Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction: the role of myocardial energy deficiency

T. T. Phan, K. Abozguia, T. Nallur Shivu, M. Gnanadevan, Irfan Ahmed, Lynda Williams, G. Dwivedi, K. Patel, P. Steendijk, H. Ashrafian, A. Henning, Michael Frenneaux

Research output: Contribution to journalArticle

Abstract

Background: Patients with heart failure with preserved ejection fraction (HFpEF) have dyspnoea on exertion and limited exercise capacity. In this study we evaluated the role of exercise-related changes in left ventricular relaxation and of vasculoventricular coupling (VVC) as the mechanism of this limitation and whether cardiac energetic impairment may underlie these abnormalities.

Methods: We prospectively studied 37 patients with HFpEF. All had signs and/or symptoms of heart failure and a normal ejection fraction (>50%). Twenty age and gender-matched healthy volunteers were also studied. VVC and left ventricular filling characteristics were assessed at rest and on exercise by multiple uptake gated acquisition scan, and time to peak filling (nTTPF) was corrected for the RR interval (an indirect measure of the rate of left ventricular active relaxation) was derived. In vivo myocardial energetic state was assessed by 31P magnetic resonance spectroscopy at 3 Tesla. All subjects also underwent metabolic exercise testing, pulmonary function test and echocardiography.

Results: nTTPF and the VVC ratio were similar in patients and controls. The cardiac phosphocreatine/adenosine triphosphate ratio was lower in patients than controls (1.57 ± 0.52 and 2.09 ± 0.62, respectively, p = 0.006). Peak maximum oxygen consumption (VO2max) was lower in patients compared with controls (19 ± 4 ml/kg per minute and 36 ± 8 ml/kg per minute, respectively, p<0.001). During maximal exercise the increase in heart rate was lower in patients than controls (52 ± 16 and 81 ± 14 bpm, respectively, p<0.001) and the relative increases in stroke volume and cardiac output during submaximal exercise were lower in patients than controls (0.99 ± 0.34 vs 1.29 ± 0.48, p = 0.02; 1.36 ± 0.45 vs 2.25 ± 0.69, p<0.001). Whereas nTTPF fell during exercise in controls it paradoxically lengthened in patients (–0.03 ± 12 s and +0.07 ± 0.11 s, respectively, p = 0.005). The VVC ratio decreased on exercise in controls but was essentially unchanged in patients (–0.01 ± 0.15 and –0.25 ± 0.19, respectively, p<0.001). Heart rate, VVC ratio and nTTPF were independent predictors of peak VO2max (mean ± SD) (see fig).

Original languageEnglish
Pages (from-to)114
Number of pages2
JournalHeart
Volume95
Issue numberSuppl. 1
Publication statusPublished - Jun 2009

Cite this

Phan, T. T., Abozguia, K., Shivu, T. N., Gnanadevan, M., Ahmed, I., Williams, L., ... Frenneaux, M. (2009). Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction: the role of myocardial energy deficiency. Heart, 95(Suppl. 1), 114.

Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction : the role of myocardial energy deficiency. / Phan, T. T.; Abozguia, K.; Shivu, T. Nallur; Gnanadevan, M.; Ahmed, Irfan; Williams, Lynda; Dwivedi, G.; Patel, K.; Steendijk, P.; Ashrafian, H.; Henning, A.; Frenneaux, Michael.

In: Heart, Vol. 95, No. Suppl. 1, 06.2009, p. 114.

