Heart Failure With Midrange Ejection Fraction—What Is It, If Anything?

Boulet, Jacinthe; Massie, Emmanuelle; Rouleau, Jean‐Lucien

doi:10.1016/j.cjca.2020.11.013

Cited by 7 publications

(3 citation statements)

References 87 publications

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“…clasificación centrada en la FE 29 . Recientemente, una recomendación de consenso de la asociación de insuficiencia cardíaca de la Sociedad Europea de Cardiología, señala que el problema con la FE es que la estimación de la función global no informa sobre el volumen ventricular o el VS 30 .…”

Section: Discussionunclassified

La serendipia en torno la fracción de eyección: una revisión de la historia, la casualidad y la cuasi-funcionalidad de una métrica aplaudida

Kerkhof¹,

Díaz-Navarro²,

Heyndrickx³

et al. 2022

Rev. méd. Chile

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A critical analysis of ejection fraction Ejection fraction (EF) is defined by the ratio of end-systolic volume (ESV) and end-diastolic volume (EDV). The resulting fraction is a dimensionless number whose interpretation is ambiguous and most likely misleading. Despite this limitation, EF is widely accepted as a clinical marker of cardiac function. In this article we analyze the role of ESV, a fundamental variable of ventricular mechanics, compared with the popular EF. Common physiology-based mathematics can explain a simple association between EF and ESV. This concept is illustrated by a detailed analysis of the information obtained from angiocardiography, echocardiography and cardiac magnetic resonance studies. EF versusESV produces a non-linear curve. For a small ESV, the EF approaches 100%, while for a large ESV, the EF gradually decreases toward zero. This elemental relationship is commonly observed in innervated natural hearts. Thus, the popularity of EF mostly derives from a fortuitous connection with the pivotal variable ESV. Alongside this finding, we unfold historical events that facilitated the emergence of EF as a result of serendipity. Our physiology-based approach denounces the circumstantial theories invoked to justify the importance of EF as an index of cardiac function, which are critically discussed. EF appears to be nothing more than a blessing in disguise. For this reason, we propose the ESV as a more logical metric for the analysis of ventricular function.

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Section: Discussionunclassified

La serendipia en torno la fracción de eyección: una revisión de la historia, la casualidad y la cuasi-funcionalidad de una métrica aplaudida

Kerkhof¹,

Díaz-Navarro²,

Heyndrickx³

et al. 2022

Rev. méd. Chile

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“…Finally, we could assume that analyzing the various biomarker profiles in all HF population does not take into account the several mechanisms that are shared across the entire EF range. Some processes are more relevant at the extremities (HFrEF myocyte death vs. HFpEF inflammation or fibrosis), and in this spectrum, HFmrEF represents a continuum without a predominant underlying pathophysiology (32,33). In this era in which a new precision phenotype is emerging in patients with HF, knowledge of different pathophysiologic pathways and of the laboratory profile of each patient may contribute to therapeutic decision and prognostic stratification (Table 2).…”

Section: Laboratory Profile Of Hfmrefmentioning

confidence: 99%

Are HFpEF and HFmrEF So Different? The Need to Understand Distinct Phenotypes

Palazzuoli

Beltrami

2021

Front. Cardiovasc. Med.

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Traditionally, patients with heart failure (HF) are divided according to ejection fraction (EF) threshold more or <50%. In 2016, the ESC guidelines introduced a new subgroup of HF patients including those subjects with EF ranging between 40 and 49% called heart failure with midrange EF (HFmrEF). This group is poorly represented in clinical trials, and it includes both patients with previous HFrEF having a good response to therapy and subjects with initial preserved EF appearance in which systolic function has been impaired. The categorization according to EF has recently been questioned because this variable is not really a representative of the myocardial contractile function and it could vary in relation to different hemodynamic conditions. Therefore, EF could significantly change over a short-term period and its measurement depends on the scan time course. Finally, although EF is widely recognized and measured worldwide, it has significant interobserver variability even in the most accredited echo laboratories. These assumptions imply that the same patient evaluated in different periods or by different physicians could be classified as HFmrEF or HFpEF. Thus, the two HF subtypes probably subtend different responses to the underlying pathophysiological mechanisms. Similarly, the adaptation to hemodynamic stimuli and to metabolic alterations could be different for different HF stages and periods. In this review, we analyze similarities and dissimilarities and we hypothesize that clinical and morphological characteristics of the two syndromes are not so discordant.

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“…Patients with HF and mid-range ejection fraction (HFmrEF) showed an intermediary profile with abnormal biomarker levels of both cardiac stretch and inflammation. It may be that while there is an underlying group of mechanisms that may be common across the EF range, the contribution of inflammation may be more specific and predominant at one end of the spectrum [ 7 ]. The inflammatory/pro-fibrotic paradigm describes one such group of mechanisms believed to drive disease pathogenesis in HFpEF [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Inflammation in heart failure: pathophysiology and therapeutic strategies

Boulet,

Sridhar,

Bouabdallaoui

et al. 2024

Inflamm. Res.

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A role for inflammation in the development and progression of heart failure (HF) has been proposed for decades. Multiple studies have demonstrated the potential involvement of several groups of cytokines and chemokines in acute and chronic HF, though targeting these pathways in early therapeutic trials have produced mixed results. These studies served to highlight the complexity and nuances of how pro-inflammatory pathways contribute to the pathogenesis of HF. More recent investigations have highlighted how inflammation may play distinct roles based on HF syndrome phenotypes, findings that may guide the development of novel therapies. In this review, we propose a contemporary update on the role of inflammation mediated by the innate and adaptive immune systems with HF, highlighting differences that exist across the ejection fraction spectrum. This will specifically be looked at through the lens of established and novel biomarkers of inflammation. Subsequently, we review how improvements in inflammatory pathways may mediate clinical benefits of existing guideline-directed medical therapies for HF, as well as future therapies in the pipeline targeting HF and inflammation.

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Heart Failure With Midrange Ejection Fraction—What Is It, If Anything?

Cited by 7 publications

References 87 publications

La serendipia en torno la fracción de eyección: una revisión de la historia, la casualidad y la cuasi-funcionalidad de una métrica aplaudida

La serendipia en torno la fracción de eyección: una revisión de la historia, la casualidad y la cuasi-funcionalidad de una métrica aplaudida

Are HFpEF and HFmrEF So Different? The Need to Understand Distinct Phenotypes

Inflammation in heart failure: pathophysiology and therapeutic strategies

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