Abstract
Background
Dysphagia is common in older patients with heart failure (HF), but evidence regarding sarcopenic dysphagia remains limited. The purpose of this retrospective study was to clarify the prevalence of sarcopenic dysphagia and its relationship with swallowing-related measures and prognosis in older patients with HF.
Methods and Results
The study group included patients aged ≥65 years admitted with HF between June 2021 and December 2023. Patients were classified into 3 groups using the diagnostic algorithm for sarcopenic dysphagia at discharge: robust (without sarcopenia), sarcopenia (with sarcopenia only), and sarcopenic dysphagia (with sarcopenia and dysphagia). Outcomes were swallowing-related measures (maximal tongue pressure, geniohyoid muscle area, and geniohyoid muscle echogenicity) and a 1-year composite outcome (all-cause death or HF-related readmission). Of 524 screened patients, 363 were analyzed (median age 83 years [Q1–Q3: 78–90 years], 46.6% women); 61 patients were robust (16.8%), 215 had sarcopenia (59.2%), and 87 had sarcopenic dysphagia (24.0%). In the analysis of covariance, swallowing-related measures were poorer in the sarcopenic dysphagia group compared with the robust group (P<0.05). In the Cox regression analysis compared with robust, sarcopenia was not statistically significantly associated with prognosis, but sarcopenic dysphagia was associated with a higher risk (hazard ratio 2.53, 95% confidence interval 1.30–4.90, P=0.006).
Conclusions
Sarcopenic dysphagia affected 24.0% of patients with HF, and was associated with poorer swallowing-related measures and prognosis.
Key Words: Acute disease, Deglutition disorders, Heart failure, Sarcopenia
Central Figure.
Population aging is increasing the burden of heart failure (HF) among older adults in Japan, and clinical outcomes remain suboptimal.1 In older patients with HF, prognosis is influenced not only by cardiac dysfunction but also by non-cardiac complications.2 Among these, dysphagia is increasingly recognized as a common and clinically relevant problem, with recent studies reporting a prevalence of 23–36% in older HF populations.3–6 These observations support the clinical importance of routinely evaluating swallowing function in older patients with HF.
Recent evidence suggests that whole-body sarcopenia contributes to the development of dysphagia in older adults.7 In addition, sarcopenia related to malnutrition has been associated with marked declines in swallowing-related measures in older patients with HF.3 This emerging phenotype, in which dysphagia develops in the context of systemic sarcopenia, has been termed sarcopenic dysphagia.7 Identifying sarcopenic dysphagia is clinically important because it has been associated with higher mortality rates than dysphagia due to non-sarcopenic causes, and may capture a clinically vulnerable phenotype in which systemic sarcopenia and swallowing-related problems coexist.8 This may provide insight into the pathophysiology of dysphagia in older patients with HF and help guide nutritional and rehabilitation strategies.
However, the epidemiology of this condition in patients with HF remains limited, and the prevalence and clinical outcomes that underpin potential interventions are still unclear. Although a prior study suggested that possible sarcopenia at admission may be associated with dysphagia at discharge in patients with HF,9 detailed swallowing-related measures and prognosis were not systematically evaluated. Therefore, in this study we aimed to determine the prevalence of sarcopenic dysphagia and to examine its associations with swallowing-related measures and prognosis in older patients with HF.
Methods
Study Design and Patient Population
The study design was a retrospective review of an initial cohort of 524 consecutive patients aged ≥65 years who were hospitalized with HF between June 2021 and December 2023, including only those who could follow instructions. The diagnosis of HF was based on the Framingham criteria and confirmed by experienced cardiologists.10 The exclusion criteria were: (1) cerebrovascular disease, (2) undergoing maintenance hemodialysis, (3) pacemaker implantation, (4) in-hospital death, and (5) missing data on skeletal muscle mass index. The study protocol conformed to the Strengthening the Reporting of Observational Studies in Epidemiology guidelines and ethical principles of the 1975 Declaration of Helsinki. It was approved by the Institutional Ethics Committee of the Sagamihara Kyodo Hospital (No. 221). Patient consent was deemed non-applicable as this observational study utilized de-identified data. Therefore, the Institutional Review Board did not require patient consent. An opt-out mechanism was available, allowing patients to withdraw from the study as detailed in the study protocol on the hospital website, in accordance with the committee’s recommendations.
