Treating Anemia in Older Adults With Heart Failure With a Preserved Ejection Fraction With Epoetin Alfa

Maurer, Mathew S.; Teruya, Sergio; Chakraborty, Bibhas; Helmke, Stephen; Mancini, Donna

doi:10.1161/circheartfailure.112.969717

Cited by 46 publications

(40 citation statements)

References 53 publications

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“…Evidence for improved outcomes after IV iron therapy is lacking. Small-scale studies treating HFpEF patients with erythropoietin-stimulating agents or oral iron reported no effect on left ventricular end-diastolic volume and left ventricular mass and no improvement in the submaximal exercise capacity or QoL [30, 31]. These findings are consistent with a report from Kasner et al [32], who did not find an association between functional iron deficiency and exercise capacity in patients with HFpEF.…”

Section: Iron In Diastolic Hfsupporting

confidence: 85%

Management of Iron Deficiency in Heart Failure

2019

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Anemia is a common finding in patients with heart failure (HF). The cause for anemia is multifactorial, with iron deficiency being the most common cause. Anemia with HF is an established predictor of morbidity and mortality. Iron deficiency in systolic HF, even without anemia, has been associated with increased mortality, increased hospitalizations, and decreased functional capacity and quality of life measures. Data from several randomized controlled trials and meta-analyses of iron deficiency and systolic HF show a beneficial effect for intravenous (IV) iron in terms of quality of life and functional capacity (improvements in 6-min walk test, and improvements in New York Heart Association functional class), as well as decreased hospitalizations for HF and reduction in cardiovascular mortality rates. Limited evidence exists for a beneficial effect of IV iron in diastolic dysfunction. Patients with symptomatic systolic HF should undergo an anemia diagnostic work-up. When iron deficiency (defined as ferritin <100 ng/mL or serum ferritin 100–299 ng/mL and transferrin saturation <20%) is present, current evidence supports treating HF patients with iron deficiency with IV iron.

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Section: Iron In Diastolic Hfsupporting

confidence: 85%

Management of Iron Deficiency in Heart Failure

2019

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“…The severity of anaemia predicts mortality, but the role of treatment is uncertain. 42 As described above, peripheral endothelial dysfunction has been reported in HFpEF, 27 and might impair dynamic flow-mediated dilatation responses during exercise while also impairing matching of perfusion to regional demand in skeletal muscle microcirculation. 35,123 Combined cardiovascular reserve limitation Clearly, HFpEF is not simply caused by one pathophysiological factor, but in fact is a complex, highly-integrated, multisystem loss of cardiac and vascular reserve capacity -affecting the left and right ventricles, diastolic and systolic function, atrial reserve, heart rate and rhythm, autonomic control, the vasculature and microcirculation, and the periphery (Figure 3).…”

Section: Vascular Stiffening and Dysfunctionmentioning

confidence: 92%

The pathophysiology of heart failure with preserved ejection fraction

2014

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Approximately half of all patients with heart failure have preserved ejection fraction (HFpEF) and, as life expectancies continue to increase in western societies, the prevalence of HFpEF will continue to grow. In contrast to heart failure with reduced ejection fraction (HFrEF), no treatment has been proven in pivotal clinical trials to be effective for HFpEF, largely because of the pathophysiological heterogeneity that exists within the broad spectrum of HFpEF. This syndrome was historically considered to be caused exclusively by left ventricular diastolic dysfunction, but research has identified several other contributory factors, including limitations in left ventricular systolic reserve, systemic and pulmonary vascular function, nitric oxide bioavailability, chronotropic reserve, right heart function, autonomic tone, left atrial function, and peripheral impairments. Multiple individual mechanisms frequently coexist within the same patient to cause symptomatic heart failure, but between patients with HFpEF the extent to which each component is operative can differ widely, confounding treatment approaches. This Review focuses on our current understanding of the pathophysiological mechanisms underlying HFpEF, and how they might be mechanistically related to typical risk factors for HFpEF, including ageing, obesity, and hypertension.

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“…Although these findings are inconclusive, treatment of anemia may be of benefit in some HFpEF patients. 47 …”

Section: Discussionmentioning

confidence: 99%

Resting Ventricular–Vascular Function and Exercise Capacity in Heart Failure With Preserved Ejection Fraction

Mohammed

Borlaug

McNulty

et al. 2014

Circ: Heart Failure

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Background Exercise intolerance is a hallmark of heart failure (HF), but factors associated with impaired exercise capacity in HF with preserved EF (HFpEF) are unclear. We hypothesized that in HFpEF, the severity of resting ventricular and vascular dysfunction are associated with impairment in exercise tolerance as assessed by peak oxygen consumption (pVO2). Methods and Results Subjects with HFpEF enrolled in the PhosphodiesteRasE-5 Inhibition to Improve CLinical Status And EXercise Capacity in Diastolic Heart Failure (RELAX) clinical trial (n=216) underwent baseline Doppler echocardiography, cardiopulmonary exercise testing and cardiac magnetic resonance imaging. RELAX participants were elderly (median age 69 years) and 48% were women. EF (60%) and stroke volume (77 ml) were normal, while diastolic dysfunction (medial E/e′ 16, deceleration time 185 msec, left atrial volume 44 ml/m2) and increased arterial load (arterial elastance (Ea) 1.51 mmHg/ml) were evident. PVO2 was reduced (11.7 ml/kg/min, 1141 ml/min) and age, sex, body mass index (BMI), hemoglobin and chronotropic response collectively explained 64% of the variance in raw pVO2 (ml/min). After adjustment for these variables, LV structure (diastolic dimension (1.5%, p=0.008) and LV mass (1.6%, p=0.008)), resting stroke volume (2.0%, p=0.002), LV diastolic dysfunction (deceleration time (0.9%, p=0.03) and E/e′ (1.4%, p=0.009), and arterial function (Ea (2.1%, p=0.002) and systemic arterial compliance (1.5%, p=0.007)), each explained only a small additional portion of the variance in pVO2. Conclusions In HFpEF, potentially modifiable factors (obesity, anemia and chronotropic incompetence) are strongly associated with exercise capacity whereas resting measures of ventricular and vascular structure and function are not. Clinical Trial Registration ;URL: http://www.clinicaltrials.gov. Unique identifier: NCT00763867.

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Treating Anemia in Older Adults With Heart Failure With a Preserved Ejection Fraction With Epoetin Alfa

Cited by 46 publications

References 53 publications

Management of Iron Deficiency in Heart Failure

Management of Iron Deficiency in Heart Failure

The pathophysiology of heart failure with preserved ejection fraction

Resting Ventricular–Vascular Function and Exercise Capacity in Heart Failure With Preserved Ejection Fraction

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