Research output: Contribution to journalArticle

Phan, TT, Abozguia, K, Shivu, TN, Gnanadevan, M, Ahmed, I, Williams, L, Dwivedi, G, Patel, K, Steendijk, P, Ashrafian, H, Henning, A & Frenneaux, M 2009, 'Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction: the role of myocardial energy deficiency' Heart, vol. 95, no. Suppl. 1, pp. 114.
Phan, T. T. ; Abozguia, K. ; Shivu, T. Nallur ; Gnanadevan, M. ; Ahmed, Irfan ; Williams, Lynda ; Dwivedi, G. ; Patel, K. ; Steendijk, P. ; Ashrafian, H. ; Henning, A. ; Frenneaux, Michael. / Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction : the role of myocardial energy deficiency. In: Heart. 2009 ; Vol. 95, No. Suppl. 1. pp. 114.
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abstract = "Background: Patients with heart failure with preserved ejection fraction (HFpEF) have dyspnoea on exertion and limited exercise capacity. In this study we evaluated the role of exercise-related changes in left ventricular relaxation and of vasculoventricular coupling (VVC) as the mechanism of this limitation and whether cardiac energetic impairment may underlie these abnormalities. Methods: We prospectively studied 37 patients with HFpEF. All had signs and/or symptoms of heart failure and a normal ejection fraction (>50{\%}). Twenty age and gender-matched healthy volunteers were also studied. VVC and left ventricular filling characteristics were assessed at rest and on exercise by multiple uptake gated acquisition scan, and time to peak filling (nTTPF) was corrected for the RR interval (an indirect measure of the rate of left ventricular active relaxation) was derived. In vivo myocardial energetic state was assessed by 31P magnetic resonance spectroscopy at 3 Tesla. All subjects also underwent metabolic exercise testing, pulmonary function test and echocardiography. Results: nTTPF and the VVC ratio were similar in patients and controls. The cardiac phosphocreatine/adenosine triphosphate ratio was lower in patients than controls (1.57 ± 0.52 and 2.09 ± 0.62, respectively, p = 0.006). Peak maximum oxygen consumption (VO2max) was lower in patients compared with controls (19 ± 4 ml/kg per minute and 36 ± 8 ml/kg per minute, respectively, p<0.001). During maximal exercise the increase in heart rate was lower in patients than controls (52 ± 16 and 81 ± 14 bpm, respectively, p<0.001) and the relative increases in stroke volume and cardiac output during submaximal exercise were lower in patients than controls (0.99 ± 0.34 vs 1.29 ± 0.48, p = 0.02; 1.36 ± 0.45 vs 2.25 ± 0.69, p<0.001). Whereas nTTPF fell during exercise in controls it paradoxically lengthened in patients (–0.03 ± 12 s and +0.07 ± 0.11 s, respectively, p = 0.005). The VVC ratio decreased on exercise in controls but was essentially unchanged in patients (–0.01 ± 0.15 and –0.25 ± 0.19, respectively, p<0.001). Heart rate, VVC ratio and nTTPF were independent predictors of peak VO2max (mean ± SD) (see fig).",
author = "Phan, {T. T.} and K. Abozguia and Shivu, {T. Nallur} and M. Gnanadevan and Irfan Ahmed and Lynda Williams and G. Dwivedi and K. Patel and P. Steendijk and H. Ashrafian and A. Henning and Michael Frenneaux",
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T1 - Dynamic changes in left ventricular function on exercise in heart failure with preserved ejection fraction

T2 - the role of myocardial energy deficiency

AU - Phan, T. T.

AU - Abozguia, K.

AU - Shivu, T. Nallur

AU - Gnanadevan, M.

AU - Ahmed, Irfan

AU - Williams, Lynda

AU - Dwivedi, G.

AU - Patel, K.

AU - Steendijk, P.

AU - Ashrafian, H.

AU - Henning, A.

