Abstract
Inflamed skeletal muscle promotes chronic inflammation in atherosclerotic plaques, thereby contributing to the increased risk of coronary artery disease (CAD). In this study, we evaluated the metabolic activity of psoas muscle, using 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT), and its association with carotid artery inflammation and acute myocardial infarction (AMI). In total, 90 participants (32 AMI, 33 chronic stable angina (CSA), and 25 control) were enrolled in this prospective study. Metabolic activity of skeletal muscle (SM) was measured by using maximum standardized uptake value (SUVmax) of psoas muscle, and corresponding psoas muscle area (SM area) was also measured. Carotid artery inflammation was evaluated by using the target-to background ratio (TBR) of carotid artery. SM SUVmax was highest in AMI, intermediate in CSA, and lowest in control group. SM SUVmax was significantly correlated with carotid artery TBR and systemic inflammatory surrogate markers. Furthermore, SM SUVmax was independently associated with carotid artery TBR and showed better predictability than SM area for the prediction of AMI. Metabolic activity of psoas muscle assessed by 18F-FDG PET/CT was associated with coronary plaque vulnerability and synchronized with the carotid artery inflammation in the participants with CAD. Furthermore, it may also be useful to predict AMI.
Highlights
Cardiovascular disease (CVD) is the leading cause of death globally, and around 40%of these deaths are due to coronary artery disease (CAD) [1,2]
CAD is usually caused by atherosclerosis, which can further lead to plaque erosion or rupture that results in angina and/or acute myocardial infarction (AMI) [3]
Several previous studies have reported that increased inflammation in skeletal muscle (SM) could contribute to the upregulation of systemic inflammation, which may lead to the promotion of the chronic inflammatory process in atherosclerotic arterial lesions [4,5,6]
Summary
Cardiovascular disease (CVD) is the leading cause of death globally, and around 40%of these deaths are due to coronary artery disease (CAD) [1,2]. Cardiovascular disease (CVD) is the leading cause of death globally, and around 40%. CAD is usually caused by atherosclerosis, which can further lead to plaque erosion or rupture that results in angina and/or acute myocardial infarction (AMI) [3]. Several previous studies have reported that increased inflammation in skeletal muscle (SM) could contribute to the upregulation of systemic inflammation, which may lead to the promotion of the chronic inflammatory process in atherosclerotic arterial lesions [4,5,6]. Inflamed SM secretes large numbers of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and monocyte chemotactic protein-1 (MCP-1) thereby promoting inflammatory cells infiltration into SM with predominant M1-polarized macrophages, which further contribute to insulin resistance with systemic inflammation and increase the risk of atherosclerotic plaque rupture [4,5,6]. Inflamed SM could play a key role in the development of CVD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
