Heart failure (HF) with preserved ejection fraction (HFpEF) is the most rapidly increasing form of HF, occurs primarily in older women, and is associated with high rates of morbidity, mortality, and ...health care expenditures. In the highest age decile (≥90 years old), nearly all patients with HFpEF. As our understanding of the disease has grown in the last few years, we now know that HFpEF is a systemic disorder influenced by aging processes. The involvement of this broad collection of abnormalities in HFpEF, the recognition of the high frequency and impact of noncardiac comorbidities, and systemic, multiorgan involvement, and its nearly exclusive existence in older persons, has led to the recognition of HFpEF as a true geriatric syndrome. Most of the conventional therapeutics used in other cardiac diseases have failed to improve HFpEF patient outcomes significantly. Several recent studies have evaluated exercise training (ET) as a therapeutic management strategy in patients with HFpEF. Although these studies were not designed to address clinical endpoints, such as HF hospitalizations and mortality, they have shown that ET is a safe and effective intervention to improve peak oxygen consumption, physical function, and quality of life in clinically stable HF patients. Recently, a progressive, multidomain physical rehabilitation study among older adults showed that it is feasible in older patients with acute decompensated HF who have high frailty and comorbidities and showed improvement in physical function. However, the lack of Centers for Medicare and Medicaid Services coverage can be a major barrier to formal cardiac rehabilitation in older HFpEF patients. Unfortunately, insistence upon demonstration of mortality improvement before approving reimbursement overlooks the valuable and demonstrated benefits of physical function and life quality.
Objectives The purpose of this study was to evaluate the mechanisms for improved exercise capacity after endurance exercise training (ET) in elderly patients with heart failure and preserved ejection ...fraction (HFPEF). Background Exercise intolerance, measured objectively by reduced peak oxygen consumption (VO2 ), is the primary chronic symptom in HFPEF and is improved by ET. However, the mechanisms are unknown. Methods Forty stable, compensated HFPEF outpatients (mean age 69 ± 6 years) were examined at baseline and after 4 months of ET (n = 22) or attention control (n = 18). The VO2 and its determinants were assessed during rest and peak upright cycle exercise. Results After ET, peak VO2 in those patients was higher than in control patients (16.3 ± 2.6 ml/kg/min vs. 13.1 ± 3.4 ml/kg/min; p = 0.002). That was associated with higher peak heart rate (139 ± 16 beats/min vs. 131 ± 20 beats/min; p = 0.03), but no difference in peak end-diastolic volume (77 ± 18 ml vs. 77 ± 17 ml; p = 0.51), stroke volume (48 ± 9 ml vs. 46 ± 9 ml; p = 0.83), or cardiac output (6.6 ± 1.3 l/min vs. 5.9 ± 1.5 l/min; p = 0.32). However, estimated peak arterial-venous oxygen difference was significantly higher in ET patients (19.8 ± 4.0 ml/dl vs. 17.3 ± 3.7 ml/dl; p = 0.03). The effect of ET on cardiac output was responsible for only 16% of the improvement in peak VO2. Conclusions In elderly stable compensated HFPEF patients, peak arterial-venous oxygen difference was higher after ET and was the primary contributor to improved peak VO2 . This finding suggests that peripheral mechanisms (improved microvascular and/or skeletal muscle function) contribute to the improved exercise capacity after ET in HFPEF. (Prospective Aerobic Reconditioning Intervention Study PARIS; NCT01113840 )
Exercise intolerance is the primary chronic symptom in heart failure with preserved ejection fraction (HFpEF), the most common form of heart failure in older patients; however its pathophysiology is ...not well understood. Recent data suggest that peripheral factors such as skeletal muscle (SM) dysfunction may be important contributors. Therefore, 38 participants, 23 patients with HFpEF (69 ± 7 years) and 15 age-matched healthy controls (HCs), underwent magnetic resonance imaging and cardiopulmonary exercise testing to assess for SM, intermuscular fat (IMF), subcutaneous fat, total thigh, and thigh compartment (TC) areas and peak exercise oxygen consumption (peak VO2 ). There were no significant intergroup differences in total thigh area, TC, subcutaneous fat, or SM. However, in the HFpEF versus HC group, IMF area (35.6 ± 11.5 vs 22.3 ± 7.6 cm2 , p = 0.01), percent IMF/TC (26 ± 5 vs 20 ± 5%, p = 0.005), and the ratio of IMF/SM (0.38 ± 0.10 vs 0.28 ± 0.09, p = 0.007) were significantly increased, whereas percent SM/TC was significantly reduced (70 ± 5 vs 75 ± 5, p = 0.009). In multivariate analyses, IMF area (partial r = −0.51, p = 0.002) and IMF/SM ratio (partial r = −0.45, p = 0.006) were independent predictors of peak VO2 whereas SM area was not (partial r = −0.14, p = 0.43). Thus, older patients with HFpEF have greater thigh IMF and IMF/SM ratio compared with HCs, and these are significantly related to their severely reduced peak VO2 . These data suggest that abnormalities in SM composition may contribute to the severely reduced exercise capacity in older patients with HFpEF. This implicates potential targets for novel therapeutic strategies in this common debilitating disorder of older persons.
