JPEN J Parenter Enteral Nutr. 2025 Dec 17. doi: 10.1002/jpen.70039. Online ahead of print.
ABSTRACT
BACKGROUND: Patients with visceral obesity experience an amplified systemic inflammatory response during the perioperative period, increasing infection risk. Significant skeletal muscle loss following invasive cardiovascular surgery presents a considerable clinical challenge. This study aimed to investigate the association between preoperative visceral fat mass and postoperative skeletal muscle loss, emphasizing the clinical utility of computed tomography-based body composition analysis.
METHODS: This retrospective cohort study included Japanese patients who underwent elective cardiovascular surgery (May 2020 to December 2023). Preoperative computed tomography was used to calculate the visceral fat area, subcutaneous fat area, and psoas muscle area as indicators of skeletal muscle mass. Skeletal muscle loss was assessed by the change in the psoas muscle area between the preoperative period and the first postoperative week.
RESULTS: Of the 159 patients included in the final analysis, 69.2% were classified as having visceral obesity. Preoperative visceral fat area was significantly correlated with peak postoperative C-reactive protein (CRP) levels (r = 0.361) and changes in psoas muscle area (r = -0.374), whereas subcutaneous fat area showed no such correlation. In the multivariate logistic regression analysis, after adjusting for clinical characteristics, including age, body mass index, operative time, preoperative CRP level, EuroSCORE II, and preoperative 6-min walk distance, higher visceral fat area was significantly associated with postoperative skeletal muscle loss (odds ratio [OR]: 1.01; 95% CI: 1.00-1.02), whereas subcutaneous fat area was not (OR: 1.01; 95% CI: 0.99-1.02).
CONCLUSIONS: Preoperative visceral fat area measured using computed tomography is a robust predictor of postoperative skeletal muscle loss. Visceral obesity, linked to heightened systemic inflammation, may accelerate muscle degradation through proinflammatory pathways.
PMID:41408882 | DOI:10.1002/jpen.70039