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      Functional impact of exercise pulmonary hypertension in patients with borderline resting pulmonary arterial pressure

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          Abstract

          Borderline resting mean pulmonary arterial pressure (mPAP) is associated with adverse outcomes and affects the exercise pulmonary vascular response. However, the pathophysiological mechanisms underlying exertional intolerance in borderline mPAP remain incompletely characterized. In the current study, we sought to evaluate the prevalence and functional impact of exercise pulmonary hypertension (ePH) across a spectrum of resting mPAP’s in consecutive patients with contemporary resting right heart catheterization (RHC) and invasive cardiopulmonary exercise testing. Patients with resting mPAP <25 mmHg and pulmonary arterial wedge pressure ≤15 mmHg (n = 312) were stratified by mPAP < 13, 13–16, 17–20, and 21–24 mmHg. Those with ePH (n = 35) were compared with resting precapillary pulmonary hypertension (rPH; n = 16) and to those with normal hemodynamics (non-PH; n = 224). ePH prevalence was 6%, 8%, and 27% for resting mPAP 13–16, 17–20, and 21–24 mmHg, respectively. Within each of these resting mPAP epochs, ePH negatively impacted exercise capacity compared with non-PH (peak oxygen uptake 70 ± 16% versus 92 ± 19% predicted, P < 0.01; 72 ± 13% versus 86 ± 17% predicted, P < 0.05; and 64 ± 15% versus 82 ± 19% predicted, P < 0.001, respectively). Overall, ePH and rPH had similar functional limitation (peak oxygen uptake 67 ± 15% versus 68 ± 17% predicted, P > 0.05) and similar underlying mechanisms of exercise intolerance compared with non-PH (peak oxygen delivery 1868 ± 599 mL/min versus 1756 ± 720 mL/min versus 2482 ± 875 mL/min, respectively; P < 0.05), associated with chronotropic incompetence, increased right ventricular afterload and signs of right ventricular/pulmonary vascular uncoupling. In conclusion, ePH is most frequently found in borderline mPAP, reducing exercise capacity in a manner similar to rPH. When borderline mPAP is identified at RHC, evaluation of the pulmonary circulation under the stress of exercise is warranted.

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          Most cited references30

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          Right heart adaptation to pulmonary arterial hypertension: physiology and pathobiology.

          Survival in patients with pulmonary arterial hypertension (PAH) is closely related to right ventricular (RV) function. Although pulmonary load is an important determinant of RV systolic function in PAH, there remains a significant variability in RV adaptation to pulmonary hypertension. In this report, the authors discuss the emerging concepts of right heart pathobiology in PAH. More specifically, the discussion focuses on the following questions. 1) How is right heart failure syndrome best defined? 2) What are the underlying molecular mechanisms of the failing right ventricle in PAH? 3) How are RV contractility and function and their prognostic implications best assessed? 4) What is the role of targeted RV therapy? Throughout the report, the authors highlight differences between right and left heart failure and outline key areas of future investigation. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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            Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review.

            According to current guidelines, pulmonary arterial hypertension (PAH) is diagnosed when mean pulmonary arterial pressure (Ppa) exceeds 25 mmHg at rest or 30 mmHg during exercise. Issues that remain unclear are the classification of Ppa values 30 mmHg during exercise is always pathological. We performed a comprehensive literature review and analysed all accessible data obtained by right heart catheter studies from healthy individuals to determine normal Ppa at rest and during exercise. Data on 1,187 individuals from 47 studies in 13 countries were included. Data were stratified for sex, age, geographical origin, body position and exercise level. Ppa at rest was 14.0+/-3.3 mmHg and this value was independent of sex and ethnicity. Resting Ppa was slightly influenced by posture (supine 14.0+/-3.3 mmHg, upright 13.6+/-3.1 mmHg) and age ( or = 50 yrs: 14.7+/-4.0 mmHg). Ppa during exercise was dependent on exercise level and age. During mild exercise, Ppa was 19.4+/-4.8 mmHg in subjects aged or = 50 yrs (p<0.001). In conclusion, while Ppa at rest is virtually independent of age and rarely exceeds 20 mmHg, exercise Ppa is age-related and frequently exceeds 30 mmHg, especially in elderly individuals, which makes it difficult to define normal Ppa values during exercise.
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              Pulmonary hypertension in chronic lung diseases.

