Abstract 15264: Clinical Outcomes and Cardiovascular Responses to Exercise Training in Heart Failure Patients with Preserved Ejection Fraction: A Systematic Review and Meta-Analysis

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Gudrun Dieberg ◽  
Hashbullah Ismail ◽  
Francesco Giallauria ◽  
Neil A Smart
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Diastolic Function ◽  
Short Form ◽  
Systolic Dysfunction ◽  
Cardiovascular Responses ◽  
Preserved Ejection Fraction ◽  
Medline Search ◽  
Heart Failure Patients

Background: Exercise training induces physical adaptations for heart failure patients with systolic dysfunction but less is known about those patients with preserved ejection fraction. Objectives: To establish if exercise training produces changes in peak VO 2 and related measures, quality of life, general health and diastolic function in heart failure patients with preserved ejection fraction (HFpEF). Methods: We conducted a MEDLINE search (1985 to March 2014), for exercise based rehabilitation trials in heart failure, using search terms ‘exercise training, heart failure with preserved ejection fraction, heart failure with normal ejection fraction, peak VO 2 and diastolic heart dysfunction’. Seven intervention studies were included providing a total of 144 exercising subjects and 114 control subjects, a total of 258 participants. Results: Peak VO 2 increased by a mean difference (MD) 2.13 ml.kg -1 .min -1 (95% C.I. 1.54 to 2.71, p<0.00001) in exercise training versus sedentary control, equating to a 17% improvement from baseline. The corresponding data for V E /VCO 2 slope MD 0.85 ml.kg -1 .min -1 (95% C.I. 0.05 to 1.65, p=0.04); maximum heart rate MD 5.60 bpm (95% C.I. 3.95 to 7.25, p<0.00001); and 6 Minute Walk Test (6MWT) MD 32.1m (95% C.I. 17.2 to 47.1, p<0.0001); diastolic function; E/A ratio MD 0.07 (95% C.I. 0.02 to 0.12, p=0.005); E/E’ ratio MD -2.31 (95% C.I. -3.44 to -1.19, p<0.0001); Deceleration time (D T ) MD -13.2 msec (95% C.I. -19.8 to -6.5, p=0.0001); Minnesota Living with Heart Failure Questionnaire (MLHFQ) MD -6.50 (95% C.I. -9.47 to -3.53, p<0.0001); Short Form (36) Health Survey MD 15.6 (95% C.I. 7.4 to 23.8, p=0.0002). In 3,744 hours patient-hours of training, not one death was directly attributable to exercise. Conclusions: Exercise training appears to effect several health-related improvements in people with heart failure and preserved ejection fraction.

scholarly journals Exercise training in heart failure patients with preserved ejection fraction: a systematic review and meta-analysis

2016 ◽  
Vol 86 (1-2) ◽  
Author(s):  
Erick Chan ◽  
Francesco Giallauria ◽  
Carlo Vigorito ◽  
Neil A. Smart
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Diastolic Function ◽  
Short Form ◽  
Meta Analysis ◽  
Systolic Dysfunction ◽  
Preserved Ejection Fraction ◽  
Medline Search ◽  
Heart Failure Patients

<p>Exercise training induces physical adaptations for heart failure patients with systolic dysfunction but less is known about those patients with preserved ejection fraction. This study's aims were to establish if exercise training produces changes in peak VO<sub>2</sub> and related measures, quality of life, general health and diastolic function in heart failure patients with preserved ejection fraction (HFpEF). We conducted a MEDLINE search (1985 to September 1, 2015), for exercise based rehabilitation trials in heart failure, using search terms ‘exercise training, heart failure with preserved ejection fraction, heart failure with  normal ejection fraction, peak VO<sub>2</sub> and diastolic heart dysfunction’. Eight intervention studies were included providing a total of 174 exercising subjects and 143 control subjects, a total of 317 participants. Peak VO<sub>2</sub> increased by a mean difference (MD) 2.08 mL kg<sup>-1 </sup>min<sup>-1</sup> (95% C.I. 1.51 to 2.65, p&lt;0.00001) in exercise training versus sedentary control, equating to a 17% improvement from baseline. V<sub>E</sub>/VCO<sub>2</sub> slope was not different between groups, MD -3.10 mL kg<sup>-1 </sup>min<sup>-1</sup> (95% C.I. -7.47 to 1.27, p=0.16); maximum heart rate was significantly increased in exercise groups, MD 3.46 bpm (95% C.I. 2.41 to 4.51, p&lt;0.00001); 6 Minute Walk Distance (6MWT) MD 32.1m (95% C.I. 17.2 to 47.1, p&lt;0.0001); diastolic  function; the ratio of early to late filling (E/A ratio) was improved after exercise training MD 0.07 (95% C.I. 0.02 to 0.12, p=0.006); as was filling pressure E/E’ ratio MD -2.38 (95% C.I. -3.47 to -1.28, p&lt;0.0001); Deceleration time (D<sub>T</sub>) MD -13.2 msec (95% C.I. -19.8 to -6.5, p=0.0001); Minnesota Living with Heart Failure Questionnaire (MLHFQ) MD -6.77 (95% C.I. -9.70 to -3.84, p&lt;0.00001); Short Form (36) Health Survey MD 11.38 (95% C.I. 5.28 to 17.48, p=0.0003).  In 3222 patient-hours of training, not a single death was directly attributable to exercise. Exercise training appears to effect several health-related improvements in people with heart failure and preserved ejection fraction.</p>