Data Collection
All clinical data at discharge were collected from electronic medical records. Prognostic risk was quantified using the Meta-analysis Global Group in Chronic Heart Failure (MAGGIC) risk score, a validated tool for estimating all-cause mortality in patients with HF.11,12 The score is calculated from 13 routinely available clinical parameters and ranges from 0 to 56, with higher values indicating higher predicted mortality risk.11,12 Nutritional status was evaluated using the Mini Nutritional Assessment Short-Form, which includes 6 components addressing recent weight loss, reduced food intake, mobility, recent psychological stress or acute illness, neuropsychological problems, and body mass index. The total score ranges from 0 to 14, with lower scores indicating worse nutritional status.13 In our hospital, based on previous studies,3 handgrip strength, usual gait speed, maximal tongue pressure, the Food Intake LEVEL Scale, and geniohyoid ultrasonography are routinely performed as part of clinical care during hospitalization in older patients with HF. Handgrip strength was measured using a digital dynamometer (TKK 5101 Grip-D; Takei, Tokyo, Japan).14 The patients were seated with their elbows flexed at 90°, and 2×3-s maximal isometric voluntary contractions were measured for each hand. The highest value was used in the analysis. Usual gait speed was assessed on a 10-m walkway, with patients instructed to walk at their usual speed.15 The Food Intake LEVEL Scale was assessed at discharge by speech therapists and well-trained nurses and physical therapists who performed bedside swallowing evaluations, which included assessments of the patient’s level of consciousness, mouth and tongue function, vocal capabilities, oral hygiene, and cough reflex.3,4 Subsequently, a water-swallowing test was conducted for patients deemed to have adequate swallowing competence, and dietary patterns were established based on the test results. Food Intake LEVEL Scale ≤8 was used to identify dysphagia because this threshold indicates that patients require some form of dietary modification or swallowing-related management rather than taking a regular diet without restriction, and it has been used in previous studies of dysphagia.3,4
Assessment of Sarcopenia and Sarcopenic Dysphagia
Participants were categorized into 3 groups according to the published diagnostic algorithm for sarcopenic dysphagia:7 robust (no sarcopenia), sarcopenia (sarcopenia without dysphagia), and sarcopenic dysphagia (concurrent sarcopenia and dysphagia) (Figure 1). The algorithm is a 3-step procedure. First, low muscle strength and/or low physical performance were identified using handgrip strength (men <26 kg; women <18 kg) and/or usual gait speed (≤0.8 m/s). These thresholds were used to maintain consistency with the published diagnostic algorithm for sarcopenic dysphagia.7 Second, low muscle mass was defined by the skeletal muscle mass index (men <7.0 kg/m2; women <5.7 kg/m2). Third, dysphagia was determined using the Food Intake LEVEL Scale, with levels ≤8 indicating dysphagia.3,4 For the present analysis, patients without sarcopenia or dysphagia were classified as robust; those with sarcopenia but without dysphagia were classified as sarcopenia; and those with both sarcopenia and dysphagia were classified as sarcopenic dysphagia. The 9 patients with dysphagia without sarcopenia were excluded from the primary three-group analyses.
Figure 1.
Flow chart of the study population. BIA, bioelectrical impedance analysis; SMI, skeletal muscle mass index.
Outcomes
Outcomes were swallowing-related measures, assessed by maximal tongue pressure, geniohyoid muscle area, and geniohyoid echogenicity during hospitalization, and a 1-year composite outcome of all-cause death or HF-related readmission.
Geniohyoid muscle area and echogenicity were evaluated using submental ultrasonography with a convex probe (SONIMAGE MX1, C5-2; KONICA MINOLTA, Tokyo, Japan) under standardized settings by a single physical therapist blinded to other clinical information.3 Participants were examined while in a 60° reclined position with the head neutral. The transducer was positioned at the midline beneath the chin, and resting images of the geniohyoid region were obtained for analysis. Muscle area was quantified by manual tracing within the fascial border, and echogenicity was calculated as the mean grayscale value within the region of interest (0–255), with higher values indicating greater echogenicity. Maximal tongue pressure was measured in the same posture using a tongue-pressure device (JMS, Hiroshima, Japan).4 After calibration, participants compressed the balloon against the hard palate with maximal effort. Three trials were performed, and the maximum value was used. These measurements were performed according to previously reported protocols with established reproducibility.16,17
For the prognostic outcome, time-to-event was calculated from discharge to the first occurrence of death or HF-related readmission. Follow-up information within 1 year after discharge was obtained from medical records and, when necessary, confirmed by telephone contact with patients or family members for outcome ascertainment, with data collection through December 2024.
