Right ventricular dysfunction in left-sided heart failure with preserved versus reduced ejection fraction

Lena Bosch; Carolyn S.P. Lam; Lingli Gong; Siew Pang Chan; David Sim; Daniel Yeo; Fazlur Jaufeerally; Kui Toh Gerard Leong; Hean Yee Ong; Tze Pin Ng; Arthur Mark Richards; Fatih Arslan; Lieng H. Ling

doi:10.1002/ejhf.873

Right ventricular dysfunction in left-sided heart failure with preserved versus reduced ejection fraction

Lena Bosch, Carolyn S.P. Lam, Lingli Gong, Siew Pang Chan, David Sim, Daniel Yeo, Fazlur Jaufeerally, Kui Toh Gerard Leong, Hean Yee Ong, Tze Pin Ng, Arthur Mark Richards, Fatih Arslan, Lieng H. Ling^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

7 Citations (Scopus)

Abstract

Background: Right ventricular (RV) dysfunction is recognized as a major prognostic factor in left-sided heart failure (HF). However, the relative contribution of RV dysfunction in HF with preserved (HFpEF) vs. reduced ejection fraction (HFrEF) is unclear. Methods and results: Right ventricular longitudinal strain (RVLS), tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) were determined by echocardiography in 657 age- and gender-matched groups of patients with HFpEF [left ventricular ejection fraction (LVEF) ≥50%; n=219] and HFrEF (LVEF <50%; n=219) and in controls without HF (n=219) from an Asian population-based cohort study. Across control to HFpEF and HFrEF groups, RV function deteriorated as measured by RVLS (−26.7 ± 5%, −22.7±6.6% and −18.2 ± 6.7%, respectively) and TAPSE (21.0 ± 3.9, 17.5 ± 5.1 and 14.7 ± 4.7 mm, respectively), whereas PASP increased (26.8 ± 7.1, 34.5 ± 11.9 and 39.3 ± 16.2 mmHg, respectively) (all P<0.001). Controlling for PASP in control, HFpEF and HFrEF subjects, the magnitude of RVLS/PASP (−1.06 ± 0.32, −0.75 ± 0.32 and −0.56 ± 0.36, respectively) and TAPSE/PASP ratios (0.83 ± 0.23, 0.54 ± 0.24 and 0.55 ± 0.29, respectively) similarly decreased across groups. Right ventricular dysfunction (by both TAPSE and RVLS) was independently associated with left ventricular systolic dysfunction and atrial fibrillation, but not with PASP. Among patients with HF, both TAPSE/PASP and RVLS/PASP ratios were related to the composite endpoint of all-cause death and HF hospitalization, even after multivariable adjustment [hazard ratio (HR) 0.33; 95% confidence interval (CI) 0.14–0.74 and HR 3.09; 95% CI 1.52–6.26, respectively], with no difference between HFrEF and HFpEF. Conclusions: Right ventricular dysfunction is present in HFpEF and is even more pronounced in HFrEF for any given degree of pulmonary hypertension. It is independently predicted by left ventricular dysfunction but not by PASP. Right ventricular–arterial coupling is prognostically important in HF regardless of LVEF.

Original language	English
Pages (from-to)	1664-1671
Number of pages	8
Journal	European Journal of Heart Failure
Volume	19
Issue number	12
DOIs	https://doi.org/10.1002/ejhf.873
Publication status	Published - 1 Dec 2017

Keywords

Deformation imaging
Echocardiography
Heart failure
Preserved ejection fraction
Pulmonary hypertension
Right ventricular dysfunction

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10.1002/ejhf.873

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@article{8cdd7e19ace14ccd9be99353d44c6acc,

title = "Right ventricular dysfunction in left-sided heart failure with preserved versus reduced ejection fraction",