Clinical outcomes and cardiovascular responses to exercise training in heart failure patients with preserved ejection fraction: a systematic review and meta-analysis

2015 ◽  
Vol 119 (6) ◽  
pp. 726-733 ◽  
Author(s):  
Gudrun Dieberg ◽  
Hashbullah Ismail ◽  
Francesco Giallauria ◽  
Neil A. Smart
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Diastolic Function ◽  
Short Form ◽  
Cardiovascular Responses ◽  
Preserved Ejection Fraction ◽  
Heart Failure Patients

Exercise training induces physical adaptations for heart failure patients with systolic dysfunction, but less is known about those patients with preserved ejection fraction. To establish whether exercise training produces changes in peak V̇o2 and related measures, quality of life, general health, and diastolic function in heart failure patients with preserved ejection fraction. We conducted a MEDLINE search (1985 to October 10, 2014), for exercise-based rehabilitation trials in heart failure, using search terms “exercise training, heart failure with preserved ejection fraction, heart failure with normal ejection fraction, peak V̇o2, and diastolic heart dysfunction”. Seven intervention studies were included providing a total of 144 exercising subjects and 114 control subjects, a total of 258 participants. Peak V̇o2 increased by a mean difference (MD) 2.13 ml·kg−1·min−1 [95% confidence interval (CI) 1.54 to 2.71, P < 0.00001] in exercise training vs. sedentary control, equating to a 17% improvement from baseline. The corresponding data are provided for the following exercise test variables: V̇e/V̇co2 slope, MD 0.85 ml·kg−1·min−1 (95% CI 0.05 to 1.65, P = 0.04); maximum heart rate, MD 5.60 beats per minute (95% CI 3.95 to 7.25, P < 0.00001); Six-Minute Walk Test, MD 32.1 m (95% CI 17.2 to 47.1, P < 0.0001); and indices of diastolic function: E/A ratio, MD 0.07 (95% CI 0.02 to 0.12, P = 0.005); E/E′ ratio MD −2.31 (95% CI −3.44 to −1.19, P < 0.0001); deceleration time (DT), MD −13.2 ms (95% CI −19.8 to −6.5, P = 0.0001); and quality of life: Minnesota Living with Heart Failure Questionnaire, MD −6.50 (95% CI −9.47 to −3.53, P < 0.0001); and short form-36 health survey (physical dimension), MD 15.6 (95% CI 7.4 to 23.8, P = 0.0002). In 3,744 h patient-hours of training, not one death was directly attributable to exercise. Exercise training appears to effect several health-related improvements in people with heart failure and preserved ejection fraction.

scholarly journals Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function

2013 ◽  
Vol 114 (1) ◽  
pp. 131-147 ◽  
Author(s):  
Kurt D. Marshall ◽  
Brittany N. Muller ◽  
Maike Krenz ◽  
Laurin M. Hanft ◽  
Kerry S. McDonald ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Diastolic Function ◽  
Myocardial Oxygen Consumption ◽  
Preserved Ejection Fraction ◽  
Miniature Swine ◽  
Interval Exercise ◽  
Low Intensity ◽  
Physiol Heart Circ

We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary vascular dysfunction in miniature swine with left ventricular (LV) hypertrophy (Emter CA, Baines CP. Am J Physiol Heart Circ Physiol 299: H1348–H1356, 2010; Emter CA, et al. Am J Physiol Heart Circ Physiol 301: H1687–H1694, 2011). The purpose of this study was to test two hypotheses: 1) chronic low-intensity interval training preserves normal myocardial oxygen supply/demand balance; and 2) training-dependent attenuation of LV fibrotic remodeling improves diastolic function in aortic-banded sedentary, exercise-trained (HF-TR), and control sedentary male Yucatan miniature swine displaying symptoms of heart failure with preserved ejection fraction. Pressure-volume loops, coronary blood flow, and two-dimensional speckle tracking ultrasound were utilized in vivo under conditions of increasing peripheral mean arterial pressure and β-adrenergic stimulation 6 mo postsurgery to evaluate cardiac function. Normal diastolic function in HF-TR animals was characterized by prevention of increased time constant of isovolumic relaxation, normal LV untwisting rate, and enhanced apical circumferential and radial strain rate. Reduced fibrosis, normal matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase-4 mRNA expression, and increased collagen III isoform mRNA levels ( P < 0.05) accompanied improved diastolic function following chronic training. Exercise-dependent improvements in coronary blood flow for a given myocardial oxygen consumption ( P < 0.05) and cardiac efficiency (stroke work to myocardial oxygen consumption, P < 0.05) were associated with preserved contractile reserve. LV hypertrophy in HF-TR animals was associated with increased activation of Akt and preservation of activated JNK/SAPK. In conclusion, chronic low-intensity interval exercise training attenuates diastolic impairment by promoting compliant extracellular matrix fibrotic components and preserving extracellular matrix regulatory mechanisms, preserves myocardial oxygen balance, and promotes a physiological molecular hypertrophic signaling phenotype in a large animal model resembling heart failure with preserved ejection fraction.

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