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Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling

Deep phenotyping of pulmonary hypertension (PH) with multimodal diagnostic exercise interventions can lead to early focused therapeutic interventions. Herein, we report methods to simultaneously assess pulmonary impedance, differential biventricular myocardial strain, and right ventricular:pulmonary...

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Autores principales: Raza, Farhan, Kozitza, Callyn, Lechuga, Chris, Seiter, Daniel, Corrado, Philip, Merchant, Mohammed, Dharmavaram, Naga, Korcarz, Claudia, Eldridge, Marlowe, Francois, Christopher, Wieben, Oliver, Chesler, Naomi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228647/
https://www.ncbi.nlm.nih.gov/pubmed/35774590
http://dx.doi.org/10.1093/function/zqac022
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author Raza, Farhan
Kozitza, Callyn
Lechuga, Chris
Seiter, Daniel
Corrado, Philip
Merchant, Mohammed
Dharmavaram, Naga
Korcarz, Claudia
Eldridge, Marlowe
Francois, Christopher
Wieben, Oliver
Chesler, Naomi
author_facet Raza, Farhan
Kozitza, Callyn
Lechuga, Chris
Seiter, Daniel
Corrado, Philip
Merchant, Mohammed
Dharmavaram, Naga
Korcarz, Claudia
Eldridge, Marlowe
Francois, Christopher
Wieben, Oliver
Chesler, Naomi
author_sort Raza, Farhan
collection PubMed
description Deep phenotyping of pulmonary hypertension (PH) with multimodal diagnostic exercise interventions can lead to early focused therapeutic interventions. Herein, we report methods to simultaneously assess pulmonary impedance, differential biventricular myocardial strain, and right ventricular:pulmonary arterial (RV:PA) uncoupling during exercise, which we pilot in subjects with suspected PH. As proof-of-concept, we show that four subjects with different diagnoses [pulmonary arterial hypertension (PAH); chronic thromboembolic disease (CTEPH); PH due to heart failure with preserved ejection fraction (PH-HFpEF); and noncardiac dyspnea (NCD)] have distinct patterns of response to exercise. RV:PA coupling assessment with exercise was highest-to-lowest in this order: PAH > CTEPH > PH-HFpEF > NCD. Input impedance (Z(0)) with exercise was highest in precapillary PH (PAH, CTEPH), followed by PH-HFpEF and NCD. Characteristic impedance (Z(C)) tended to decline with exercise, except for the PH-HFpEF subject (initial Zc increase at moderate workload with subsequent decrease at higher workload with augmentation in cardiac output). Differential myocardial strain was normal in PAH, CTEPH, and NCD subjects and lower in the PH-HFpEF subject in the interventricular septum. The combination of these metrics allowed novel insights into mechanisms of RV:PA uncoupling. For example, while the PH-HFpEF subject had hemodynamics comparable to the NCD subject at rest, with exercise coupling dropped precipitously, which can be attributed (by decreased myocardial strain of interventricular septum) to poor support from the left ventricle (LV). We conclude that this deep phenotyping approach may distinguish afterload sensitive vs. LV-dependent mechanisms of RV:PA uncoupling in PH, which may lead to novel therapeutically relevant insights.
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spelling pubmed-92286472022-06-28 Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling Raza, Farhan Kozitza, Callyn Lechuga, Chris Seiter, Daniel Corrado, Philip Merchant, Mohammed Dharmavaram, Naga Korcarz, Claudia Eldridge, Marlowe Francois, Christopher Wieben, Oliver Chesler, Naomi Function (Oxf) Research Article Deep phenotyping of pulmonary hypertension (PH) with multimodal diagnostic exercise interventions can lead to early focused therapeutic interventions. Herein, we report methods to simultaneously assess pulmonary impedance, differential biventricular myocardial strain, and right ventricular:pulmonary arterial (RV:PA) uncoupling during exercise, which we pilot in subjects with suspected PH. As proof-of-concept, we show that four subjects with different diagnoses [pulmonary arterial hypertension (PAH); chronic thromboembolic disease (CTEPH); PH due to heart failure with preserved ejection fraction (PH-HFpEF); and noncardiac dyspnea (NCD)] have distinct patterns of response to exercise. RV:PA coupling assessment with exercise was highest-to-lowest in this order: PAH > CTEPH > PH-HFpEF > NCD. Input impedance (Z(0)) with exercise was highest in precapillary PH (PAH, CTEPH), followed by PH-HFpEF and NCD. Characteristic impedance (Z(C)) tended to decline with exercise, except for the PH-HFpEF subject (initial Zc increase at moderate workload with subsequent decrease at higher workload with augmentation in cardiac output). Differential myocardial strain was normal in PAH, CTEPH, and NCD subjects and lower in the PH-HFpEF subject in the interventricular septum. The combination of these metrics allowed novel insights into mechanisms of RV:PA uncoupling. For example, while the PH-HFpEF subject had hemodynamics comparable to the NCD subject at rest, with exercise coupling dropped precipitously, which can be attributed (by decreased myocardial strain of interventricular septum) to poor support from the left ventricle (LV). We conclude that this deep phenotyping approach may distinguish afterload sensitive vs. LV-dependent mechanisms of RV:PA uncoupling in PH, which may lead to novel therapeutically relevant insights. Oxford University Press 2022-04-30 /pmc/articles/PMC9228647/ /pubmed/35774590 http://dx.doi.org/10.1093/function/zqac022 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of American Physiological Society. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Research Article
Raza, Farhan
Kozitza, Callyn
Lechuga, Chris
Seiter, Daniel
Corrado, Philip
Merchant, Mohammed
Dharmavaram, Naga
Korcarz, Claudia
Eldridge, Marlowe
Francois, Christopher
Wieben, Oliver
Chesler, Naomi
Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title_full Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title_fullStr Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title_full_unstemmed Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title_short Multimodality Deep Phenotyping Methods to Assess Mechanisms of Poor Right Ventricular–Pulmonary Artery Coupling
title_sort multimodality deep phenotyping methods to assess mechanisms of poor right ventricular–pulmonary artery coupling
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228647/
https://www.ncbi.nlm.nih.gov/pubmed/35774590
http://dx.doi.org/10.1093/function/zqac022
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