = .010). Elevated DPG was associated with more advanced pulmonary vascular remodeling.

Conclusions:  DPG identifies patients with “out-of-proportion” PH who have significant pulmonary vascular disease and increased mortality. We propose a diagnostic algorithm, using pulmonary capillary wedge pressure, TPG, and DPG in sequence to diagnose pulmonary vascular disease superimposed on left-sided pressure elevation.

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