Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction

Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Methods and re...

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Veröffentlicht in:	European journal of heart failure Jg. 15; H. 7; S. 776 - 785
Hauptverfasser:	Abudiab, Muaz M., Redfield, Margaret M., Melenovsky, Vojtech, Olson, Thomas P., Kass, David A., Johnson, Bruce D., Borlaug, Barry A.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England Blackwell Publishing Ltd 01.07.2013 Oxford University Press
Schlagworte:	Aged Cardiac output Cardiac Output - physiology Diastolic heart failure Exercise Exercise Physiology Exercise Test Exercise Tolerance - physiology Female Follow-Up Studies Heart Failure - metabolism Heart Failure - physiopathology Heart rate Humans Male Middle Aged Oxygen - metabolism Oxygen consumption Oxygen Consumption - physiology Prognosis Retrospective Studies Stroke volume Stroke Volume - physiology Ventricular Function, Left - physiology Heart rate Diastolic heart failure Oxygen consumption Exercise Cardiac output Stroke volume
ISSN:	1388-9842, 1879-0844, 1879-0844
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Abstract	Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Methods and results Patients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non‐invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial–venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial–venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually. Conclusion While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.
AbstractList	Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF.AIMSExercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF.Patients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non-invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial-venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial-venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually.METHODS AND RESULTSPatients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non-invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial-venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial-venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually.While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.CONCLUSIONWhile diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs. Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Patients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non-invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial-venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial-venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually. While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs. Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Methods and results Patients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non‐invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial–venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial–venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P < 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually. Conclusion While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.
Author	Abudiab, Muaz M. Olson, Thomas P. Johnson, Bruce D. Kass, David A. Borlaug, Barry A. Melenovsky, Vojtech Redfield, Margaret M.
AuthorAffiliation	3 Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA 1 Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA 2 Department of Cardiology, Institute of Clinical and Experimental Medicine-IKEM, Prague, Czech Republic
AuthorAffiliation_xml	– name: 3 Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA – name: 1 Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA – name: 2 Department of Cardiology, Institute of Clinical and Experimental Medicine-IKEM, Prague, Czech Republic
Author_xml	– sequence: 1 givenname: Muaz M. surname: Abudiab fullname: Abudiab, Muaz M. organization: Division of Cardiovascular Diseases, Mayo Clinic, MN, Rochester, USA – sequence: 2 givenname: Margaret M. surname: Redfield fullname: Redfield, Margaret M. organization: Division of Cardiovascular Diseases, Mayo Clinic, MN, Rochester, USA – sequence: 3 givenname: Vojtech surname: Melenovsky fullname: Melenovsky, Vojtech organization: Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA – sequence: 4 givenname: Thomas P. surname: Olson fullname: Olson, Thomas P. organization: Division of Cardiovascular Diseases, Mayo Clinic, MN, Rochester, USA – sequence: 5 givenname: David A. surname: Kass fullname: Kass, David A. organization: Division of Cardiology, Johns Hopkins Medical Institutions, MD, Baltimore, USA – sequence: 6 givenname: Bruce D. surname: Johnson fullname: Johnson, Bruce D. organization: Division of Cardiovascular Diseases, Mayo Clinic, MN, Rochester, USA – sequence: 7 givenname: Barry A. surname: Borlaug fullname: Borlaug, Barry A. email: borlaug.barry@mayo.edu organization: Division of Cardiovascular Diseases, Mayo Clinic, MN, Rochester, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/23426022$$D View this record in MEDLINE/PubMed
