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

Thanh T. Phan, Khalid Abozguia, Ganesh Nallur Shivu, Gnanadevan Mahadevan, Ibrar Ahmed, Lynne Williams, Girish Dwivedi, Kiran Patel, Paul Steendijk, Houman Ashrafian, Anke Henning, Michael Frenneaux

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Abstract

Objectives We sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients.

Background To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF.

Methods We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of P-31 magnetic resonance spectroscopy at 3-T.

Results When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).

Conclusions Patients with HFpEF have reduced cardiac energetic reserve that may underlie marked dynamic slowing of LV active relaxation and abnormal VVC during exercise. (J Am Coll Cardiol 2009; 54: 402-9) (C) 2009 by the American College of Cardiology Foundation

Original languageEnglish
Pages (from-to)402-409
Number of pages8
JournalJournal of the American College of Cardiology
Volume54
Issue number5
Early online date22 Jul 2009
DOIs
Publication statusPublished - 28 Jul 2009

Keywords

  • heart failure
  • diastole
  • radionuclide ventriculography
  • spectroscopy
  • exercise
  • troponin-I phosphorylation
  • magnetic-resonance spectroscopy
  • coronary-artery disease
  • diastolic dysfunction
  • hypertrophic cardiomyopathy
  • metabolic modulation
  • passive stiffness
  • cardiac troponin
  • stroke volume
  • filling rate

Cite this

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. / Phan, Thanh T.; Abozguia, Khalid; Shivu, Ganesh Nallur; Mahadevan, Gnanadevan; Ahmed, Ibrar; Williams, Lynne; Dwivedi, Girish; Patel, Kiran; Steendijk, Paul; Ashrafian, Houman; Henning, Anke; Frenneaux, Michael.

In: Journal of the American College of Cardiology, Vol. 54, No. 5, 28.07.2009, p. 402-409.

Research output: Contribution to journalArticle

Phan, Thanh T. ; Abozguia, Khalid ; Shivu, Ganesh Nallur ; Mahadevan, Gnanadevan ; Ahmed, Ibrar ; Williams, Lynne ; Dwivedi, Girish ; Patel, Kiran ; Steendijk, Paul ; Ashrafian, Houman ; Henning, Anke ; Frenneaux, Michael. / 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. In: Journal of the American College of Cardiology. 2009 ; Vol. 54, No. 5. pp. 402-409.
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title = "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",
abstract = "Objectives We sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients.Background To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF.Methods We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of P-31 magnetic resonance spectroscopy at 3-T.Results When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).Conclusions Patients with HFpEF have reduced cardiac energetic reserve that may underlie marked dynamic slowing of LV active relaxation and abnormal VVC during exercise. (J Am Coll Cardiol 2009; 54: 402-9) (C) 2009 by the American College of Cardiology Foundation",
keywords = "heart failure, diastole, radionuclide ventriculography, spectroscopy, exercise, troponin-I phosphorylation, magnetic-resonance spectroscopy, coronary-artery disease, diastolic dysfunction, hypertrophic cardiomyopathy, metabolic modulation, passive stiffness, cardiac troponin , stroke volume, filling rate",
author = "Phan, {Thanh T.} and Khalid Abozguia and Shivu, {Ganesh Nallur} and Gnanadevan Mahadevan and Ibrar Ahmed and Lynne Williams and Girish Dwivedi and Kiran Patel and Paul Steendijk and Houman Ashrafian and Anke Henning and Michael Frenneaux",
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language = "English",
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TY - JOUR

T1 - 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

AU - Phan, Thanh T.

AU - Abozguia, Khalid

AU - Shivu, Ganesh Nallur

AU - Mahadevan, Gnanadevan

AU - Ahmed, Ibrar

AU - Williams, Lynne

AU - Dwivedi, Girish

AU - Patel, Kiran

AU - Steendijk, Paul

AU - Ashrafian, Houman

AU - Henning, Anke

AU - Frenneaux, Michael

PY - 2009/7/28

Y1 - 2009/7/28

N2 - Objectives We sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients.Background To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF.Methods We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of P-31 magnetic resonance spectroscopy at 3-T.Results When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).Conclusions Patients with HFpEF have reduced cardiac energetic reserve that may underlie marked dynamic slowing of LV active relaxation and abnormal VVC during exercise. (J Am Coll Cardiol 2009; 54: 402-9) (C) 2009 by the American College of Cardiology Foundation

AB - Objectives We sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients.Background To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF.Methods We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of P-31 magnetic resonance spectroscopy at 3-T.Results When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).Conclusions Patients with HFpEF have reduced cardiac energetic reserve that may underlie marked dynamic slowing of LV active relaxation and abnormal VVC during exercise. (J Am Coll Cardiol 2009; 54: 402-9) (C) 2009 by the American College of Cardiology Foundation

KW - heart failure

KW - diastole

KW - radionuclide ventriculography

KW - spectroscopy

KW - exercise

KW - troponin-I phosphorylation

KW - magnetic-resonance spectroscopy

KW - coronary-artery disease

KW - diastolic dysfunction

KW - hypertrophic cardiomyopathy

KW - metabolic modulation

KW - passive stiffness

KW - cardiac troponin

KW - stroke volume

KW - filling rate

U2 - 10.1016/j.jacc.2009.05.012

DO - 10.1016/j.jacc.2009.05.012

M3 - Article

VL - 54

SP - 402

EP - 409

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 5

ER -