Beyond ejection fraction: back to the myocardium in the assessment of cardiac function
Year: 2026
Type: editorial
Abstract: This editorial refers to ‘Reappraising cardiac function with myocardial contraction fraction: normal values, disease detection and prognostication’, by H. Kurdi et al., https://doi.org/10.1093/ehjci/jeag019. For more than half a century, left ventricular ejection fraction (LVEF) has been the dominant quantitative measure of cardiac systolic function. It is deeply embedded in clinical guidelines, therapeutic algorithms, and trial eligibility criteria. Yet its limitations are equally well recognized: LVEF is geometry-dependent, insensitive to early myocardial disease, and frequently discordant with symptoms, prognosis, and true contractile performance.1,2 In this context, the study by Kurdi et al.3 offers a timely and compelling reappraisal of myocardial contraction fraction (MCF) as a complementary—and in many respects more physiologically coherent—metric of cardiac function.3 The conceptual limitation of LVEF lies in its denominator. By expressing stroke volume relative to end-diastolic chamber volume, LVEF implicitly assumes that cavity size is a suitable surrogate for myocardial ‘health’. This assumption fails in many common disease states.4–6 Concentric hypertrophy, infiltrative cardiomyopathies, paradoxical low-flow aortic stenosis, and hypertensive heart disease all exemplify situations in which myocardial performance is impaired despite a preserved or even ‘supranormal’ ejection fraction.7–9 MCF, defined as stroke volume divided by myocardial volume, reframes systolic function as output per unit of myocardium. In doing so, it directly interrogates myocardial efficiency rather than chamber emptying.4–6 This distinction is not semantic; it is physiological. By anchoring function to myocardial mass, MCF mitigates the confounding effects of ventricular geometry and offers a more faithful representation of how effectively myocardial tissue generates forward flow.3 A major barrier to clinical adoption of MCF has been the lack of robust, sex-specific reference ranges derived from large populations. Kurdi et al.3 decisively address this gap by leveraging more than 3500 healthy participants from the UK Biobank, complemented by an independent healthy cohort.3 Their findings are striking: MCF is strongly sex-dependent but largely age-independent, with consistently higher values in women than in men. Importantly, this sex difference persists even after indexing to body surface area, reinforcing the decision to preserve MCF as a dimensionless, non-indexed parameter—mirroring the convention used for LVEF. These data provide the essential interpretive framework required for clinical translation and move MCF from a conceptual construct to a quantifiable biomarker with defined normal limits.10–12 One of the most compelling aspects of the study is its ability to distinguish physiological adaptation from pathological remodelling. Veteran athletes demonstrated preserved MCF, paralleling normal LVEF, despite increased myocardial mass—an elegant demonstration that MCF respects adaptive hypertrophy without falsely signalling dysfunction.4–6 In contrast, MCF was consistently reduced across a spectrum of pathological conditions, including hypertrophic cardiomyopathy, cardiac amyloidosis, severe aortic stenosis, hypertension, and dilated cardiomyopathy. Notably, in most of these conditions, LVEF remained within the normal range. This dissociation underscores a central message of the paper: preserved LVEF does not equate to preserved myocardial performance.7–9,12 The data are particularly persuasive in infiltrative and hypertrophic diseases, where myocardial mass increases disproportionately to stroke volume. In these settings, MCF captures the progressive inefficiency of the myocardium long before cavity-based metrics deteriorate. Perhaps the most provocative finding is the divergent behaviour of MCF and LVEF across increasing grades of hypertension. As blood pressure values increased, LVEF paradoxically rose, whereas MCF declined in a directionally coherent manner. This observation elegantly illustrates how LVEF can misrepresent disease progression by conflating compensatory geometric changes with preserved contractility. By contrast, the monotonic decline in MCF aligns with the known pathophysiology of hypertensive heart disease, characterized by increasing myocardial mass, fibrosis, and impaired efficiency. This capacity to track disease severity, rather than merely detect disease presence, positions MCF as a potentially valuable tool for longitudinal assessment and follow-up.4–6 The prognostic analyses further strengthen