Why the study?
Because diabetes impairs muscle protein metabolism and promotes adipose accumulation, sarcopenic obesity may be a high-risk phenotype in HFrEF, but its clinical profiles, LV remodeling, and prognostic implications remained unclear.
Does sarcopenic obesity worsen the composite of heart failure readmission, cardiovascular mortality, and heart transplantation in patients with HFrEF and diabetes mellitus?
Does sarcopenic obesity worsen the composite of heart failure readmission, cardiovascular mortality, and heart transplantation in patients with HFrEF and diabetes mellitus?
Sarcopenic obesity is a high-risk phenotype in patients with HFrEF and diabetes, associated with adverse left ventricular remodeling and a 3-fold increased risk of adverse cardiovascular outcomes.
SO may flag higher-risk diabetic HF; hypothesis-generating for body-composition interventions in prospective trials.
BACKGROUND: Obesity is common in the heart failure (HF) population and is regarded as an important risk factor for developing HF. Greater skeletal muscle mass has shown to be the underlying protective factor against cardiac failure. Since diabetic mellitus (DM) can impair muscle protein metabolism, leading to skeletal muscle wasting, accompanied by adipose tissue accumulation, sarcopenic obesity (SO) may be a high-risk phenotype with poor outcomes in this specific population, especially in HF with reduced ejection fraction (HFrEF). Thus, the aim of this study was to clarify the clinical profiles, left ventricular (LV) remodeling, and prognostic implications of SO in patients with HFrEF and DM. METHODS: ). Obesity in conjunction with a SMI lower than the median is referred to as SO. The LV volume and function, as well as the systolic strain, were measured. The clinical characteristics and cardiovascular outcomes (heart failure readmission, cardiovascular mortality and heart transplantation) were recorded. RESULTS: Patients with SO had a greater level of amino-terminal pro-B-type natriuretic peptide and were more likely than nonsarcopenic patients with obesity to present with hypoproteinemia. Among patients with obesity, those with sarcopenia displayed greater LV expansion and more profound LV dysfunction, together with an increase in LV mass. During a median follow-up duration of 35.1 months, a total of 73 (25.8%) subjects reached the composite endpoint, with a worst outcome in the group of patients with SO (log-rank P = 0.04). Multivariable Cox analysis revealed that patients with SO had an approximately 3-fold greater risk of experiencing adverse outcomes than did those with neither sarcopenia nor obesity (hazard ratio: 3.03, 95% confidence interval: 1.39 to 6.63; P = 0.005). CONCLUSIONS: SO is a potentially high-risk phenotype with adverse LV remodeling and poor clinical outcomes in diabetic patients with HFrEF that may require more attention.
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Shi et al. (2025) studied this question.
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