abstract = "Background: Right ventricular (RV) dysfunction is recognized as a major prognostic factor in left-sided heart failure (HF). However, the relative contribution of RV dysfunction in HF with preserved (HFpEF) vs. reduced ejection fraction (HFrEF) is unclear. Methods and results: Right ventricular longitudinal strain (RVLS), tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) were determined by echocardiography in 657 age- and gender-matched groups of patients with HFpEF [left ventricular ejection fraction (LVEF) ≥50%; n=219] and HFrEF (LVEF <50%; n=219) and in controls without HF (n=219) from an Asian population-based cohort study. Across control to HFpEF and HFrEF groups, RV function deteriorated as measured by RVLS (−26.7 ± 5%, −22.7±6.6% and −18.2 ± 6.7%, respectively) and TAPSE (21.0 ± 3.9, 17.5 ± 5.1 and 14.7 ± 4.7 mm, respectively), whereas PASP increased (26.8 ± 7.1, 34.5 ± 11.9 and 39.3 ± 16.2 mmHg, respectively) (all P<0.001). Controlling for PASP in control, HFpEF and HFrEF subjects, the magnitude of RVLS/PASP (−1.06 ± 0.32, −0.75 ± 0.32 and −0.56 ± 0.36, respectively) and TAPSE/PASP ratios (0.83 ± 0.23, 0.54 ± 0.24 and 0.55 ± 0.29, respectively) similarly decreased across groups. Right ventricular dysfunction (by both TAPSE and RVLS) was independently associated with left ventricular systolic dysfunction and atrial fibrillation, but not with PASP. Among patients with HF, both TAPSE/PASP and RVLS/PASP ratios were related to the composite endpoint of all-cause death and HF hospitalization, even after multivariable adjustment [hazard ratio (HR) 0.33; 95% confidence interval (CI) 0.14–0.74 and HR 3.09; 95% CI 1.52–6.26, respectively], with no difference between HFrEF and HFpEF. Conclusions: Right ventricular dysfunction is present in HFpEF and is even more pronounced in HFrEF for any given degree of pulmonary hypertension. It is independently predicted by left ventricular dysfunction but not by PASP. Right ventricular–arterial coupling is prognostically important in HF regardless of LVEF.",

keywords = "Deformation imaging, Echocardiography, Heart failure, Preserved ejection fraction, Pulmonary hypertension, Right ventricular dysfunction",

author = "Lena Bosch and Lam, {Carolyn S.P.} and Lingli Gong and Chan, {Siew Pang} and David Sim and Daniel Yeo and Fazlur Jaufeerally and Leong, {Kui Toh Gerard} and Ong, {Hean Yee} and Ng, {Tze Pin} and Richards, {Arthur Mark} and Fatih Arslan and Ling, {Lieng H.}",

note = "Funding Information: This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. Funding Information: This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. The authors would like to thank the clinicians, clinical research coordinators and sonographers in their institutions who assisted with the conduct of this study. This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. Publisher Copyright: {\textcopyright} 2017 The Authors. European Journal of Heart Failure {\textcopyright} 2017 European Society of Cardiology",

year = "2017",

month = dec,

day = "1",

doi = "10.1002/ejhf.873",

language = "English",

volume = "19",

pages = "1664--1671",

journal = "European Journal of Heart Failure",

issn = "1388-9842",

publisher = "Oxford University Press",

number = "12",

}

TY - JOUR

T1 - Right ventricular dysfunction in left-sided heart failure with preserved versus reduced ejection fraction

AU - Bosch, Lena

AU - Lam, Carolyn S.P.

AU - Gong, Lingli

AU - Chan, Siew Pang

AU - Sim, David

AU - Yeo, Daniel

AU - Jaufeerally, Fazlur

AU - Leong, Kui Toh Gerard

AU - Ong, Hean Yee

AU - Ng, Tze Pin

AU - Richards, Arthur Mark

AU - Arslan, Fatih

AU - Ling, Lieng H.

N1 - Funding Information: This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. Funding Information: This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. The authors would like to thank the clinicians, clinical research coordinators and sonographers in their institutions who assisted with the conduct of this study. This work was supported by a Centre Grant from the National Medical Research Council of Singapore (grant number R-172-003-2190511) and by the Alexandre Suerman MD/PhD programme from the UMC Utrecht. Conflict of interest: C.S.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Thermofisher, Medtronic, and Vifor Pharma; and has consulted for Bayer, Novartis, Takeda, Merck, Astra Zeneca, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim and Abbott Diagnostics. A.M.R is supported by a Senior Translational Research Award from the National Medical Research Council of Singapore and is Principal Investigator for the Centre Grant made to the National University Heart Centre, Singapore, which funded this study. He has consulted for, and received research support from, Bayer, Novartis, Merck, Medtronic, Pfizer, Boehringer Ingelheim, Astra Zeneca, Roche Diagnostics, Thermo Fisher, Alere, Critical Diagnostics, and Abbott Diagnostics. All other authors have no conflicts of interest to declare. Publisher Copyright: © 2017 The Authors. European Journal of Heart Failure © 2017 European Society of Cardiology

