Predicting Atrial Fibrillation With Manganese Superoxide Dismutase Levels

By Patrick Daly - Last Updated: September 13, 2022

Citing growing evidence linking inflammation and oxidative stress to the pathogenesis of atrial fibrillation, researchers evaluated whether plasma manganese superoxide dismutase (MnSOD) levels were associated with atrial fibrillation. In their study, published in the Journal of Clinical Medicine, they identified an independent association between increased circulating MnSOD and incidence of paroxysmal atrial fibrillation.

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The study enrolled 87 and 43 patients with paroxysmal and persistent atrial fibrillation, respectively, and 58 patients without atrial fibrillation as controls. Researchers used the ELISA method to measure nicotinamide-adenine dinucleotide phosphate oxidase 4 (NOX4) and MnSOD levels in plasma. Comparisons between groups were based on Spearmen correlation, multivariable logistic regression, and area under the curve (AUC) of receiver operating characteristic (ROC) curve analyses.

Plasma MnSOD Levels Predict Atrial Fibrillation

According to the report, plasma MnSOD levels were the highest in the paroxysmal group, followed by the persistent group, and then the controls. The difference between the paroxysmal and control groups was statistically significant (P=.002), although the differences between the paroxysmal and persistent groups and the persistent and control groups were not.

The authors found a significantly negative correlation between MnSOD and left atrial diameter (r=-0.232; P=.008) and a positive correlation between MnSOD and red cell distribution width variation coefficient (r=0.214; P=.014) in patients with atrial fibrillation.

Additionally, MnSOD levels were found to be an independent risk factor for paroxysmal atrial fibrillation (odds ratio [OR], 1.003; 95% CI, 1.001-1.005; P=.002). Lastly, the ROC curve analyses determined that MnSOD at a best cut-off value of 311.49 ug/mL predicted paroxysmal atrial fibrillation with a sensitivity of 52.9% and specificity of 77.6% (AUC=0.668).

Limitations of the study included its single-center design and a small number of eligible patients, and the researchers acknowledged that the prospective nature of the study could only establish association and not causation.

Regardless, the study’s authors concluded that “oxidative stress underlies the pathogenesis of AF and may play a stronger role in paroxysmal AF than persistent AF.” They called for larger studies to further explore the potential role of MnSOD in atrial remodeling and atrial fibrillation.

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