Pulmonary Vascular Distensibility and Early Pulmonary Vascular Remodeling in Pulmonary Hypertension
Exercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea,...
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Published in | Chest Vol. 156; no. 4; pp. 724 - 732 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
01.10.2019
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Abstract | Exercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea, including pulmonary hypertension (PH) and/or heart failure with preserved ejection fraction (HFpEF). We investigated rest and exercise invasive pulmonary hemodynamics, ventilation, and gas exchange in patients with unexplained dyspnea, including 44 patients with HFpEF (of whom 20 had a normal pulmonary vascular resistance [PVR] during exercise [ie, passive HFpEF] and 24 had a higher than normal exercise PVR), 22 patients with exercise PH, 19 patients with pulmonary arterial hypertension (PAH), and 24 age- and sex-matched normal control subjects.
A PV distensibility coefficient α (%/mm Hg) was determined from multipoint PV pressure-flow plots. RV-PA coupling was quantified from the analysis of RV pressure curves to determine ratios of end-systolic to arterial elastances (Ees/Ea). Aerobic exercise capacity was estimated by peak oxygen consumption.
The α coefficient decreased from 1.35 ± 0.58%/mm Hg in control subjects and 1.1 ± 0.48%/mm Hg in patients with passive HFpEF to 0.62 ± 0.32%/mm Hg in exercise PH, 0.54 ± 0.27%/mm Hg in HFpEF with high exercise PVR, and 0.18 ± 0.16%/mm Hg in PAH. On multivariate analysis, PV distensibility was associated with decreased Ees/Ea and maximal volume of oxygen consumed.
PV distensibility is an early and sensitive hemodynamic marker of PV disease that is associated with RV-PA uncoupling and decreased aerobic exercise capacity. |
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AbstractList | Exercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea, including pulmonary hypertension (PH) and/or heart failure with preserved ejection fraction (HFpEF). We investigated rest and exercise invasive pulmonary hemodynamics, ventilation, and gas exchange in patients with unexplained dyspnea, including 44 patients with HFpEF (of whom 20 had a normal pulmonary vascular resistance [PVR] during exercise [ie, passive HFpEF] and 24 had a higher than normal exercise PVR), 22 patients with exercise PH, 19 patients with pulmonary arterial hypertension (PAH), and 24 age- and sex-matched normal control subjects.
A PV distensibility coefficient α (%/mm Hg) was determined from multipoint PV pressure-flow plots. RV-PA coupling was quantified from the analysis of RV pressure curves to determine ratios of end-systolic to arterial elastances (Ees/Ea). Aerobic exercise capacity was estimated by peak oxygen consumption.
The α coefficient decreased from 1.35 ± 0.58%/mm Hg in control subjects and 1.1 ± 0.48%/mm Hg in patients with passive HFpEF to 0.62 ± 0.32%/mm Hg in exercise PH, 0.54 ± 0.27%/mm Hg in HFpEF with high exercise PVR, and 0.18 ± 0.16%/mm Hg in PAH. On multivariate analysis, PV distensibility was associated with decreased Ees/Ea and maximal volume of oxygen consumed.
PV distensibility is an early and sensitive hemodynamic marker of PV disease that is associated with RV-PA uncoupling and decreased aerobic exercise capacity. Exercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea, including pulmonary hypertension (PH) and/or heart failure with preserved ejection fraction (HFpEF). We investigated rest and exercise invasive pulmonary hemodynamics, ventilation, and gas exchange in patients with unexplained dyspnea, including 44 patients with HFpEF (of whom 20 had a normal pulmonary vascular resistance [PVR] during exercise [ie, passive HFpEF] and 24 had a higher than normal exercise PVR), 22 patients with exercise PH, 19 patients with pulmonary arterial hypertension (PAH), and 24 age- and sex-matched normal control subjects.BACKGROUNDExercise stress testing of the pulmonary circulation may uncover decreased pulmonary vascular (PV) distensibility as a cause of impaired aerobic exercise capacity and right ventricular (RV)-pulmonary arterial (PA) uncoupling. As such, it may help in the differential diagnosis of unexplained dyspnea, including pulmonary hypertension (PH) and/or heart failure with preserved ejection fraction (HFpEF). We investigated rest and exercise invasive pulmonary hemodynamics, ventilation, and gas exchange in patients with unexplained dyspnea, including 44 patients with HFpEF (of