the case for MCF. In a large, external, all-comers clinical cohort, MCF outperformed LVEF, left ventricular mass index, end-diastolic volume index, and stroke volume in predicting all-cause mortality. Crucially, neither stroke volume nor myocardial mass alone showed consistent prognostic power—highlighting that it is their ratio, not their absolute values, that carries biological meaning.7–9,12 This finding reinforces the notion that MCF is not merely a mathematical rearrangement of existing parameters but an integrative marker capturing the interplay between structure and function. The incremental prognostic value of MCF when added to models containing LVEF further supports its role as a complementary, rather than competing, metric.4–6 Modern cardiac imaging increasingly embraces deformation-based metrics such as global longitudinal strain (GLS) and, more recently, myocardial work indices derived from pressure–strain loops. These tools have advanced the field by offering greater sensitivity to subclinical dysfunction and partial adjustment for loading conditions.4–6 MCF occupies a distinct and complementary niche within this ecosystem. While GLS primarily reflects longitudinal fibre shortening and remains load-sensitive, MCF integrates global myocardial performance relative to total myocardial volume. The modest correlation between LVEF and MCF observed in this study reinforces that these metrics interrogate different dimensions of systolic function.7–9 Rather than viewing MCF as a replacement for strain or myocardial work, the data argue for a multiparametric approach in which MCF contributes a geometry-robust, volumetric perspective on myocardial efficiency.3 A key strength of this work is its demonstration that MCF can be derived automatically using validated artificial intelligence–based CMR segmentation, without additional acquisition time or complex post-processing. Stroke volume and myocardial mass are already routinely measured; reporting their ratio is therefore a low-cost, high-yield addition4–6 (Figure 1). summary slide about the need to reconsider the central role of left ventricular ejection fraction. The authors appropriately acknowledge current limitations. MCF, like LVEF, may overestimate effective forward function in the presence of significant valvular regurgitation, and its behaviour in acute conditions such as myocarditis or myocardial infarction remains to be defined. Moreover, clinically meaningful thresholds for change over time and disease-specific severity cut-offs require longitudinal outcome-driven validation. Nevertheless, these limitations should be viewed as opportunities for future investigation rather than barriers to adoption.3 The relevance of MCF may be particularly profound in heart failure with preserved ejection fraction (HFpEF), a syndrome defined more by what LVEF fails to capture than by what it reveals. In conditions such as hypertensive heart disease and amyloidosis (core substrates of HFpEF) MCF may enable earlier identification of impaired myocardial performance and more refined risk stratification.13–15 By re-centring assessment on the myocardium itself, MCF aligns closely with the evolving conceptualization of heart failure as a disorder of myocardial efficiency rather than simply pump failure. Kurdi et al.3 deliver a rigorous, methodologically robust, and conceptually important study that repositions MCF as a clinically relevant imaging biomarker.1,3 By establishing normative values, demonstrating superior disease discrimination, resolving paradoxes inherent to LVEF, and confirming independent prognostic value, this work provides a strong foundation for broader adoption of MCF in cardiovascular imaging. In an era increasingly defined by precision phenotyping and automated quantification, MCF offers a simple yet powerful reminder: to understand cardiac function, we must look beyond how much the ventricle empties and refocus on how effectively the myocardium works. The Cardiac Echo-corelab team, CHU Rennes [email protected]. Erwan Donal (MD, PhD (Conceptualization [lead]; Formal analysis [lead]; Supervision [lead]; Validation [lead]; Visualization [lead]; Writing—original draft [lead]; Writing—review & editing [lead])), Paul-Calin CRACIUN MD (Conceptualization [equal]; Validation [lead]; Writing—original draft [equal]; Writing—review & editing [equal])), and Bogdan A. POPESCU (Validation [equal]; Visualization [equal]; Writing—review & editing [equal]) None declared. The data underlying this article will be shared on reasonable request to the corresponding author.
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7125508845
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