Statistical Analysis
Continuous variables were summarized as medians with interquartile ranges, and categorical variables as counts and percentages. Baseline characteristics were compared across groups using one-way analysis of variance or the Kruskal–Wallis test for continuous variables, as appropriate, and the chi-square test for categorical variables.
Swallowing-related measures were compared among the robust, sarcopenia, and sarcopenic dysphagia groups using analysis of covariance, with maximal tongue pressure, geniohyoid muscle area, and geniohyoid echogenicity as dependent variables. Analysis of covariance was used to compare model-based estimates while adjusting for potential confounders, including age, sex, body mass index, log-transformed N-terminal pro-B-type natriuretic peptide (NT-proBNP), and New York Heart Association class.3–6 Model assumptions were assessed by evaluating residual normality and homogeneity of variances using Q–Q plots and Levene’s test, respectively. Post hoc pairwise comparisons were performed using estimated marginal means with Tukey adjustment.
For the 1-year composite outcome of all-cause death or HF-related readmission, event-free survival was evaluated using Kaplan–Meier curves and compared with the log-rank test. Cox proportional hazards models were used to estimate hazard ratios (HR) with 95% confidence intervals (CI), using the robust group as the reference. Models were adjusted for the MAGGIC risk score and log-transformed NT-proBNP; the MAGGIC score has been validated in Japanese HF cohorts.12
Missing covariate data were addressed using multiple imputation by chained equations, generating 20 imputed datasets that were pooled using Rubin’s rules.18 Analyses were conducted in R version 4.1.3 (R Foundation for Statistical Computing, Vienna, Austria). Statistical tests were two-sided, and P values <0.05 were considered significant.
Results
Patients’ Characteristics
In this study, 161 of the 524 patients with HF were excluded, leaving 363 patients for analysis (Figure 1). In the cross-tabulation of sarcopenia and Food Intake LEVEL Scale ≤8, 9 patients had dysphagia without sarcopenia and they were excluded from the primary three-group analyses; their descriptive characteristics are shown in the Supplementary Table. Compared with patients with sarcopenic dysphagia, patients with dysphagia without sarcopenia were younger and had higher skeletal muscle mass index, handgrip strength, and maximal tongue pressure, while Food Intake LEVEL Scale and geniohyoid muscle area were similar and geniohyoid muscle echogenicity was slightly lower. Table 1 displays the baseline characteristics of all patients and the results of between-group comparisons. The median age of the study population was 83 years (Q1–Q3: 78–90 years), and 46.6% of the participants were women. Of these, 61 (16.8%) were classified as robust, 215 (59.2%) as having sarcopenia, and 87 (24.0%) as having sarcopenic dysphagia. Sarcopenic dysphagia was characterized by older age, lower body mass index, more severe HF, poorer nutritional status, and a higher prevalence of dementia. In addition, patients with reductions in all 3 sarcopenia components, namely low skeletal muscle mass, low handgrip strength, and low gait speed (severe sarcopenia), were observed in 88 patients with sarcopenia alone (40.9%) and in 70 patients with sarcopenic dysphagia (80.5%).
Table 1.
