Comprehensive Physiology Wiley Online Library

Imaging in Pulmonary Vascular Disease—Understanding Right Ventricle‐Pulmonary Artery Coupling

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Abstract

The right ventricle (RV) and pulmonary arterial (PA) tree are inextricably linked, continually transferring energy back and forth in a process known as RV‐PA coupling. Healthy organisms maintain this relationship in optimal balance by modulating RV contractility, pulmonary vascular resistance, and compliance to sustain RV‐PA coupling through life's many physiologic challenges. Early in states of adaptation to cardiovascular disease—for example, in diastolic heart failure—RV‐PA coupling is maintained via a multitude of cellular and mechanical transformations. However, with disease progression, these compensatory mechanisms fail and become maladaptive, leading to the often‐fatal state of “uncoupling.” Noninvasive imaging modalities, including echocardiography, magnetic resonance imaging, and computed tomography, allow us deeper insight into the state of coupling for an individual patient, providing for prognostication and potential intervention before uncoupling occurs. In this review, we discuss the physiologic foundations of RV‐PA coupling, elaborate on the imaging techniques to qualify and quantify it, and correlate these fundamental principles with clinical scenarios in health and disease. © 2022 American Physiological Society. Compr Physiol 12: 3705–3730, 2022.

Figure 1. Figure 1. Normal right ventricular pressure‐volume loop.
Figure 2. Figure 2. Sequential right ventricular pressure‐volume loops at decreasing preload, as in vena caval occlusion. SV, stroke volume; ESPVR, end‐systolic pressure‐volume relationship; Ea, artrial elastance; Ees, end‐systolic elastance; Pes, end‐systolic pressure.
Figure 3. Figure 3. Resistance × compliance time curve, where C, compliance; R, resistance; τ, RC time constant. Reproduced, with permission, Lankhaar J‐W, et al., 2008 58, Oxford University Press.
Figure 4. Figure 4. RV‐PV loops at sequentially increasing exercise in a healthy individual.
Figure 5. Figure 5. Model for progression to RV failure with decreased pulmonary arterial compliance. Reproduced, with permission, from Thenappan T, et al., 2016 100, American Thoracic Society. © 2021 American Thoracic Society. All rights reserved. Annals of the American Thoracic Society is an official journal of the American Thoracic Society.
Figure 6. Figure 6. Reduction of preload in heart failure with preserved ejection fraction (HFpEF; left column) and controls (middle column) to determine load‐independent markers of contractility (Ees slope) and stiffness (β; right column). Ees, end‐systolic elastance. Reproduced, with permission, from Pantoja JL, et al., 2017 73, Wolters Kluwer Health, Inc.
Figure 7. Figure 7. Natural history of pulmonary hypertension. CO, cardiac output; NYHA, New York Heart Association functional class; PAP, pulmonary arterial pressure; PVR, pulmonary vascular resistence.
Figure 8. Figure 8. Transthoracic echocardiography in short‐axis view showing systolic flattening of the interventricular septum (D‐shaped septum) consistent with RV pressure overload.
Figure 9. Figure 9. M‐Mode measurement of the tricuspid annular plane systolic excursion (TAPSE) showing reduced value in patient with PH.
Figure 10. Figure 10. Tissue Doppler imaging of the tricuspid annulus in a patient with reduced RV systolic function.
Figure 11. Figure 11. Transthoracic echocardiography in apical four‐chamber view showing dilated RV with reduced fractional area change (FAC). FAC is measured as end‐diastolic area (A) minus end‐systolic area (B), divided by end‐diastolic area.
Figure 12. Figure 12. Calculation of the right ventricular index of myocardial performance (RIMP) from the lateral tricuspid annular tissue Doppler recording. Y marks the duration of ejection time. X marks the total interval during which the tricuspid valve is closed, which is the sum of isovolumic contraction, ejection time, and isovolumic relaxation. RIMP is then calculated using formula (X−Y)/Y.
Figure 13. Figure 13. Longitudinal strain of the RV free wall and the global RV assessed by speckle tracking from transthoracic echocardiogram showing abnormally low values.
Figure 14. Figure 14. Pulse wave Doppler (PW) recording in the RVOT demonstrating notching of the PW signal and short acceleration time indicating elevated PA pressure.
Figure 15. Figure 15. (A) Continuous wave (CW) Doppler recording through the tricuspid valve in apical four‐chamber view showing increased peak tricuspid regurgitation velocity and elevated RVSP. (B) CW Doppler through the pulmonic valve showing significant pulmonic regurgitation. Note increased early diastolic pulmonic regurgitation velocity indicating elevated mPAP and increased end‐diastolic regurgitation velocity indicating elevated PADP.
Figure 16. Figure 16. Pulse wave (PW) Doppler recording of the hepatic veins. Prominent diastolic flow suggesting elevated RAP.
Figure 17. Figure 17. End‐diastolic (A and C) and end‐systolic (B and D) still frames of cardiac MRI SSFP cine images showing severe dilation of RV and RA, as well as prominent flattening of the interventricular septum with leftward shifting in systole.
Figure 18. Figure 18. Cardiac MRI feature tracking RV free wall longitudinal strain (FT‐FWLS). RV endocardial and epicardial borders are defined manually for one cine frame, followed by automated tracking of myocardial displacement during the rest of the cardiac cycle. Peak FT‐FWLS of −8% in this PH patient suggests RV dysfunction.
Figure 19. Figure 19. Cardiac MRI phase‐sensitive inversion recovery (PSIR) image in short axis view showing mid‐wall delayed gadolinium enhancement of the LV at the RV insertion points in a patient with PH.
Figure 20. Figure 20. The arterial Windkessel. Reproduced, with permission, from Tsuchiya N., et al., 2018 102, from Springer Nature.
Figure 21. Figure 21. Circuit diagram of the pulmonary vasculature. L_MainPA, impedance of the main pulmonary artery; R_MainPA, resistance of the main pulmonary artery; L_Artery, lumped impedance of the peripheral pulmonary vasculature; R_Artery_Cp_Composite, lumped resistance of the peripheral pulmonary vasculature; R_Vn, pulmonary venous resistance; C_MainPA, main pulmonary artery compliance; C_Artery, lumped compliance of the peripheral pulmonary vasculature; C_Vn, pulmonary venous compliance.
Figure 22. Figure 22. Flow diagram of linked finite element model with 0‐D lumped parameter model of the pulmonary circulation. LV, left ventricle; RV, right ventricle; VCO, vena caval occlusion; PAC, pulmonary artery constriction. Reproduced, with permission, from Wenk JF, et al., 2013 109, Taylor & Francis Ltd.
Figure 23. Figure 23. Stress at end‐diastole in the myofiber direction 10 mm below the ventricular base in canine hearts for (A) normal and (B) induced CHF/dilated cardiomyopathy model. Scale bar is in kiloPascals. Reproduced, with permission, from Wenk JF, et al., 2013 109, Taylor & Francis Ltd.
Figure 24. Figure 24. Sequential RV PV loops during simulated pulmonary arterial constriction, created using the OD model in Figure 21.