AU - Frenneaux, Michael

PY - 2009/6

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N2 - Background: Patients with heart failure with preserved ejection fraction (HFpEF) have dyspnoea on exertion and limited exercise capacity. In this study we evaluated the role of exercise-related changes in left ventricular relaxation and of vasculoventricular coupling (VVC) as the mechanism of this limitation and whether cardiac energetic impairment may underlie these abnormalities. Methods: We prospectively studied 37 patients with HFpEF. All had signs and/or symptoms of heart failure and a normal ejection fraction (>50%). Twenty age and gender-matched healthy volunteers were also studied. VVC and left ventricular filling characteristics were assessed at rest and on exercise by multiple uptake gated acquisition scan, and time to peak filling (nTTPF) was corrected for the RR interval (an indirect measure of the rate of left ventricular active relaxation) was derived. In vivo myocardial energetic state was assessed by 31P magnetic resonance spectroscopy at 3 Tesla. All subjects also underwent metabolic exercise testing, pulmonary function test and echocardiography. Results: nTTPF and the VVC ratio were similar in patients and controls. The cardiac phosphocreatine/adenosine triphosphate ratio was lower in patients than controls (1.57 ± 0.52 and 2.09 ± 0.62, respectively, p = 0.006). Peak maximum oxygen consumption (VO2max) was lower in patients compared with controls (19 ± 4 ml/kg per minute and 36 ± 8 ml/kg per minute, respectively, p<0.001). During maximal exercise the increase in heart rate was lower in patients than controls (52 ± 16 and 81 ± 14 bpm, respectively, p<0.001) and the relative increases in stroke volume and cardiac output during submaximal exercise were lower in patients than controls (0.99 ± 0.34 vs 1.29 ± 0.48, p = 0.02; 1.36 ± 0.45 vs 2.25 ± 0.69, p<0.001). Whereas nTTPF fell during exercise in controls it paradoxically lengthened in patients (–0.03 ± 12 s and +0.07 ± 0.11 s, respectively, p = 0.005). The VVC ratio decreased on exercise in controls but was essentially unchanged in patients (–0.01 ± 0.15 and –0.25 ± 0.19, respectively, p<0.001). Heart rate, VVC ratio and nTTPF were independent predictors of peak VO2max (mean ± SD) (see fig).

AB - Background: Patients with heart failure with preserved ejection fraction (HFpEF) have dyspnoea on exertion and limited exercise capacity. In this study we evaluated the role of exercise-related changes in left ventricular relaxation and of vasculoventricular coupling (VVC) as the mechanism of this limitation and whether cardiac energetic impairment may underlie these abnormalities. Methods: We prospectively studied 37 patients with HFpEF. All had signs and/or symptoms of heart failure and a normal ejection fraction (>50%). Twenty age and gender-matched healthy volunteers were also studied. VVC and left ventricular filling characteristics were assessed at rest and on exercise by multiple uptake gated acquisition scan, and time to peak filling (nTTPF) was corrected for the RR interval (an indirect measure of the rate of left ventricular active relaxation) was derived. In vivo myocardial energetic state was assessed by 31P magnetic resonance spectroscopy at 3 Tesla. All subjects also underwent metabolic exercise testing, pulmonary function test and echocardiography. Results: nTTPF and the VVC ratio were similar in patients and controls. The cardiac phosphocreatine/adenosine triphosphate ratio was lower in patients than controls (1.57 ± 0.52 and 2.09 ± 0.62, respectively, p = 0.006). Peak maximum oxygen consumption (VO2max) was lower in patients compared with controls (19 ± 4 ml/kg per minute and 36 ± 8 ml/kg per minute, respectively, p<0.001). During maximal exercise the increase in heart rate was lower in patients than controls (52 ± 16 and 81 ± 14 bpm, respectively, p<0.001) and the relative increases in stroke volume and cardiac output during submaximal exercise were lower in patients than controls (0.99 ± 0.34 vs 1.29 ± 0.48, p = 0.02; 1.36 ± 0.45 vs 2.25 ± 0.69, p<0.001). Whereas nTTPF fell during exercise in controls it paradoxically lengthened in patients (–0.03 ± 12 s and +0.07 ± 0.11 s, respectively, p = 0.005). The VVC ratio decreased on exercise in controls but was essentially unchanged in patients (–0.01 ± 0.15 and –0.25 ± 0.19, respectively, p<0.001). Heart rate, VVC ratio and nTTPF were independent predictors of peak VO2max (mean ± SD) (see fig).

M3 - Article

VL - 95

SP - 114

JO - Heart

JF - Heart

SN - 1355-6037

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ER -