Mitochondrial Dysfunction Contributes to Sustained Muscle Loss After Cardiac Surgery: A Prospective Observational...

Area of Science:

• Cardiology
• Metabolomics
• Muscle Physiology

Background:

• Cardiac surgery is a major systemic insult leading to significant muscle loss (sarcopenia).
• Muscle mass and strength loss after surgery is highly variable (0%-40% rectus femoris cross-sectional area).
• Understanding muscle recovery beyond the first week is crucial for patient outcomes.

Purpose of the Study:

• To investigate muscle phenotype, body composition, and quality of life up to outpatient follow-up after cardiac surgery.
• To correlate muscle recovery with protein and metabolomic markers.
• To identify predictors of poor muscle outcomes post-cardiac surgery.

Main Methods:

• Recruitment of patients undergoing elective aortic valve surgery.
• Assessment of muscle mass (RFcsa), strength (handgrip, knee extension, spirometry), body composition, and quality of life pre-operatively, at 7 days, and at follow-up.
• Plasma metabolome analysis at multiple time points (Days 0, 3, 7, and follow-up).

Main Results:

• Mean rectus femoris cross-sectional area (RFcsa) loss was 6.44% at Day 7 and 9.69% at follow-up.
• Muscle strength and functionality recovered to baseline by follow-up, contrasting with persistent muscle bulk loss in some patients.
• Quality of life correlated positively with muscle bulk and strength at follow-up.
• Mitochondrial dysfunction markers (short-chain acyl-carnitines) correlated with muscle loss and reduced strength.

Conclusions:

• A significant proportion of patients experience persistent muscle bulk loss despite strength recovery after aortic surgery.
• Baseline and acute mitochondrial dysfunction predict poor muscle outcomes up to outpatient follow-up.
• These findings highlight the importance of monitoring muscle mass and identifying patients at risk for sarcopenia post-cardiac surgery.