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Title: | Pulmonary vascular disease in pulmonary hypertension due to left heart disease: pathophysiologic implications | Authors: | Omote, Kazunori Sorimachi, Hidemi Obokata, Masaru Reddy, Yogesh N., V VERBRUGGE, Frederik Omar, Massar DuBrock, Hilary M. Redfield, Margaret M. Borlaug, Barry A. |
Issue Date: | 2022 | Publisher: | OXFORD UNIV PRESS | Source: | European heart journal, 43 (36) , p. 3417-3431 | Abstract: | Aims Pulmonary hypertension (PH) and pulmonary vascular disease (PVD) are common and associated with adverse outcomes in left heart disease (LHD). This study sought to characterize the pathophysiology of PVD across the spectrum of PH in LHD. Methods and results Patients with PH-LHD [mean pulmonary artery (PA) pressure >20 mmHg and PA wedge pressure (PAWP) >= 15 mmHg] and controls free of PH or LHD underwent invasive haemodynamic exercise testing with simultaneous echocardiography, expired air and blood gas analysis, and lung ultrasound in a prospective study. Patients with PH-LHD were divided into isolated post-capillary PH (IpcPH) and PVD [combined post- and pre-capillary PH (CpcPH)] based upon pulmonary vascular resistance (PVR <3.0 or >= 3.0 WU). As compared with controls (n = 69) and IpcPH-LHD (n = 55), participants with CpcPH-LHD (n = 40) displayed poorer left atrial function and more severe right ventricular (RV) dysfunction at rest. With exercise, patients with CpcPH-LHD displayed similar PAWP to IpcPH-LHD, but more severe RV-PA uncoupling, greater ventricular interaction, and more severe impairments in cardiac output, O-2 delivery, and peak O-2 consumption. Despite higher PVR, participants with CpcPH developed more severe lung congestion compared with both IpcPH-LHD and controls, which was associated lower arterial O-2 tension, reduced alveolar ventilation, decreased pulmonary O-2 diffusion, and greater ventilation-perfusion mismatch. Conclusions Pulmonary vascular disease in LHD is associated with a distinct pathophysiologic signature marked by greater exercise-induced lung congestion, arterial hypoxaemia, RV-PA uncoupling, ventricular interdependence, and impairment in O-2 delivery, impairing aerobic capacity. Further study is required to identify novel treatments targeting the pulmonary vasculature in PH-LHD. | Notes: | Borlaug, BA (corresponding author), Mayo Clin & Mayo Fdn, Dept Cardiovasc Med, 200 First St SW, Rochester, MN 55905 USA. borlaug.barry@mayo.edu |
Keywords: | Heart failure;Left heart disease;Pulmonary hypertension;Combined post- and pre-capillary pulmonary hypertension;Pulmonary vascular resistance;Exercise haemodynamics | Document URI: | http://hdl.handle.net/1942/37805 | ISSN: | 0195-668X | e-ISSN: | 1522-9645 | DOI: | 10.1093/eurheartj/ehac184 | ISI #: | 000821569600001 | Rights: | The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com Free access | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2023 |
Appears in Collections: | Research publications |
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ehac184 3417..3431.pdf | Published version | 1.2 MB | Adobe PDF | View/Open |
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