To the editor

I read with interest the cohort study by Guo et al¹ published in a recent issue of Polish Archives of Internal Medicine, showing that the combination of a high body mass index (BMI) and a high circulating lipoprotein(a) (Lp[a]) level helped predict the occurrence of atrial fibrillation (AF). This is a highly relevant report, since the prevention and management of AF remain important in patient care, and the clinical significance of Lp(a) in relation to AF is an attractive point.^1,2 I would like to add some comments that were inspired by the findings of the authors.

The first comment concerns the pathophysiological view of the BMI–Lp(a) association in the context of AF. Oxidative stress and inflammation are involved in the pathophysiology of AF.² Lp(a) is susceptible to oxidative modifications, and high Lp(a) levels are induced by inflammatory conditions.² Obesity, as reflected by high BMI, is also well known to be associated with oxidative stress and inflammatory state. Thus, the effect of BMI and Lp(a) on the risk of AF development is considered mechanistically acceptable. On the other hand, although there is still no consensus on the matter, some studies reported an inverse correlation between BMI and Lp(a) levels, which might be partly mediated by the adipocyte biology.^3,4 In this context, the combination of high BMI and elevated Lp(a) levels may be a specific, unnatural phenotypic entity that contributes to the development of AF. Notably, unnatural activation of the autonomic nervous system (ie, upregulation of the sympathetic system and abnormal responsiveness of the parasymphatetic system) has already been considered as a specific entity that leads to AF.⁵ Therefore, assuming the presence of such entities merits further investigation.

The second comment regards the practical view of the BMI–Lp(a) connection in AF. BMI is easily measurable, and treatment for obesity includes lifestyle intervention and / or recent pharmaceutical drugs (ie, glucagon‑like peptide 1‑receptor agonist). Screening of Lp(a) levels has been recently advocated for cardiovascular risk stratification, and Lp(a)-targeting drugs (ie, Lp[a] inhibitors) are expected to appear in the near future. The strategy of screening and adjusting treatment based on BMI and Lp(a) levels would be useful for reducing the occurrence of AF. Therefore, the report by Guo et al,¹ showing the joint of association of elevated BMI and Lp(a) levels with the increased prevalence of AF provides valuable insights into the prevention and management of this arrhythmia.