Monocyte-to-HDL-cholesterol ratio and left atrial remodelling in atrial fibrillation

I was grateful to read an interesting paper by Suzuki et al.1 which revealed that the ratio of circulating intermediate CD14++CD16+ monocytes was significantly higher in patients with atrial fibrillation (AF) compared with control group. Intermediate CD14++CD16+ monocytes also showed a strongly negative correlation with left atrial appendage (LAA) flow during sinus rhythm. Moreover, the ratio of circulating intermediate CD14++CD16+ monocytes was found as an independent predictor for the presence of AF. Atrial fibrillation is initiated and maintained by a complex interaction between electrical, contractile, and structural remodelling.2 Inflammation, oxidative stress, and subsequent atrial fibrosis are shown to be significant contributors of structural remodelling process.3 It has been already shown that the extent of atrial fibrosis as a hallmark for structural remodelling has had a prognostic and therapeutic role in AF patients.4 Monocytes are the most important sources of pro-inflammatory and pro-oxidant cytokines at inflammatory sites, which leads to atrial adverse electrical and/or structural remodelling and may represent a prerequisite for AF.4 Because of its anti-inflammatory and anti-oxidant actions, the relationship between high-density lipoprotein cholesterol (HDL-C) and AF has also been investigated. In our recent study,5 we combined both parameters as ‘monocyte count-to-HDL-C ratio (MHR)’ and evaluated its prognostic value among AF patients undergoing catheter ablation. For the first time in the literature, we demonstrated that MHR was found as an independent predictor of AF recurrence after cryoballoon-based AF ablation. We also showed that MHR has been significantly correlated with LA diameter and duration of AF history. These findings supported that the monocyte accumulation and reduced HDL-C may participate in atrial remodelling by the release of activated substances, including oxygen-free radicals, proteases, and pro-inflammatory cytokines. One of the important limitations of our study was using an automatically counted monocyte numbers rather than the proportion of monocyte subsets. Thus, the study by Suzuki et al.1 may support and confirm our previous findings when the ratio of circulating intermediate CD14++CD16+ monocytes to HDL-C levels has been calculated and analysed. Because MHR combines the two detrimental processes like inflammation and oxidative stress, it could be used as a novel marker for prediction of the severity of atrial remodelling. However, additional large-scale prospective studies in different populations are needed to confirm the role of MHR and/or circulating intermediate CD14++CD16+ monocytes/HDL-C in the pathophysiology and prognosis of AF. Conflict of interest: none declared.