Objectives The purpose of this study was to determine the mechanisms responsible for reduced aerobic capacity (peak V o2 ) in patients with heart failure with preserved ejection fraction (HFPEF). ...Background HFPEF is the predominant form of heart failure in older persons. Exercise intolerance is the primary symptom among patients with HFPEF and a major determinant of reduced quality of life. In contrast to patients with heart failure and reduced ejection fraction, the mechanism of exercise intolerance in HFPEF is less well understood. Methods Left ventricular volumes (2-dimensional echocardiography), cardiac output, V o2 , and calculated arterial-venous oxygen content difference (A-V o2 Diff) were measured at rest and during incremental, exhaustive upright cycle exercise in 48 HFPEF patients (age 69 ± 6 years) and 25 healthy age-matched controls. Results In HFPEF patients compared with healthy controls, V o2 was reduced at peak exercise (14.3 ± 0.5 ml·kg·min−1 vs. 20.4 ± 0.6 ml·kg·min−1 ; p < 0.0001) and was associated with a reduced peak cardiac output (6.3 ± 0.2 l·min−1 vs. 7.6 ± 0.2 l·min−1 ; p < 0.0001) and A-V o2 Diff (17 ± 0.4 ml·dl−1 vs. 19 ± 0.4 ml·dl−1 , p < 0.0007). The strongest independent predictor of peak V o2 was the change in A-V o2 Diff from rest to peak exercise (A-V o2 Diff reserve) for both HFPEF patients (partial correlate, 0.58; standardized β coefficient, 0.66; p = 0.0002) and healthy controls (partial correlate, 0.61; standardized β coefficient, 0.41; p = 0.005). Conclusions Both reduced cardiac output and A-V o2 Diff contribute significantly to the severe exercise intolerance in elderly HFPEF patients. The finding that A-V o2 Diff reserve is an independent predictor of peak V o2 suggests that peripheral, noncardiac factors are important contributors to exercise intolerance in these patients.
Cardiovascular disease (CVD) is the leading cause of death globally. Advancements in the treatment of CVD have reduced mortality rates, yet the global burden of CVD remains high. Considering that CVD ...is still largely a preventable disease, prioritizing preventative measures through healthy lifestyle (HL) behaviors is necessary to lessen the burden of CVD. HL behaviors, such as regular exercise, healthy eating habits, adequate sleep, and smoking cessation, can influence a number of traditional CVD risk factors as well as a less commonly measured risk factor, cardiorespiratory fitness (CRF). It is important to note that cardiac rehabilitation programs, which traditionally have focused on secondary prevention, also emphasize the importance of making comprehensive HL behavior changes. This review discusses preventative measures to reduce the burden of CVD through an increased uptake and assessment of HL behaviors. An overview of the importance of CRF as a risk factor is discussed along with how to improve CRF and other risk factors through HL behavior interventions. The role of the clinician for promoting HL behaviors to prevent CVD is also reviewed.
Almost half of all heart failure (HF) disease burden is due to HF with preserved ejection fraction (HFpEF). The primary symptom in patients with HFpEF, even when well compensated, is severe exercise ...intolerance and is associated with their reduced quality of life. Recently, studies showed that HFpEF patients have multiple skeletal muscle (SM) abnormalities, and these are associated with decreased exercise intolerance. The SM abnormalities are likely intrinsic to the HFpEF syndrome, not a secondary consequence of an epiphenomenon. These abnormalities are decreased muscle mass, reduced type I (oxidative) muscle fibers, and reduced type I-to-type II fiber ratio as well as a reduced capillary-to-fiber ratio, abnormal fat infiltration into the thigh SM, increased levels of atrophy genes and proteins, reduction in mitochondrial content, and rapid depletion of high-energy phosphate during exercise with markedly delayed repletion of high-energy phosphate during recovery in mitochondria. In addition, patients with HFpEF have impaired nitric oxide bioavailability, particularly in the microvasculature. These SM abnormalities may be responsible for impaired diffusive oxygen transport and/or impaired SM oxygen extraction. To date, exercise training (ET) and caloric restriction are some of the interventions shown to improve outcomes in HFpEF patients. Improvements in exercise tolerance following aerobic ET are largely mediated through peripheral SM adaptations with minimal change in central hemodynamics and highlight the importance of targeting SM to improve exercise intolerance in HFpEF. Focusing on the abnormalities mentioned above may improve the clinical condition of patients with HFpEF.
The study sought to evaluate the effects of endurance exercise training (ET) on endothelial-dependent flow-mediated arterial dilation (FMD) and carotid artery stiffness, and their potential ...contributions to the training-related increase in peak exercise oxygen consumption (Vo2) in older patients with heart failure with preserved ejection fraction (HFPEF).
Elderly HFPEF patients have severely reduced peak Vo2, which improves with ET, however, the mechanisms of this improvement are unclear. FMD and arterial distensibility are critical components of the exercise response and are reduced with aging. However, it is unknown whether these improve with ET in elderly HFPEF or contribute to the training-related improvement in peak Vo2.
A total of 63 HFPEF patients (age 70 ± 7 years) were randomized to 16 weeks of ET (walking, arm and leg ergometry, n = 32) or attention control (CT) (n = 31). Peak Vo2, brachial artery FMD in response to cuff ischemia, carotid artery distensibility by high-resolution ultrasound, left ventricular function, and quality of life were measured at baseline and follow-up.
ET increased peak Vo2 (ET: 15.8 ± 3.3 ml/kg/min vs. CT: 13.8 ± 3.1 ml/kg/min, p = 0.0001) and quality of life. However, brachial artery FMD (ET: 3.8 ± 3.0% vs. CT: 4.3 ± 3.5%, p = 0.88), and carotid arterial distensibility (ET: 0.97 ± 0.56 vs. CT: 1.07 ± 0.34 × 10(-3) mm·mm Hg(-2); p = 0.65) were unchanged. Resting left ventricular systolic and diastolic function were unchanged by ET.
In elderly HFPEF patients, 16 weeks of ET improved peak Vo2 without altering endothelial function or arterial stiffness. This suggests that other mechanisms, such as enhanced skeletal muscle perfusion and/or oxygen utilization, may be responsible for the ET-mediated increase in peak Vo2 in older HFPEF patients. (Prospective Aerobic Reconditioning Intervention Study PARIS; NCT01113840).
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