Sarcopenia is defined as the loss of skeletal muscle mass and function. Despite being part of the normal aging process, it can accelerate and become more pronounced in the presence of chronic diseases.1 Sarcopenia could be found in 20–45% of heart failure (HF) patients2–4 and has a significant impact on their functional capacity and quality of life.3 The diagnosis can be confirmed by the existence of low muscle strength (evaluated by handgrip strength [HGS] or the chair stand test), in association with a low muscle quantity or quality (by means of magnetic resonance imaging or computed tomography).5 An isolated decrease in muscle strength identifies probable patients with sarcopenia.5 Muscle strength is also considered a better marker for adverse outcomes other than muscle mass.3,5 HGS correlates well with overall strength, making it a reliable and easy to measure biomarker.5

Handgrip strength is a valuable prognostic marker in HF and reduced strength is associated with higher mortality and worse outcomes.6,7 QoL is also a key clinical parameter in HF, as lower scores, assessed through validated tools like the KCCQ-23, increase hospitalization and mortality.6,7 Declining QoL correlates with disease progression.8

In this study, we tested the hypothesis that decreased muscle strength, as evaluated by means of HGS, is independently associated with worse QoL in patients with HF.

During the inclusion period, a total of 178 patients with HF were identified, but only 114 met the study inclusion criteria. Figure 1 summarizes the sample selection and reasons for exclusion.

Figure 1.

Sample selection - After exclusions, a total of 54 patients were considered for data analysis.

The study population characteristics are presented in Table 1. A total of 25 (46.3%) males were included, with a mean age of 74.8±10.2 years. The population was complex and characterized by multiple comorbidities – median Charlson Comorbidity Index of 5 (4–6) points. The mean BMI was 29.2±5.5 kg/m2. Applying the CFS, 49% presented a CFS ≤3. The median ejection fraction (EF) was 50 (40.5–57.5)%, with only one fourth of the patients presenting HFrEF. Regarding symptom severity, most patients were in NYHA class II (59.3%). Hypertensive and valvular etiologies accounted for 22.2% and 18.5% of cases, respectively. Only 11.1% of patients had ischemic etiology.

According to the KCCQ-23, QoL was rated as good to excellent in 44.4% of the patients, fair to good in 33.3% of the patients, poor to fair in 18.5% of the patients and very poor to poor in 3.7% of the patients.

Sarcopenia was present in 54.5% of patients, with no significant differences between genders (men: 60%; women: 50%, p=0.458).

The mean HGS was 20.9±8.4 kg. When comparing the HGS between the four categories of KCCQ-23, good to excellent QoL was associated with higher HGS (23.6±9 kg) than fair to good (20.2 (16.4–24.1) kg), poor to fair (14.5 (12.3–14.5) kg) and very poor to poor (11.6 (9.5–11.6) kg) (p=0.02).

Figure 2 depicts a scatterplot that shows the correlation between HGS and QoL. Overall, these variables correlated positively, with a v Pearson's r value of 0.46 (p<0.001). Besides QoL, HGS negatively correlated with other variables, namely NYHA class (r=−0.33; p=0.016) and CFS (r=−0.50; p<0.001) (Supplementary material).

Figure 2.

Correlation between HGS (kg) and QoL (KCCQ-23).

In the univariate analysis (Table 2), age (β=−0.18, p=0.012), HGS (β=1.3, p<0.001), NYHA scale (β=−28, p<0.001) and CFS (β=−13.0, p<0.001) were found to be significantly associated with QoL. On multivariable analysis (Table 2, Model 3), the effects of age, HGS, NYHA scale and CFS remained significant. For each increase in one NYHA class, QoL decreased 20 points on the KCCQ-23, whereas for each 10 kg increase in HGS, QoL increased 8.7 points on the KCCQ-23. Additionally, for every 10-year increase in patient age, there was an improvement of 6.9 points in the KCCQ-23 score. Conversely, an increase in the category of the CFS was associated with a decline of 6.0 points in quality of life as measured by the KCCQ-23.

In this research, the association between HGS, as a marker of muscle strength, and HF symptoms, frailty and QoL was studied in a population of patients with chronic HF.