Figure 1. Normal right ventricular pressure‐volume loop.


Figure 2. Sequential right ventricular pressure‐volume loops at decreasing preload, as in vena caval occlusion. SV, stroke volume; ESPVR, end‐systolic pressure‐volume relationship; Ea, artrial elastance; Ees, end‐systolic elastance; Pes, end‐systolic pressure.


Figure 3. Resistance × compliance time curve, where C, compliance; R, resistance; τ, RC time constant. Reproduced, with permission, Lankhaar J‐W, et al., 2008 58, Oxford University Press.


Figure 4. RV‐PV loops at sequentially increasing exercise in a healthy individual.


Figure 5. Model for progression to RV failure with decreased pulmonary arterial compliance. Reproduced, with permission, from Thenappan T, et al., 2016 100, American Thoracic Society. © 2021 American Thoracic Society. All rights reserved. Annals of the American Thoracic Society is an official journal of the American Thoracic Society.


Figure 6. Reduction of preload in heart failure with preserved ejection fraction (HFpEF; left column) and controls (middle column) to determine load‐independent markers of contractility (Ees slope) and stiffness (β; right column). Ees, end‐systolic elastance. Reproduced, with permission, from Pantoja JL, et al., 2017 73, Wolters Kluwer Health, Inc.


Figure 7. Natural history of pulmonary hypertension. CO, cardiac output; NYHA, New York Heart Association functional class; PAP, pulmonary arterial pressure; PVR, pulmonary vascular resistence.


Figure 8. Transthoracic echocardiography in short‐axis view showing systolic flattening of the interventricular septum (D‐shaped septum) consistent with RV pressure overload.