Demographic and Clinical Characteristics of the Study Patients
| Characteristic | Missing data (%) |
Overall (n=363) |
Robust (n=61) |
Sarcopenia (n=215) |
Sarcopenic dysphagia (n=87) |
P value |
|---|---|---|---|---|---|---|
| Age [years] | 0 (0.0) | 83 [78–90] | 80 [73–85] | 83 [78–90] | 84 [81–92] | <0.001 |
| Sex, women (%) | 0 (0.0) | 169 (46.6) | 33 (54.1) | 89 (41.4) | 47 (54.0) | 0.069 |
| Body mass index [kg/m2] | 0 (0.0) | 20.2 [18.3–23.1] | 23.6 [20.7–26.4] | 20.0 [18.3–22.6] | 18.9 [17.2–21.5] | <0.001 |
| SBP [mmHg] | 0 (0.0) | 142 [121–163] | 142 [120–164] | 144 [121–163] | 142 [123–161] | 0.813 |
| DBP [mmHg] | 0 (0.0) | 87 [71–103] | 89 [75–110] | 85 [71–100] | 87 [71–101] | 0.243 |
| Heart rate [beats/min] | 0 (0.0) | 90 [73–113] | 96 [77–114] | 87 [70–114] | 88 [72–105] | 0.250 |
| LVEF [%] | 0 (0.0) | 53.0 [39.6–64.3] | 53.1 [42.9–62.7] | 51.6 [39.3–64.8] | 53.8 [39.4–65.2] | 0.987 |
| Heart failure phenotype (%) | 0.500 | |||||
| HFrEF | 0 (0.0) | 95 (26.2) | 13 (21.3) | 59 (27.4) | 23 (26.4) | |
| HFmrEF | 0 (0.0) | 67 (18.5) | 15 (24.6) | 40 (18.6) | 12 (13.8) | |
| HFpEF | 0 (0.0) | 201 (55.4) | 33 (54.1) | 116 (54.0) | 52 (59.8) | |
| NYHA class III/IV (%) | 0 (0.0) | 29 (8.0) | 2 (3.3) | 13 (6.0) | 14 (16.1) | 0.018 |
| MAGGIC risk score | 0 (0.0) | 29 [25–32] | 27 [24–29] | 29 [25–32] | 30 [27–34] | 0.001 |
| MNA-SF [points] | 0 (0.0) | 9 [7–11] | 10 [8–11] | 9 [6–10] | 6 [4–8] | <0.001 |
| Food Intake LEVEL Scale | 0 (0.0) | 10 [10–10] | 10 [10–10] | 10 [10–10] | 7 [6–8] | <0.001 |
| Comorbidities (%) | ||||||
| Dementia | 0 (0.0) | 70 (19.3) | 2 (3.3) | 25 (11.6) | 43 (49.4) | <0.001 |
| Hypertension | 0 (0.0) | 255 (70.2) | 44 (72.1) | 149 (69.3) | 62 (71.3) | 0.888 |
| Diabetes | 0 (0.0) | 135 (37.2) | 24 (39.3) | 75 (34.9) | 36 (41.4) | 0.531 |
| Atrial fibrillation | 0 (0.0) | 210 (57.9) | 37 (60.7) | 118 (54.9) | 55 (63.2) | 0.368 |
| Chronic renal failure | 0 (0.0) | 157 (43.3) | 24 (39.3) | 82 (38.1) | 51 (58.6) | 0.004 |
| Laboratory data | ||||||
| NT-proBNP [pg/mL] | 35 (9.6) | 1,637 [671–5,583] | 1,922 [868–3,266] | 1,338 [689–3,362] | 3,070 [764–8,652] | 0.036 |
| Hemoglobin A1c [%] | 24 (6.6) | 6.0 [5.6–6.5] | 6.1 [5.8–6.6] | 6.0 [5.7–6.5] | 6.0 [5.5–6.5] | 0.048 |
| Creatinine [mg/dL] | 14 (3.9) | 1.1 [0.8–1.6] | 1.2 [0.9–1.7] | 1.1 [0.9–1.7] | 1.1 [0.8–1.6] | 0.190 |
| eGFR [mL/min/1.73 m2] | 11 (3.0) | 38.5 [26.1–52.1] | 34.7 [21.3–49.6] | 37.2 [22.2–49.8] | 39.2 [24.7–53.1] | 0.736 |
| Albumin [g/dL] | 0 (0.0) | 3.2 [2.9–3.5] | 3.4 [3.0–3.8] | 3.2 [2.9–3.6] | 3.1 [2.7–3.4] | <0.001 |
| Hemoglobin [g/dL] | 0 (0.0) | 11.7 [10.2–13.2] | 12.2 [10.9–14.0] | 11.5 [10.3–13.2] | 11.5 [9.9–12.7] | <0.001 |
| C-reactive protein [mg/dL] | 0 (0.0) | 0.5 [0.2–1.2] | 0.4 [0.2–0.9] | 0.5 [0.2–1.1] | 0.6 [0.2–1.4] | 0.058 |
| Medications (%) | ||||||
| β-blocker | 0 (0.0) | 270 (74.4) | 56 (91.8) | 161 (74.9) | 53 (60.9) | 0.001 |
