MAPSE in critical illness: from prognostic association to clinical utility

Dear editor

We read with great interest the study by Cavefors et al. [1]. In this exploratory secondary analysis of a prospective ICU cohort, MAPSE was feasible in 90% of patients, and MAPSE ≤ 10 mm remained associated with 90-day mortality after adjustment for age, Simplified Acute Physiology Score 3, and cardiac index (adjusted odds ratio [OR] 2.48, 95% confidence interval [CI] 1.31–4.71). The authors should be commended for evaluating a simple longitudinal systolic index in a mixed population of critically ill patients. However, three issues merit consideration before MAPSE is incorporated into routine clinical decision-making.

First, prognostic association alone does not establish clinical utility. The nested-model analysis suggests that MAPSE adds prognostic information to a baseline model; however, the study does not show whether MAPSE-guided assessment changes management or improves outcomes beyond standard clinical and haemodynamic evaluation. An isolated reduction in MAPSE cannot determine whether a patient is preload responsive, afterload sensitive, or likely to benefit from inotropic support. For example, in a patient with an LVEF of 60% but a MAPSE of 7 mm, this finding might reasonably prompt closer monitoring or further haemodynamic assessment, but would not, by itself, justify initiating an inotrope. Reduced MAPSE may reflect altered loading conditions, transient myocardial stunning, or established myocardial injury, each with different therapeutic implications. Serial measurements, analyses of treatment–MAPSE interactions, and clinical-impact studies are therefore needed to establish whether MAPSE is actionable rather than simply prognostic.

Second, the same MAPSE threshold may not have the same biological meaning across different clinical aetiologies. Although the authors appropriately performed exploratory analyses in patients with sepsis, respiratory failure, cardiac disease, and other conditions, the confidence intervals were wide and the reported clinical categories were broad and potentially overlapping. In sepsis, reduced longitudinal function may reflect sepsis-associated myocardial dysfunction, with potentially different degrees of reversibility [2]. In acute or chronic cardiac disease, it may instead reflect ischaemic injury, regional dysfunction, or established myocardial fibrosis. Neurological indications accounted for 40% of admissions in the “other conditions” category; in such patients, catecholamine-mediated myocardial injury or autonomic dysregulation may be relevant [3]. Similar directions of association across subgroups should not be interpreted as evidence of a common mechanism or comparable treatment responsiveness. Future studies should therefore prespecify aetiological strata, test for interactions, and evaluate serial changes in MAPSE during recovery.

Third, structural annular disease may limit the specificity of MAPSE as a marker of myocardial contractility. The authors appropriately acknowledge angle dependency, cursor alignment, off-axis annular motion, and variation according to the sampled annular region [1]. In addition, three-dimensional imaging has shown that mitral annular calcification (MAC) is associated with altered mitral annular dynamics [4]. Because MAPSE quantifies annular displacement rather than myocardial shortening directly, advanced MAC could affect the relationship between a low MAPSE and intrinsic longitudinal myocardial function. This issue may be clinically relevant in an older ICU population with multiple comorbidities. It would not invalidate the association between MAPSE and mortality, but it could alter the physiological interpretation of a low value: MAPSE may reflect a combination of myocardial dysfunction, annular structure, and loading conditions rather than isolated longitudinal contractility. Future studies should report the presence and severity of MAC and assess whether it modifies the association between MAPSE and outcome.

In summary, Cavefors et al. provide valuable evidence that MAPSE is feasible and prognostically informative in critically ill patients. We suggest that its initial clinical implementation, if pursued, should be framed as a trigger for integrated haemodynamic assessment and serial reassessment, rather than as a stand-alone indication for inotropic therapy. Determining whether MAPSE-guided care improves outcomes, whether its meaning varies by aetiology, and whether annular disease affects its validity will be essential to translate prognostic association into patient benefit.

Abbreviations

CI

Confidence interval

GLS

Global longitudinal strain

LVEF

Left ventricular ejection fraction

MAC

Mitral annular calcification

MAPSE

Mitral annular plane systolic excursion

Author contributions

YYH and XJH conceived the comment and drafted the manuscript. YYH and XJH critically revised the manuscript for important intellectual content. All authors read and approved the final manuscript.

Funding

No funding was received for this work.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.