Objectives: Lower-extremity peripheral arterial disease (PAD) results in limb ischemia and is strongly associated with sarcopenia. This study aimed to retrospectively evaluate the association between the quantity of muscle mass in the lower extremities and the severity of vascular stenosis in PAD patients.
Methods: Between January 2018 and August 2021, 128 patients with PAD and 53 individuals without PAD, diagnosed by computed tomography, were enrolled. The severity of stenosis of lower-extremity arteries was measured using a grading system. The muscle and fat mass areas were calculated in the abdomen at the L3 or L4 level, mid-thigh, and lower leg. Multivariable logistic regression was conducted to clarify the risk associated with low muscle mass. The difference in muscle mass between PAD and non-PAD patients was evaluated by using propensity score matching.
Results: A strong positive correlation between the abdomen muscle area and leg muscle area was observed. The muscle area and muscle index of the leg were lower in PAD patients. These changes occurred earlier than in the abdomen muscle area. The group with more severe artery stenosis had more muscle wasting in the lower extremities. Greater age, female, lower BMI, and PAD were associated with low muscle mass. After propensity score matching, the leg muscle area was still lower in PAD patients.
Conclusions: There is a direct association between PAD and regional muscle wasting. This occurs earlier regionally in the lower extremities than in central muscles. Early diagnosis of PAD might prevent progressive muscle loss, improving disease outcome and quality of life.
Key Points: • Peripheral arterial disease is strongly associated with sarcopenia. • Muscle wasting in the lower extremities is earlier and more prominent than that in the abdomen. • More severe arterial stenoses are associated with higher muscle wasting in the lower extremities.
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http://dx.doi.org/10.1007/s00330-022-09356-4 | DOI Listing |
Age Ageing
November 2024
Department of Physical Education and Sport, Faculty of Sport Sciences, University of Granada, Granada, Spain.
J Oral Biosci
December 2024
Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan R.O.C; Marine Biology and Cetacean Research Center, National Cheng Kung University, Tainan, Taiwan R.O.C. Electronic address:
Objective: Drug resistance and subsequent adverse effects, such as cancer cachexia, limit the clinical use of cisplatin. Oligonol® (Olg), a low-molecular-weight polyphenol, exhibits NF-κB inhibitory properties. NF-κB activation has been implicated in cisplatin resistance of cancer cells and skeletal muscle wasting.
View Article and Find Full Text PDFSemin Respir Crit Care Med
December 2024
Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, Ohio.
Neuromuscular disorders can cause respiratory impairment by affecting the muscle fibers, neuromuscular junction, or innervation of respiratory muscles, leading to significant morbidity and mortality. Over the past few years, new disease-modifying therapies have been developed and made available for treating different neuromuscular disorders. Some of these therapies have remarkable effectiveness, resulting in the prevention and reduction of respiratory complications.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
December 2024
Department of Molecular Biotechnology and Health Sciences, University of Turin, Turin, Italy.
Despite significant progress in understanding the molecular aetiology of muscle atrophy, there is still a great need for new targets and drugs capable of counteracting muscle wasting. The role of an impaired proteostasis as the underlying causal mechanism of muscle atrophy is a well-established concept. From the earliest work on muscle atrophy and the identification of the first atrogenes, the hyper-activation of the proteolytic systems, such as autophagy and the ubiquitin proteasome system, has been recognized as the major driver of atrophy.
View Article and Find Full Text PDFStem Cell Res Ther
December 2024
The Affiliated Taian City Central Hospital of Qingdao University, Taian, 271000, China.
Background: In the rat knee stiffness model, the duration of traction treatment is mostly 20-40 min; however, relatively few studies have been conducted on longer traction treatment of extended knee stiffness in rats. Therefore, the aim of this study was to explore the efficacy of prolonged traction and its mechanism of action in extended knee stiffness in rats.
Methods: The model of extended knee joint stiffness was established in rats and treated with powered flexion position traction.
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