whom 20 had a normal pulmonary vascular resistance [PVR] during exercise [ie, passive HFpEF] and 24 had a higher than normal exercise PVR), 22 patients with exercise PH, 19 patients with pulmonary arterial hypertension (PAH), and 24 age- and sex-matched normal control subjects.A PV distensibility coefficient α (%/mm Hg) was determined from multipoint PV pressure-flow plots. RV-PA coupling was quantified from the analysis of RV pressure curves to determine ratios of end-systolic to arterial elastances (Ees/Ea). Aerobic exercise capacity was estimated by peak oxygen consumption.METHODSA PV distensibility coefficient α (%/mm Hg) was determined from multipoint PV pressure-flow plots. RV-PA coupling was quantified from the analysis of RV pressure curves to determine ratios of end-systolic to arterial elastances (Ees/Ea). Aerobic exercise capacity was estimated by peak oxygen consumption.The α coefficient decreased from 1.35 ± 0.58%/mm Hg in control subjects and 1.1 ± 0.48%/mm Hg in patients with passive HFpEF to 0.62 ± 0.32%/mm Hg in exercise PH, 0.54 ± 0.27%/mm Hg in HFpEF with high exercise PVR, and 0.18 ± 0.16%/mm Hg in PAH. On multivariate analysis, PV distensibility was associated with decreased Ees/Ea and maximal volume of oxygen consumed.RESULTSThe α coefficient decreased from 1.35 ± 0.58%/mm Hg in control subjects and 1.1 ± 0.48%/mm Hg in patients with passive HFpEF to 0.62 ± 0.32%/mm Hg in exercise PH, 0.54 ± 0.27%/mm Hg in HFpEF with high exercise PVR, and 0.18 ± 0.16%/mm Hg in PAH. On multivariate analysis, PV distensibility was associated with decreased Ees/Ea and maximal volume of oxygen consumed.PV distensibility is an early and sensitive hemodynamic marker of PV disease that is associated with RV-PA uncoupling and decreased aerobic exercise capacity.CONCLUSIONSPV distensibility is an early and sensitive hemodynamic marker of PV disease that is associated with RV-PA uncoupling and decreased aerobic exercise capacity. |
Author | Oliveira, Rudolf K.F. Singh, Inderjit Oldham, William M. Systrom, David M. Waxman, Aaron B. Rahaghi, Farbod N. Naeije, Robert |
Author_xml | – sequence: 1 givenname: Inderjit surname: Singh fullname: Singh, Inderjit organization: Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Yale New Haven Hospital and Yale School of Medicine, New Haven, CT – sequence: 2 givenname: Rudolf K.F. surname: Oliveira fullname: Oliveira, Rudolf K.F. organization: Division of Respiratory Medicine, Federal University of São Paulo - UNIFESP, São Paulo, Brazil – sequence: 3 givenname: Robert surname: Naeije fullname: Naeije, Robert organization: Department of Pathophysiology, Faculty of Medicine, Erasme Campus, Université Libre de Bruxelles, Brussels, Belgium – sequence: 4 givenname: Farbod N. surname: Rahaghi fullname: Rahaghi, Farbod N. organization: Division of Pulmonary and Critical Care, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA – sequence: 5 givenname: William M. surname: Oldham fullname: Oldham, William M. organization: Division of Pulmonary and Critical Care, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA – sequence: 6 givenname: David M. surname: Systrom fullname: Systrom, David M. organization: Division of Pulmonary and Critical Care, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA – sequence: 7 givenname: Aaron B. surname: Waxman fullname: Waxman, Aaron B. email: abwaxman@bwh.harvard.edu organization: Division of Pulmonary and Critical Care, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA |
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Keywords | mPAP RV PV HR HFpEF RHC PVR AUC TPR ePH pulmonary arterial hypertension WU heart failure iCPET RV-PA coupling SV CO HFpEF+PVR PAWP PA RV-PA Ees PAC pulmonary vascular distensibility PAH exercise capacity PH Vo2 Ea |
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SubjectTerms | Adult Aged Aged, 80 and over exercise capacity Exercise Tolerance Female heart failure Heart Failure - complications Heart Failure - physiopathology Humans Hypertension, Pulmonary - complications Hypertension, Pulmonary - physiopathology Male pulmonary arterial hypertension Pulmonary Artery - pathology Pulmonary Artery - physiopathology pulmonary vascular distensibility Retrospective Studies RV-PA coupling Stroke Volume Vascular Remodeling Ventricular Dysfunction, Right - complications Ventricular Dysfunction, Right - physiopathology |
Title | Pulmonary Vascular Distensibility and Early Pulmonary Vascular Remodeling in Pulmonary Hypertension |
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