scholarly journals Exercise Training for Heart Failure Patients with and without Systolic Dysfunction: An Evidence-Based Analysis of How Patients Benefit

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Neil Smart

Significant benefits can be derived by heart failure patients from exercise training. This paper provides an evidence-based assessment of expected clinical benefits of exercise training for heart failure patients. Meta-analyses and randomized, controlled trials of exercise training in heart failure patients were reviewed from a search of PubMed, Cochrane Controlled Trial Registry (CCTR), CINAHL, and EMBASE. Exercise training improves functional capacity, quality of life, hospitalization, and systolic and diastolic function in heart failure patients. Heart failure patients with preserved systolic function (HFnEF) participating in exercise training studies are more likely to be women and are 5–7 years older than their systolic heart failure (CHF) counterparts. All patients exhibit low functional capacities, although in HFnEF patients this may be age related, therefore subtle differences in exercise prescriptions are required. Published works report that exercise training is beneficial for heart failure patients with and without systolic dysfunction.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Gudrun Dieberg ◽  
Hashbullah Ismail ◽  
Francesco Giallauria ◽  
Neil A Smart

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.


2015 ◽  
Vol 308 (8) ◽  
pp. H792-H802 ◽  
Author(s):  
Carlos E. Negrao ◽  
Holly R. Middlekauff ◽  
Igor L. Gomes-Santos ◽  
Ligia M. Antunes-Correa

Neurohormonal excitation and dyspnea are the hallmarks of heart failure (HF) and have long been associated with poor prognosis in HF patients. Sympathetic nerve activity (SNA) and ventilatory equivalent of carbon dioxide (VE/VO2) are elevated in moderate HF patients and increased even further in severe HF patients. The increase in SNA in HF patients is present regardless of age, sex, and etiology of systolic dysfunction. Neurohormonal activation is the major mediator of the peripheral vasoconstriction characteristic of HF patients. In addition, reduction in peripheral blood flow increases muscle inflammation, oxidative stress, and protein degradation, which is the essence of the skeletal myopathy and exercise intolerance in HF. Here we discuss the beneficial effects of exercise training on resting SNA in patients with systolic HF and its central and peripheral mechanisms of control. Furthermore, we discuss the exercise-mediated improvement in peripheral vasoconstriction in patients with HF. We will also focus on the effects of exercise training on ventilatory responses. Finally, we review the effects of exercise training on features of the skeletal myopathy in HF. In summary, exercise training plays an important role in HF, working synergistically with pharmacological therapies to ameliorate these abnormalities in clinical practice.


2021 ◽  
Vol 93 (9) ◽  
pp. 1073-1077
Author(s):  
Sofia V. Miklishanskaya ◽  
Olga V. Stukalova ◽  
Lilia V. Solomasova ◽  
Nikolai A. Mazur

Currently, the world is constantly increasing the number of people with obesity. As was shown by the Framingham study, obesity is a risk factor for many cardiovascular diseases. The effect of obesity on the structure and function of the heart is manifested in the form of cardiac remodeling, the effect on energy metabolism in the heart and infiltration of both myocardium with lipids, and an increase in the accumulation of adipose tissue in the pericardium, imbalance of adipokines and activation of inflammatory markers. Cardiac remodeling occurs primarily due to thickening of the left ventricle (LV) walls and an increase in the LV myocardium mass. Systolic dysfunction of the heart is less common in obese individuals compared with diastolic dysfunction. However, more modern methods (tissue Doppler, visualization of the deformation of the chambers of the heart strain imaging) reveal a subclinical decrease in systolic function in people with obesity. It is not fully known whether obesity is associated with systolic dysfunction, regardless of other risk factors. In any case, it has been proven that heart failure in people with obesity can develop independently of other risk factors. As an illustration, we give an example when the presence of obesity and concomitant pathology (arterial hypertension, diabetes) led to the development of systolic dysfunction with a decrease in the LV ejection fraction to 35% (fat cardiopathy), which show the potential for the influence of both obesity itself and in combination with concomitant diseases to lead to severe systolic heart failure.


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