              Chronic obstructive lung disease (COPD) and diffuse parenchymal lung diseases (DPLD), including idiopathic pulmonary fibrosis (IPF) and sarcoidosis, are associated with a high incidence of pulmonary hypertension (PH), which is linked with exercise limitation and a worse prognosis. Patients with combined pulmonary fibrosis and emphysema (CPFE) are particularly prone to the development of PH. Echocardiography and right heart catheterization are the principal modalities for the diagnosis of COPD and DPLD. For discrimination between group 1 PH patients with concomitant respiratory abnormalities and group 3 PH patients (PH caused by lung disease), patients should be transferred to a center with expertise in both PH and lung diseases for comprehensive evaluation. The task force encompassing the authors of this article provided criteria for this discrimination and suggested using the following definitions for group 3 patients, as exemplified for COPD, IPF, and CPFE: COPD/IPF/CPFE without PH (mean pulmonary artery pressure [mPAP] <25 mm Hg); COPD/IPF/CPFE with PH (mPAP ≥25 mm Hg); PH-COPD, PH-IPF, and PH-CPFE); COPD/IPF/CPFE with severe PH (mPAP ≥35 mm Hg or mPAP ≥25 mm Hg with low cardiac index [CI <2.0 l/min/m(2)]; severe PH-COPD, severe PH-IPF, and severe PH-CPFE). The "severe PH group" includes only a minority of chronic lung disease patients who are suspected of having strong general vascular abnormalities (remodeling) accompanying the parenchymal disease and with evidence of an exhausted circulatory reserve rather than an exhausted ventilatory reserve underlying the limitation of exercise capacity. Exertional dyspnea disproportionate to pulmonary function tests, low carbon monoxide diffusion capacity, and rapid decline of arterial oxygenation upon exercise are typical clinical features of this subgroup with poor prognosis. Studies evaluating the effect of pulmonary arterial hypertension drugs currently not approved for group 3 PH patients should focus on this severe PH group, and for the time being, these patients should be transferred to expert centers for individualized patient care.
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                Author and article information

                Journal
                Pulm Circ
                Pulm Circ
                PUL
                sppul
                Pulmonary Circulation
                SAGE Publications (Sage UK: London, England )
                2045-8932
                2045-8940
                08 June 2017
                September 2017
                : 7
                : 3
                : 654-665
                Affiliations
                [1 ]Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
                [2 ]Heart & Vascular Center, Brigham and Women’s Hospital, Boston, MA, USA
                [3 ]Division of Respiratory Diseases, Department of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil
                [4 ]Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
                [5 ]Veterans Affairs Boston Healthcare System, Boston, MA, USA
                [6 ]Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Portugal
                Author notes
                [*]David M. Systrom, Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital, Clinics 3, 75 Francis Street, Boston, MA 02115, USA. Email: dsystrom@ 123456bwh.harvard.edu
                Article
                10.1177_2045893217709025
                10.1177/2045893217709025
                5841910
                28895507
                db2676af-ca6f-476f-8499-664eab39c6d2
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution 4.0 License ( http://www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 10 February 2017
                : 19 April 2017
                Categories
                Research Articles
                Custom metadata
                July-September 2017

                Respiratory medicine
                pulmonary hypertension,exercise,oxygen uptake,oxygen delivery,pathophysiology
                Respiratory medicine
                pulmonary hypertension, exercise, oxygen uptake, oxygen delivery, pathophysiology

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