Background There are conflicting results regarding the association between body mass index and the prognosis of cardiac arrest patients. We investigated the association of the composition and distribution of muscle and fat with neurologic outcomes at hospital discharge in successfully resuscitated out-of-hospital cardiac arrest (OHCA) patients. Methods: This prospective, single-centre, observational study involved adult OHCA patients, conducted between April 2019 and June 2021. The ratio of total skeletal muscle, upper limb muscle, lower limb muscle, and total fat to body weight was measured using InBody S10, a bioimpedance analyser, after achieving the return of spontaneous circulation. Restricted cubic spline curves with four knots were used to examine the relationship between total skeletal muscle, upper limb muscle, and lower limb muscle relative to total body weight and neurologic outcome at discharge. Multivariable logistic regression analysis was performed to assess an independent association. Results: A total of 66 patients were enrolled in the study. The proportion of total muscle and lower limb muscle positively correlated with the possibility of having a good neurologic outcome. The proportion of lower limb muscle showed an independent association in the multivariable analysis (adjusted odds ratio, 2.29; 95% confidence interval, 1.06–13.98), and its optimal cut-off value calculated through receiver operating characteristic curve analysis was 23.1%, which can predict a good neurological outcome. Conclusions: A higher proportion of lower limb muscle to body weight was independently associated with the probability of having a good neurologic outcome in OHCA patients.
Muscle wasting is commonly seen in patients with sepsis as a consequence of the catabolic response in skeletal muscle.
Muscle wasting can occur in cases that have an imbalance between degradation and synthesis of muscle proteins.
Although decrements in the synthesis of muscle proteins may contribute to sepsis-induced muscle wasting, it has been recognized that increments in its degradation play a more essential role in muscle wasting. Muscle wasting in sepsis patients has some significant clinical consequences such as reduced ambulation and exercise tolerance, and an increased risk for pulmonary and thromboembolic complications. Several mechanisms have been proposed for sepsis-induced muscle wasting. Increased proteolysis via the ubiquitin-proteasome pathway and the calpains system is one of the principal mechanisms of muscle wasting induced by sepsis. Calpains are activated by calcium, which increases in patients with sepsis. The activation of the calpains system disrupts the sarcomere of the myofibrils, resulting in the release of myofilaments that are subsequently ubiquitinated and degraded by the 26S proteasome complex. Recent studies have suggested that transcriptional factors such as NF-kappaB and FoxO, and the apoptosis and autophagy-lysosome pathways may also be involved in sepsis-induced muscle wasting. This review briefly summarizes the contribution of these mechanisms of muscle wasting in patients with sepsis and the possible therapeutic agents to treat it.
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Role of IL-15 in Sepsis-Induced Skeletal Muscle Atrophy and Proteolysis Ho Cheol Kim, Hee-Young Cho, Young-Sool Hah Tuberculosis and Respiratory Diseases.2012; 73(6): 312. CrossRef