| ACEI/ARB/ARNI | 0 (0.0) | 180 (49.6) | 25 (41.0) | 110 (51.2) | 45 (51.7) | 0.890 |
| Sarcopenia-related measures | ||||||
| Skeletal muscle mass index [kg/m2] |
0 (0.0) | 5.5 [4.3–6.3] | 6.7 [6.0–7.4] | 5.5 [4.5–6.1] | 4.0 [3.3–5.2] | <0.001 |
| Gait speed [m/s] | 5 (1.4) | 0.8 [0.6–1.0] | 1.0 [0.7–1.1] | 0.8 [0.6–0.9] | 0.6 [0.5–0.7] | <0.001 |
| Handgrip strength [kg] | 21 (5.8) | 18.8 [13.2–24.7] | 25.8 [17.3–29.5] | 18.8 [14.0–24.1] | 12.6 [6.8–17.3] | <0.001 |
| Swallowing-related measures | ||||||
| Maximal tongue pressure [kPa] | 3 (0.8) | 23.1 [18.9–26.3] | 24.9 [23.1–29.3] | 23.5 [20.2–26.7] | 18.4 [17.2–21.1] | <0.001 |
| Geniohyoid muscle area [mm2] | 49 (13.5) | 157.9 [141.6–169.6] | 161.5 [152.7–171.6] | 160.3 [143.6–170.8] | 143.1 [133.5–156.4] | <0.001 |
| Geniohyoid muscle echogenicity | 49 (13.5) | 30.1 [25.6–35.0] | 28.3 [24.5–33.1] | 29.5 [25.5–34.0] | 35.2 [28.3–41.6] | 0.014 |
Values are median [interquartile range] and n (%). ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin-receptor blocker; ARNI, angiotensin receptor–neprilysin inhibitor; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; HFmrEF, heart failure with mildly reduced ejection fraction; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; LVEF, left ventricular ejection fraction; MAGGIC, Meta-analysis Global Group in Chronic Heart Failure; MNA-SF, Mini Nutritional Assessment Short-Form; NT-proBNP, N-terminal pro-B-type natriuretic peptide; NYHA, New York Heart Association; SBP, systolic blood pressure.
Sarcopenia and Sarcopenic Dysphagia on Swallowing-Related Measures
Maximal tongue pressure data were available for 360 patients (robust, n=60; sarcopenia, n=213; sarcopenic dysphagia, n=87), with geniohyoid muscle area and echogenicity data available for 314 patients (robust, n=48; sarcopenia, n=187; sarcopenic dysphagia, n=79). Missing data reflected occasional omissions in routine clinical assessment or recording, and no specific procedural reason for unsuccessful measurement was documented. Unadjusted and adjusted estimated marginal means of swallowing-related measures according to sarcopenic dysphagia status are shown in Table 2. In the adjusted model, statistically significant overall group effects were observed for maximal tongue pressure, geniohyoid muscle area, and geniohyoid muscle echogenicity (F=17.78, P<0.001; F=4.27, P=0.015; and F=3.48, P=0.032, respectively). In post hoc comparisons using estimated marginal means with Tukey adjustment, maximal tongue pressure was statistically significantly lower in the sarcopenic dysphagia group than in both the robust and sarcopenia groups. Geniohyoid muscle area was statistically significantly lower, and geniohyoid muscle echogenicity was statistically significantly higher in the sarcopenic dysphagia group than in the robust group.
Table 2.