Fifty-five percent of patients (54.5%) were identified as having probable sarcopenia according to the HGS evaluation. The term probable sarcopenia is relatively recent, having been introduced in 2019 by the European Working Group on Sarcopenia in Older People 2 (EWGSOP2).13 Due to the lack of consensus on sarcopenia assessment methods and the novelty of this definition, determining the exact prevalence of pre-sarcopenia remains challenging. However, studies estimating the prevalence of sarcopenia in patients with HF report rates ranging from 34% to 66% and highlight the high burden of muscle dysfunction in this population.14

Handgrip strength independently predicted the quality of life in this population. Currently, the goals of HF patient management include improving symptoms and QoL, in addition to increasing survival.15 QoL was also identified as an independent predictor of mortality and hospitalization for HF.15

Several pathophysiological mechanisms have been proposed to explain the onset of sarcopenia in patients with HF including malnutrition, inflammation, hormonal changes, oxidative stress, autophagy, and apoptosis.16 A sub-analysis of the SICA-HF trial reported a sarcopenia prevalence of 19.5%.17 However, SICA-HF defined sarcopenia solely based on the evaluation of muscle mass using dual-energy X-ray absorptiometry, which may underestimate the true prevalence of sarcopenia. Additionally, although patients with muscle wasting showed significantly lower HGS, there were no significant differences in the ratio of muscle strength to muscle mass between those with and without muscle wasting.17 In the absence of confirmation of low muscle quantity or quality a diagnosis of sarcopenia cannot be accurately established. As a result, relying solely on HGS evaluation may lead to an overestimation of the presence of sarcopenia, even though muscular strength is considered a better predictor of adverse outcomes than mass.3,5 Nevertheless, this sample of patients with HF shows a worrying prevalence of reduced HGS, suggesting a likely presence of sarcopenia.

In this sample, 49% of patients were not considered frail as they presented CFS ≤ 3. A high percentage (70%) of frailty was described in the FRAIL-HF study among patients hospitalized for HF aged ≥70 years old.18 Although the mean age in this study was similar (74.8±10.2 years), patients <70 years old were not excluded. Also, patients followed in outpatient clinics may have had more stable disease, presenting HF in earlier stages and characterized by fewer physically limiting comorbidities. This may have been reflected in a lower prevalence of frailty. A close follow up of frail patients by the HF team, with regular symptom monitoring and medication adjustment is important to prevent worsening of frailty and HF decompensation.3

Handgrip strength is positively correlated with QoL and negatively with NYHA class and CFS. As expected, physical health and functioning contribute to QoL and are negatively impacted by sarcopenia.19 Independent predictors of QoL in patients with HF included HGS, NYHA scale, the CFS, and age. These results were robust since the findings from Model 2 were quite similar to those from Model 3. For every 10 kg increase in HGS, the KCCQ-23 QoL score improved by 8.7 points.

The NYHA class worsening is a well-known factor in decreasing QoL in chronic HF.16 Physical inactivity is common in frail patients due to the progression of HF. These patients often experience impaired exercise capacity and limitations in everyday activities, which contribute to muscle loss.3 Sarcopenia is age-related, and the estimated annual decline in muscle strength is 1.5% after 50 years old.1,3 Even after adjusting for NYHA class, age and frailty, HGS remains an independent predictor of QoL in patients with HF.

In this study, an older age was independently associated with a better QoL, a finding that appears counterintuitive as aging is typically associated with increased comorbidity burden, functional decline and higher HF severity. This association may reflect survival bias, as older patients attending specialized HF clinics may represent a subgroup with better disease management and physiological resilience. Moreover, psychosocial adaptation mechanisms could influence this relationship, with older patients potentially developing more effective coping strategies and adjusted expectations regarding their health status.20 Further longitudinal studies are warranted to explore these hypotheses and clarify the causal pathways underlying this association.

