To evaluate the long-term prognostic impact of delayed recovery of independent ambulation and post-operative sarcopenia progression in patients undergoing endovascular aortic aneurysm repair (EVAR).
In this multicenter retrospective cohort study, 228 patients (mean age 78.1 ± 6.5 years; 82.5% male) who underwent EVAR for abdominal aortic aneurysm between January 2015 and December 2020 were included. Independent ambulation was defined as walking ≥ 15 m. Sarcopenia was assessed using the psoas muscle index (PMI) at L3 on CT, normalized by height squared. Baseline PMI was measured within 3 months preoperatively; post-operative sarcopenia progression was calculated as ΔPMI/baseline (% change from baseline to 6 months). The primary outcome was all-cause mortality, analyzed using multivariate Cox proportional hazards models.
Over a mean follow-up of 4.6 ± 2.2 years, 52 patients (22.8%) died. Mean time to independent ambulation was 1.4 ± 1.2 days, and mean ΔPMI/baseline decreased by 4.5% ± 8.9%. After adjusting for age, sex, nutritional status, and pre-operative sarcopenia, time to independent ambulation (HR 1.25; 95% CI 1.07–1.46; p = 0.004) and ΔPMI/baseline (HR 1.13; 95% CI 1.09–1.17; p < 0.001) were independent predictors of mortality. ROC analysis identified cut-offs of ≥ 2 days for ambulation and a decrease of ≥ 6.09% in ΔPMI/baseline. Patients meeting both criteria exhibited the poorest survival, representing delayed ambulation and marked sarcopenia progression.
Delayed recovery of independent ambulation and post-operative sarcopenia progression independently predict all-cause mortality after EVAR and may serve as clinically useful indicators for risk stratification and targeted rehabilitation.
Hospital-associated sarcopenia (HAS) is a preventable and reversible condition characterized by rapid muscle loss during hospitalization. Although its prevalence is higher than that of age-related sarcopenia, the clinical recognition and structured management of this condition remain limited. In this narrative review, the pathophysiology of HAS is synthesized, the effectiveness of acute-phase interventions is evaluated, and the implementation challenges are examined to propose multifaceted strategies for optimizing treatment outcomes. The development of HAS involves a vicious cycle of activity limitation, inflammation, malnutrition, and iatrogenic stress. Initiating interventions within 48 h may aid in preserving muscle function and improving the patients' quality of life. However, protocol variability, inadequate patient stratification, fragile transitional care systems, and other challenges persist. The proposed solutions include modular protocols, electronic medical record-integrated adaptive algorithms, and strengthened team coordination. To prevent HAS progression and improve patient-centered outcomes, timely, structured multidisciplinary interventions in the acute phase are imperative. Standardized evaluations, scalable protocols, and sustainable post-discharge systems are key to advancing the clinical implementation of HAS management strategies.
We read with great interest the article by Uchida et al. [1], regarding the J-MINT study baseline data. The authors highlighted a compelling dissociation in older adults with Mild Cognitive Impairment (MCI): while clinical visual acuity (LogMAR) was largely preserved, self-reported visual difficulties were significantly associated with physical, social, and cognitive frailty. We commend the authors for establishing “self-reported vision status” (SRVS) as a sensitive marker for frailty, potentially superior to standard acuity charts in this specific population.
From a neuro-ophthalmic perspective, we suggest that this discrepancy—good acuity yet poor subjective vision—is not merely a psychological phenomenon but likely reflects specific pathophysiological changes in the early stages of neurodegeneration. Standard high-contrast visual acuity testing primarily assesses the parvocellular pathway, which is often resilient in early MCI [2]. Conversely, the magnocellular pathway and the dorsal visual stream, which process low-contrast information, motion, and depth, are known to be selectively vulnerable to early amyloid and tau pathology [3].
Therefore, the “poor vision” reported by participants, despite their 20/20 acuity, may represent a functional deficit in contrast sensitivity (CS). This “hidden” deficit explains the study's observation that poor SRVS correlates with the Fall Risk Index (FRI) [1]. Postural stability relies heavily on detecting low-contrast edges (like carpet borders) and processing optic flow, functions governed by the dorsal stream rather than the foveal acuity measured by LogMAR [4].
We propose that Uchida et al.'s findings support a paradigm shift in defining “Eye Frailty.” We suggest conceptualizing subjective vision not just as a proxy for acuity, but as a distinct neuro-visual dimension of frailty. This dimension likely captures the “cognitive cost” of processing visual information through a compromised neural network.
Moving forward, incorporating rapid contrast sensitivity assessments (e.g., Pelli-Robson charts or frequency-doubling technology) in geriatric research frameworks could objectively quantify this dimension. This would bridge the gap between the patient's lived experience and clinical metrics, ultimately refining fall prevention strategies for the growing MCI population.
The authors have nothing to report.
The authors have nothing to report.
The authors have nothing to report.
The authors have nothing to report.
The authors declare no conflicts of interest.
Data sharing is not applicable to this article as no new data were created or analyzed in this study.
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