Unadjusted and Adjusted Estimated Marginal Means of Swallowing-Related Measures According to Sarcopenic Dysphagia Status
| Variable | Robust | Sarcopenia | Sarcopenic dysphagia |
F value | P value |
|---|---|---|---|---|---|
| Maximal tongue pressure, kPa | |||||
| Unadjusted model | 25.5 (24.3–26.8) | 23.9 (23.2–24.5) | 19.1 (18.1–20.2)*,† | 36.93 | <0.001 |
| Adjusted model | 24.1 (21.9–26.3) | 23.7 (21.8–25.5) | 20.1 (18.1–22.1)*,† | 17.78 | <0.001 |
| Geniohyoid muscle area, mm2 | |||||
| Unadjusted model | 161.0 (155.3–166.6) | 158.5 (155.5–161.5) | 147.2 (141.8–152.7)* | 7.70 | <0.001 |
| Adjusted model | 159.7 (148.8–170.5) | 157.6 (148.4–166.7) | 148.3 (137.7–158.9)* | 4.27 | 0.015 |
| Geniohyoid muscle echogenicity | |||||
| Unadjusted model | 30.2 (28.0–32.2) | 31.0 (27.9–34.1) | 36.0 (33.0–39.1)* | 5.07 | 0.007 |
| Adjusted model | 30.6 (27.2–34.1) | 30.7 (29.0–32.3) | 35.5 (32.3–38.7)* | 3.48 | 0.032 |
Values are estimated marginal means with 95% confidence intervals. The adjusted model included age, sex, body mass index, log-transformed N-terminal pro-B-type natriuretic peptide, and New York Heart Association class. F values and P values indicate the overall group effect from analysis of covariance. Post hoc pairwise comparisons were performed using estimated marginal means with Tukey adjustment. *P<0.05 vs. Robust; †P<0.05 vs. Sarcopenia.
Sarcopenia and Sarcopenic Dysphagia on Prognosis
During the follow-up period, 53 (14.6%) patients died, and 82 (22.6%) were readmitted due to HF (Table 3). Kaplan–Meier analysis showed significant between-group differences in both the composite outcome and all-cause death (log-rank P<0.001 for both; Figure 2A,B). In contrast, the difference in HF-related readmission was not statistically significant (log-rank P=0.058; Figure 2C). Table 4 presents the results of the Cox proportional hazards model adjusted for the MAGGIC risk score and log-transformed NT-proBNP. In the survival analysis for the composite event using robust as the reference, the hazard for sarcopenia was not significantly different (HR 1.36, 95% CI 0.74–2.50, P=0.318), but for sarcopenic dysphagia, it was significantly higher (HR 2.53, 95% CI 1.30–4.90, P=0.006). Similarly, in the analysis for all-cause death, the hazard for sarcopenia was not significantly different (HR 0.98, 95% CI 0.47–2.10, P=0.960), but for sarcopenic dysphagia, it was significantly higher (HR 3.43, 95% CI 1.42–8.29, P=0.006). Finally, in the survival analysis for HF-related readmission using robust as the reference, the hazard was not significantly different in sarcopenia (HR 1.55; 95% CI 0.78–3.07; P=0.208) and sarcopenic dysphagia (HR 1.96; 95% CI 0.89–4.29; P=0.095).
Table 3.
Event Numbers and Follow-up Status According to Sarcopenic Dysphagia Status
| Variable | Overall (n=363) |
Robust (n=61) |
Sarcopenia (n=215) |
Sarcopenic dysphagia (n=87) |
|---|---|---|---|---|
| Composite outcome, n (%) | 106 (29.2) | 14 (23.0) | 58 (27.0) | 34 (39.1) |
| All-cause death, n (%) | 53 (14.6) | 7 (11.5) | 22 (10.2) | 24 (27.6) |
| Heart failure-related readmission, n (%) | 82 (22.6) | 11 (18.0) | 50 (23.3) | 21 (24.1) |
| 1-year outcome status ascertained, n (%) | 213 (58.7) | 41 (67.2) | 127 (59.1) | 45 (51.7) |
Values are presented as n (%). The composite outcome was defined as the first occurrence of all-cause death or HF-related readmission within 1 year after discharge.
Figure 2.
(A–C) Kaplan–Meier survival curves for prognosis.
Table 4.