Figure 9. M‐Mode measurement of the tricuspid annular plane systolic excursion (TAPSE) showing reduced value in patient with PH.


Figure 10. Tissue Doppler imaging of the tricuspid annulus in a patient with reduced RV systolic function.


Figure 11. Transthoracic echocardiography in apical four‐chamber view showing dilated RV with reduced fractional area change (FAC). FAC is measured as end‐diastolic area (A) minus end‐systolic area (B), divided by end‐diastolic area.


Figure 12. Calculation of the right ventricular index of myocardial performance (RIMP) from the lateral tricuspid annular tissue Doppler recording. Y marks the duration of ejection time. X marks the total interval during which the tricuspid valve is closed, which is the sum of isovolumic contraction, ejection time, and isovolumic relaxation. RIMP is then calculated using formula (X−Y)/Y.


Figure 13. Longitudinal strain of the RV free wall and the global RV assessed by speckle tracking from transthoracic echocardiogram showing abnormally low values.


Figure 14. Pulse wave Doppler (PW) recording in the RVOT demonstrating notching of the PW signal and short acceleration time indicating elevated PA pressure.


Figure 15. (A) Continuous wave (CW) Doppler recording through the tricuspid valve in apical four‐chamber view showing increased peak tricuspid regurgitation velocity and elevated RVSP. (B) CW Doppler through the pulmonic valve showing significant pulmonic regurgitation. Note increased early diastolic pulmonic regurgitation velocity indicating elevated mPAP and increased end‐diastolic regurgitation velocity indicating elevated PADP.


Figure 16. Pulse wave (PW) Doppler recording of the hepatic veins. Prominent diastolic flow suggesting elevated RAP.


Figure 17. End‐diastolic (A and C) and end‐systolic (B and D) still frames of cardiac MRI SSFP cine images showing severe dilation of RV and RA, as well as prominent flattening of the interventricular septum with leftward shifting in systole.


Figure 18. Cardiac MRI feature tracking RV free wall longitudinal strain (FT‐FWLS). RV endocardial and epicardial borders are defined manually for one cine frame, followed by automated tracking of myocardial displacement during the rest of the cardiac cycle. Peak FT‐FWLS of −8% in this PH patient suggests RV dysfunction.


Figure 19. Cardiac MRI phase‐sensitive inversion recovery (PSIR) image in short axis view showing mid‐wall delayed gadolinium enhancement of the LV at the RV insertion points in a patient with PH.


Figure 20. The arterial Windkessel. Reproduced, with permission, from Tsuchiya N., et al., 2018 102, from Springer Nature.


Figure 21. Circuit diagram of the pulmonary vasculature. L_MainPA, impedance of the main pulmonary artery; R_MainPA, resistance of the main pulmonary artery; L_Artery, lumped impedance of the peripheral pulmonary vasculature; R_Artery_Cp_Composite, lumped resistance of the peripheral pulmonary vasculature; R_Vn, pulmonary venous resistance; C_MainPA, main pulmonary artery compliance; C_Artery, lumped compliance of the peripheral pulmonary vasculature; C_Vn, pulmonary venous compliance.


Figure 22. Flow diagram of linked finite element model with 0‐D lumped parameter model of the pulmonary circulation. LV, left ventricle; RV, right ventricle; VCO, vena caval occlusion; PAC, pulmonary artery constriction. Reproduced, with permission, from Wenk JF, et al., 2013 109, Taylor & Francis Ltd.


Figure 23. Stress at end‐diastole in the myofiber direction 10 mm below the ventricular base in canine hearts for (A) normal and (B) induced CHF/dilated cardiomyopathy model. Scale bar is in kiloPascals. Reproduced, with permission, from Wenk JF, et al., 2013 109, Taylor & Francis Ltd.


Figure 24. Sequential RV PV loops during simulated pulmonary arterial constriction, created using the OD model in Figure 21.
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Katsiaryna Tsarova, Ashley E. Morgan, Lana Melendres‐Groves, Majd M. Ibrahim, Christy L. Ma, Irene Z. Pan, Nathan D. Hatton, Emily M. Beck, Meganne N. Ferrel, Craig H. Selzman, Dominique Ingram, Ayedh K. Alamri, Mark B. Ratcliffe, Brent D. Wilson, John J. Ryan. Imaging in Pulmonary Vascular Disease—Understanding Right Ventricle‐Pulmonary Artery Coupling. Compr Physiol 2022, 12: 3705-3730. doi: 10.1002/cphy.c210017