Chest
Volume 143, Issue 3, March 2013, Pages 758-766
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Original Research
Pulmonary Vascular Disease
Diastolic Pulmonary Vascular Pressure Gradient: A Predictor of Prognosis in “Out-of-Proportion” Pulmonary Hypertension

https://doi.org/10.1378/chest.12-1653Get rights and content

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.

Section snippets

Patients and End Points

Between May 1996 and March 2003, 3,107 patients underwent a first diagnostic right-sided heart catheterization (RHC) at the Medical University of Vienna, a national PH referral center (Fig 1). In 2,524 patients (81.2%), the procedure was combined with a left-sided heart catheterization. Catheterizations were performed for various indications, mostly for the diagnosis of elevated systolic pulmonary arterial pressure (sPAP) at echocardiography, in patients with chronic heart failure and patients

Patients

Two thousand three hundred fifty-one complete data sets were collected in 3,107 patients (Fig 2). Fourteen patients were lost to follow-up. At inclusion, 30.6% of patients were in World Health Organization functional class 1, 34.3% in class 2, 25% in class 3, and 10.1% in class 4. One thousand three hundred eighty-nine patients were diagnosed as having PH (mPAP ≥ 25 mm Hg). Cases with PH associated with congenital heart disease (n = 130), and cases with multifactorial PH (n = 28) (Fig 2) were

Discussion

PH due to LHD is a common entity and carries a poor outcome.22, 23 Today, in developed countries, it is mainly due to systolic24 and diastolic left ventricular dysfunction10 and less commonly due to valvular heart disease.25 Chronic sustained elevation of pressure in pulmonary capillaries leads to vascular remodeling that resembles the classic pulmonary arteriopathy of precapillary PH.26 However, PH due to LHD is less frequently associated with intimal proliferation and plexiform lesions, and

Acknowledgments

Author contributions: Dr Lang is the guarantor of the entire manuscript.

Mr Gerges: contributed to the database, statistical analyses, histology, and writing of the manuscript.

Dr Gerges: contributed to the database, statistical analyses, histology, and writing of the manuscript.

Ms Lang: contributed to the database, statistical analyses, and approving the manuscript.

Dr Zhang: contributed to the histology and histological images and proofread the manuscript.

Dr Jakowitsch: contributed to the

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    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.

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