Unadjusted and Adjusted Cox Regression Analyses According to Sarcopenic Dysphagia Status
| Variable | Unadjusted model | Adjusted model | ||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P value | HR | 95% CI | P value | |
| Composite outcome | ||||||
| Robust (n=61) | 1.00 | (Ref.) | 1.00 | (Ref.) | ||
| Sarcopenia (n=215) | 1.33 | 0.74–2.39 | 0.337 | 1.36 | 0.74–2.50 | 0.318 |
| Sarcopenic dysphagia (n=87) | 3.04 | 1.63–5.68 | <0.001 | 2.53 | 1.30–4.90 | 0.006 |
| All-cause death | ||||||
| Robust (n=61) | 1.00 | (Ref.) | 1.00 | (Ref.) | ||
| Sarcopenia (n=215) | 1.00 | 0.43–2.36 | 0.987 | 0.98 | 0.47–2.10 | 0.960 |
| Sarcopenic dysphagia (n=87) | 5.06 | 2.17–11.82 | <0.001 | 3.43 | 1.42–8.29 | 0.006 |
| Heart failure-related readmission | ||||||
| Robust (n=61) | 1.00 | (Ref.) | 1.00 | (Ref.) | ||
| Sarcopenia (n=215) | 1.46 | 0.76–2.80 | 0.257 | 1.55 | 0.78–3.07 | 0.208 |
| Sarcopenic dysphagia (n=87) | 2.33 | 1.12–4.85 | 0.023 | 1.96 | 0.89–4.29 | 0.095 |
Adjusted variables were the Meta-analysis Global Group in Chronic Heart Failure risk score and log-transformed N-terminal pro-B-type natriuretic peptide. CI, confidence interval; HR, hazard ratio.
Discussion
Our study provided novel evidence regarding sarcopenic dysphagia in older patients with HF. Sarcopenic dysphagia was present in 24.0% of the cohort, and swallowing-related measures differed across categories, with statistically significant post hoc differences observed between the robust and sarcopenic dysphagia groups. In the prognostic analyses, sarcopenia alone was not statistically significantly associated with different outcomes, whereas sarcopenic dysphagia was associated with a significantly higher risk of adverse events. Collectively, these findings highlight sarcopenic dysphagia as a clinically relevant phenotype for early risk stratification in HF. Identifying this phenotype may provide additional value by linking systemic sarcopenia with swallowing-related problems, thereby informing pathophysiological understanding and guiding comprehensive nutritional, swallowing, and rehabilitation assessment.
To the best of our knowledge, this is the first study to assess the prognosis of sarcopenic dysphagia in patients with HF (Figure 2). It is well known that sarcopenia is associated with prognosis in patients with HF.19 However, in this study, sarcopenia alone was not statistically significantly associated with prognosis, whereas the coexistence of sarcopenia and dysphagia was associated with poorer prognosis. Consistent with this finding, reductions in all 3 sarcopenia components were more frequent in the sarcopenic dysphagia group than in the sarcopenia-alone group. Generally, dysphagia marks a significant physiological and functional decline in frail older adults. Additionally, we found that patients with HF complicated by sarcopenia and malnutrition were more likely to develop dysphagia.3 Therefore, the coexistence of sarcopenia and dysphagia may reflect more advanced vulnerability and may be associated with a worse prognosis. Supporting this hypothesis, Wirth et al. demonstrated that dysphagia is associated with higher 6-month mortality rate among institutionalized older adults, particularly among those experiencing severe weight loss and worsening nutritional status.20 Thus, sarcopenic dysphagia, in which multiple poor prognostic factors overlap, may be associated with worse short-term outcomes. If followed over a longer period, sarcopenia alone may also be associated with prognosis, similar to previous studies.19
Another significant finding of this study was the determination of the prevalence of sarcopenic dysphagia in patients with HF. The prevalence of sarcopenic dysphagia in the study population was 24.0%. Previous studies of sarcopenic dysphagia reported mean ages of 76.0–87.1 years and prevalence rates of 10.4–43.0%,21–23 indicating that the prevalence observed in the present study was within the range reported in previous studies.