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Background: Right ventricular (RV) dysfunction is recognized as a major prognostic factor in left-sided heart failure (HF). However, the relative contribution of RV dysfunction in HF with preserved (HFpEF) vs. reduced ejection fraction (HFrEF) is unclear. Methods and results: Right ventricular longitudinal strain (RVLS), tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) were determined by echocardiography in 657 age- and gender-matched groups of patients with HFpEF [left ventricular ejection fraction (LVEF) ≥50%; n=219] and HFrEF (LVEF <50%; n=219) and in controls without HF (n=219) from an Asian population-based cohort study. Across control to HFpEF and HFrEF groups, RV function deteriorated as measured by RVLS (−26.7 ± 5%, −22.7±6.6% and −18.2 ± 6.7%, respectively) and TAPSE (21.0 ± 3.9, 17.5 ± 5.1 and 14.7 ± 4.7 mm, respectively), whereas PASP increased (26.8 ± 7.1, 34.5 ± 11.9 and 39.3 ± 16.2 mmHg, respectively) (all P<0.001). Controlling for PASP in control, HFpEF and HFrEF subjects, the magnitude of RVLS/PASP (−1.06 ± 0.32, −0.75 ± 0.32 and −0.56 ± 0.36, respectively) and TAPSE/PASP ratios (0.83 ± 0.23, 0.54 ± 0.24 and 0.55 ± 0.29, respectively) similarly decreased across groups. Right ventricular dysfunction (by both TAPSE and RVLS) was independently associated with left ventricular systolic dysfunction and atrial fibrillation, but not with PASP. Among patients with HF, both TAPSE/PASP and RVLS/PASP ratios were related to the composite endpoint of all-cause death and HF hospitalization, even after multivariable adjustment [hazard ratio (HR) 0.33; 95% confidence interval (CI) 0.14–0.74 and HR 3.09; 95% CI 1.52–6.26, respectively], with no difference between HFrEF and HFpEF. Conclusions: Right ventricular dysfunction is present in HFpEF and is even more pronounced in HFrEF for any given degree of pulmonary hypertension. It is independently predicted by left ventricular dysfunction but not by PASP. Right ventricular–arterial coupling is prognostically important in HF regardless of LVEF.

AB - Background: Right ventricular (RV) dysfunction is recognized as a major prognostic factor in left-sided heart failure (HF). However, the relative contribution of RV dysfunction in HF with preserved (HFpEF) vs. reduced ejection fraction (HFrEF) is unclear. Methods and results: Right ventricular longitudinal strain (RVLS), tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) were determined by echocardiography in 657 age- and gender-matched groups of patients with HFpEF [left ventricular ejection fraction (LVEF) ≥50%; n=219] and HFrEF (LVEF <50%; n=219) and in controls without HF (n=219) from an Asian population-based cohort study. Across control to HFpEF and HFrEF groups, RV function deteriorated as measured by RVLS (−26.7 ± 5%, −22.7±6.6% and −18.2 ± 6.7%, respectively) and TAPSE (21.0 ± 3.9, 17.5 ± 5.1 and 14.7 ± 4.7 mm, respectively), whereas PASP increased (26.8 ± 7.1, 34.5 ± 11.9 and 39.3 ± 16.2 mmHg, respectively) (all P<0.001). Controlling for PASP in control, HFpEF and HFrEF subjects, the magnitude of RVLS/PASP (−1.06 ± 0.32, −0.75 ± 0.32 and −0.56 ± 0.36, respectively) and TAPSE/PASP ratios (0.83 ± 0.23, 0.54 ± 0.24 and 0.55 ± 0.29, respectively) similarly decreased across groups. Right ventricular dysfunction (by both TAPSE and RVLS) was independently associated with left ventricular systolic dysfunction and atrial fibrillation, but not with PASP. Among patients with HF, both TAPSE/PASP and RVLS/PASP ratios were related to the composite endpoint of all-cause death and HF hospitalization, even after multivariable adjustment [hazard ratio (HR) 0.33; 95% confidence interval (CI) 0.14–0.74 and HR 3.09; 95% CI 1.52–6.26, respectively], with no difference between HFrEF and HFpEF. Conclusions: Right ventricular dysfunction is present in HFpEF and is even more pronounced in HFrEF for any given degree of pulmonary hypertension. It is independently predicted by left ventricular dysfunction but not by PASP. Right ventricular–arterial coupling is prognostically important in HF regardless of LVEF.

KW - Deformation imaging

KW - Echocardiography

KW - Heart failure

KW - Preserved ejection fraction

KW - Pulmonary hypertension

KW - Right ventricular dysfunction

UR - http://www.scopus.com/inward/record.url?scp=85020439874&partnerID=8YFLogxK

U2 - 10.1002/ejhf.873

DO - 10.1002/ejhf.873

M3 - Article

AN - SCOPUS:85020439874

SN - 1388-9842

VL - 19

SP - 1664

EP - 1671

JO - European Journal of Heart Failure

JF - European Journal of Heart Failure

IS - 12

ER -

Right ventricular dysfunction in left-sided heart failure with preserved versus reduced ejection fraction

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