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Copyright	Published on behalf of the European Society of Cardiology. All rights reserved. © 2013 the Authors Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2013. For permissions please email: journals.permissions@oup.com. 2013
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References_xml	– reference: Paulus WJ Tschope C Sanderson JE Rusconi C Flachskampf FA Rademakers FE Marino P Smiseth OA De Keulenaer G Leite-Moreira AF Borbely A Edes I Handoko ML Heymans S Pezzali N Pieske B Dickstein K Fraser AG Brutsaert DL How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology Eur Heart J 2007 28 2539 2550 – reference: Segers P Stergiopulos N Westerhof N Relation of effective arterial elastance to arterial system properties Am J Physiol Heart Circ Physiol 2002 282 H1041 H1046 – reference: Denolin H Kuhn H Krayenbuehl HP Loogen F Reale A The definition of heart failure Eur Heart J 1983 4 445 448 – reference: Abel FL Waldhausen JA Effects of alterations in pulmonary vascular resistance on right ventricular function J Thorac Cardiovasc Surg 1967 54 886 894 – reference: Kitzman DW Higginbotham MB Cobb FR Sheikh KH Sullivan MJ Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism J Am Coll Cardiol 1991 17 1065 1072 – reference: Tedford RJ Hassoun PM Mathai SC Girgis RE Russell SD Thiemann DR Cingolani OH Mudd JO Borlaug BA Redfield MM Lederer DJ Kass DA Pulmonary capillary wedge pressure augments right ventricular pulsatile loading Circulation 2012 125 289 297 – reference: Kitzman DW Brubaker PH Morgan TM Stewart KP Little WC Exercise training in older patients with heart failure and preserved ejection fraction: a randomized, controlled, single-blind trial Circ Heart Fail 2010 3 659 667 – reference: Tan YT Wenzelburger F Lee E Heatlie G Leyva F Patel K Frenneaux M Sanderson JE The pathophysiology of heart failure with normal ejection fraction: exercise echocardiography reveals complex abnormalities of both systolic and diastolic ventricular function involving torsion, untwist, and longitudinal motion J Am Coll Cardiol 2009 54 36 46 – reference: Lang CC Agostoni P Mancini DM Prognostic significance and measurement of exercise-derived hemodynamic variables in patients with heart failure J Card Fail 2007 13 672 679 – reference: Phan TT Abozguia K Nallur Shivu G Mahadevan G Ahmed I Williams L Dwivedi G Patel K Steendijk P Ashrafian H Henning A Frenneaux M Heart failure with preserved ejection fraction is characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency J Am Coll Cardiol 2009 54 402 409 – reference: McMurray JJ Adamopoulos S Anker SD Auricchio A Bohm M Dickstein K Falk V Filippatos G Fonseca C Gomez-Sanchez MA Jaarsma T Kober L Lip GY Maggioni AP Parkhomenko A Pieske BM Popescu BA Ronnevik PK Rutten FH Schwitter J Seferovic P Stepinska J Trindade PT Voors AA Zannad F Zeiher A Bax JJ Baumgartner H Ceconi C Dean V Deaton C Fagard R Funck-Brentano C Hasdai D Hoes A Kirchhof P Knuuti J Kolh P McDonagh T Moulin C Reiner Z Sechtem U Sirnes PA Tendera M Torbicki A Vahanian A Windecker S Bonet LA Avraamides P Ben Lamin HA Brignole M Coca A Cowburn P Dargie H Elliott P Flachskampf FA Guida GF Hardman S Iung B Merkely B Mueller C Nanas JN Nielsen OW Orn S Parissis JT Ponikowski PESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of CardiologyDeveloped in collaboration with the Heart Failure Association (HFA) of the ESC Eur J Heart Fail 2012 14 803 869 – reference: Maeder MT Thompson BR Brunner-La Rocca HP Kaye DM Hemodynamic basis of exercise limitation in patients with heart failure and normal ejection fraction J Am Coll Cardiol 2010 56 855 863 – reference: Di Salvo TG Mathier M Semigran MJ Dec GW Preserved right ventricular ejection fraction predicts exercise capacity and survival in advanced heart 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Snippet	Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought... Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to...
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SubjectTerms	Aged Cardiac output Cardiac Output - physiology Diastolic heart failure Exercise Exercise Physiology Exercise Test Exercise Tolerance - physiology Female Follow-Up Studies Heart Failure - metabolism Heart Failure - physiopathology Heart rate Humans Male Middle Aged Oxygen - metabolism Oxygen consumption Oxygen Consumption - physiology Prognosis Retrospective Studies Stroke volume Stroke Volume - physiology Ventricular Function, Left - physiology
Title	Cardiac output response to exercise in relation to metabolic demand in heart failure with preserved ejection fraction
URI	https://api.istex.fr/ark:/67375/WNG-NL6CBH36-5/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1093%2Feurjhf%2Fhft026 https://www.ncbi.nlm.nih.gov/pubmed/23426022 https://www.proquest.com/docview/1371268285 https://pubmed.ncbi.nlm.nih.gov/PMC3857919
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