In this study, statistically significant differences in swallowing-related measures were observed between the robust and sarcopenic dysphagia groups (Table 2). This pattern suggested that, although sarcopenia is often captured primarily as a decline in appendicular muscle,19 deterioration in swallowing-related measures may become more apparent at a stage where multiple factors (i.e., undernutrition, inflammation-driven catabolism, and greater HF severity) converge.3,24,25 Supporting this interpretation, the Mini Nutritional Assessment Short-Form score, an indicator of nutritional status, showed a graded decrease across groups and was markedly lower in the sarcopenic dysphagia group. Because undernutrition can plausibly accelerate muscle loss, swallowing-related muscle dysfunction may remain less evident in sarcopenia alone, yet become more pronounced when nutritional reserve is substantially compromised.26 Moreover, impaired swallowing may restrict oral intake and diet texture, thereby aggravating undernutrition and further promoting functional decline, suggesting a potentially self-reinforcing relationship between dysphagia and poor nutritional status.27,28 Collectively, these observed phenomena may help inform our understanding of the pathophysiology of sarcopenic dysphagia in older patients with HF.
Study Limitations
First, this was a single-center, retrospective, observational study, and sample size calculations were not performed a priori. Second, the follow-up period was short (1 year). Third, changes in dietary intake and nutritional status were not monitored. However, sarcopenic dysphagia and nutritional status are closely related,3 and if changes in nutritional status were monitored, these could not have been included as covariates due to potential multicollinearity. Fourth, because this study prioritized consistency with the published diagnostic algorithm for sarcopenic dysphagia, applying the latest sarcopenia criteria may have altered the classification in some patients. Moreover, because this study included only patients who could follow instructions, the reported proportion of sarcopenic dysphagia should be interpreted as the proportion within this selected, evaluable cohort. Fifth, although we described the distribution of patients with reductions in all 3 sarcopenia components, the primary analyses did not directly account for the severity of sarcopenia. Patients with sarcopenic dysphagia had lower skeletal muscle mass index, handgrip strength, and gait speed than those with sarcopenia alone, and patients with reductions in all 3 components were more frequent in the sarcopenic dysphagia group. Therefore, the observed differences in swallowing-related measures and clinical outcomes may partly reflect more advanced sarcopenia rather than the additional presence of dysphagia alone. This potential confounding should be considered when interpreting the association between sarcopenic dysphagia and prognosis. Sixth, because the Food Intake LEVEL Scale reflects oral intake status and may be influenced by factors other than swallowing impairment, this study may have identified the coexistence of sarcopenia and reduced oral intake rather than dysphagia caused primarily by sarcopenia. Seventh, because only 9 patients had dysphagia without sarcopenia, we could not separately evaluate the prognostic impact of non-sarcopenic dysphagia. Therefore, the present study cannot fully distinguish the effect of dysphagia itself from the effect of its coexistence with sarcopenia. Consequently, further research is needed to determine whether sarcopenic dysphagia is associated with poor prognosis in patients with HF. Nonetheless, this study has provided preliminary data to support the initiation of an interventional study investigating sarcopenic dysphagia in patients with HF.
Conclusions
Sarcopenic dysphagia was associated with lower maximal tongue pressure, smaller geniohyoid muscle area, greater geniohyoid muscle echogenicity, and higher risks of the composite outcome and all-cause death in older patients with HF. In contrast, HF-related readmission did not differ statistically significantly according to sarcopenic dysphagia status. These findings suggest that dysphagia may help identify patients with sarcopenia who are at higher risk of adverse outcomes.
Declaration of Generative AI and AI-Assisted Technologies in the Writing Process
During the preparation of this work the authors used ChatGPT 5.2 in order to improve sentence clarity. AI tools were not used to generate or analyze data, interpret results, or draw conclusions. The entire study, including the design, data collection, analysis, and interpretation, was conceived, conducted, and evaluated by the authors.
Data Statement
Data cannot be shared publicly because of the restrictions placed by the Ethics Committee of Sagamihara Kyodo Hospital.
Disclosures
The authors declare that there are no conflicts of interest.
IRB Information
The study complied with the Declaration of Helsinki and was approved by the Institutional Ethics Committee of Sagamihara Kyodo Hospital (No. 221). Because the study used de-identified data, the board waived the requirement for written informed consent; an opt-out was provided on the hospital website.
Supplementary Files
Supplementary Table.
Acknowledgments
The authors gratefully acknowledge all patients who kindly participated in this study.
Funding Statement
Funding Sources: This study was supported by Daiwa Securities Foundation and Japanese Circulation Society Grant for Medical staff for Clinical Research. The financial sponsor had no role in the design, methods, subject recruitment, data collection, analysis or preparation of the paper.
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Supplementary Materials
Supplementary Table.