Body mass index was not an independent predictor of QoL. BMI does not seem to be a good indicator of adiposity and has a better relationship with lean body mass in patients with HF, which is associated with better HGS.21 Oreopoulos et al. found that BMI, lean body mass and percent body fat were not associated with QoL.21 Lilamand et al. described a population of hospitalized geriatric patients with heart disease, finding that malnutrition, regardless of BMI, was an independent predictor of QoL.16

Also, a 2018 metanalysis showed that HGS is predictive of cardiac death, all causes of death and HF hospitalization in patients with cardiac disease including HF and ischemic heart disease.22 Sarcopenia impacts the functional capacity of patients with HF and is associated with an increased risk of adverse events (falls, fractures, a worse neurocognitive profile, and a low physical performance).3

Both resistance training and aerobic exercise are crucial for managing sarcopenia and improving physical performance.14 In patients with HF and sarcopenia, aerobic activity is associated with reduced hospitalizations and mortality, likely due to decreased inflammation and increase in muscle cross-sectional area.14 Nutritional interventions, especially adequate protein intake and essential nutrients, play a crucial role in mitigating the effects of sarcopenia.14 The implementation of strategies aiming to increase muscle strength and delay the onset of frailty may improve QoL for patients living with HF and reduce hospitalization and mortality. This is particularly important as HF is an increasing problem, particularly among older adults.23

Handgrip strength could be useful, not only as a clinical marker, but also as a patient awareness tool for promoting physical activity. Since sarcopenia can be mitigated through lifestyle interventions, routinely assessing and sharing HGS results with patients may encourage them to take part in physical exercise programs. Future studies should explore whether integrating HGS monitoring into HF management could enhance patient engagement and improve outcomes.

There are limitations to this study that must be acknowledged. First, a control group was not included in this study, which makes it more difficult to distinguish the effects of aging worsening HGS from muscle loss attributable to HF. Secondly, body composition, lean body mass or levels of leisure time/physical activity were not assessed; only the maximum HGS peak was evaluated. This neglects other variables of interest in the HGS evaluation, such as force development rate and strength loss rate between the peak and final strength. Thirdly, by using CCI to evaluate comorbidities, important factors that may further impact sarcopenia and QOL have potentially been overlooked, such as anemia or depression. Finally, some disease-modifying drugs, such as sacubitril-valsartan and SGLT2i,24–26 have been associated with improvements in QoL. However, due to the different therapeutic indications for each drug, considering the EF and the reduced number of patients taking these drugs, they were not considered in the analysis.

Due to the observational nature of the study, a causal relation between sarcopenia and worst QoL cannot be ascertained. Whether sarcopenia leads to a worse QoL in HF or whether disease progression leads to inactivity and a worse QoL remains to be determined. Longitudinal and interventional studies targeting muscle mass and strength are needed to clarify these associations. Such studies would allow us to determine whether an improvement in sarcopenia could lead to reduced symptoms and a better QoL in patients with HF. The small sample size also did not allow us to perform a separate analysis for patients with and without preserved EF. In fact, EF was not associated with QoL, as assessed by the KCCQ-23, in the univariate analysis.

This study was conducted in a tertiary hospital, where patients often have more advanced HF and a higher burden of comorbidities. Assessment in primary care settings could help to understand whether sarcopenia also affects QoL in the earlier HF stages. It could also show us whether early interventions, like exercise and nutrition programs, help prevent muscle decline and improve outcomes.

In conclusion, there is a high prevalence of HGS reduction in patients with chronic HF. HGS is positively correlated with QoL and negatively with symptoms in HF. The authors identified HGS as an independent predictor of QoL in patients with chronic HF, with every 10 kg decrease in HGS associated with an 8.7-point decrease in KCCQ-23.

Handgrip strength, which is easily measured in an outpatient clinic, can be a useful tool in assessing and monitoring sarcopenia risk in patients with HF, whose strength may be a limiting factor for daily activities and QoL.

Future intervention studies aiming to improve muscle strength could help clarify the causal relationship between sarcopenia and QoL while also providing insights into long-term patient outcomes.

The study was conducted in accordance with ethical principles and approved by the Unidade Local de Saude Gaia e Espinho Ethics Committee. All participants provided written informed consent.

The authors declare no conflicts of interest.