Mitral regurgitation, the left atrium and atrial fibrillation:unlikely bedfellows or natural kindreds?

This editorial refers to ‘Even mild mitral regurgitation is associated with incident atrial fibrillation in the general population’, by M. Yafasov et al., https://doi.org/10.1093/ehjci/jead337. There is a close association between mitral regurgitation (MR), left atrial (LA) size and function, and atrial fibrillation (AF). This association is highlighted in the ESC/EACTS and the ACC/AHA guidelines for the management of valvular heart disease. Indeed, in asymptomatic patients with chronic primary MR, surgical mitral valve repair should be considered in case of LA dilation [defined as an LA volume index ≥ 60 mL/m2] or the onset of new AF (both IIa, level of evidence B).1 In this issue of this issue of the journal, Yafasov et al. reported data from a prospective population-based fifth Copenhagen City Study. Of the nearly 4500 participants who had transthoracic echocardiograms, MR was quantifiable using the colour flow Doppler MR jet area indexed to LA area (MR/LA ratio) in about 90% of the participants.2 Some degree of MR was found in about 48%, and of those ones 39% had trace/mild MR. During a median follow-up duration of 5.3 years, slightly less than 5% of the participants in the study were found to have developed AF. The MR/LA ratio was independently associated with incident AF but only in participants ≤ 73 years. Additionally, this relationship persisted even in patients with mild MR. Our existing knowledge regarding the association between MR and AF and the current guideline recommendations to intervene predominantly relies on data from individuals who sought medical attention at hospital echocardiography centres or laboratories or from specifically selected communities. To that extent, the data from the Copenhagen City Study offer some additional insights. The data from the study by Yafasov et al. study emphasize the interplay between MR, LA, and AF. This intimate connection also raises the question of which came first, akin to the chicken and egg dilemma. If the cause–effect relationship between FA and MR is more plausible in primary MR, it is less so in secondary MR (SMR). This is supported by the fact that in the Copenhagen City Study, only 5% of the enrolees had SMR. It is interesting that while 43% had primary MR by predefined criteria, the rest were not categorized as primary or secondary MR. It is likely that the definitions used by the authors (SMR was defined as MR with ischaemic heart disease, heart failure, or left ventricle dilation at baseline, while primary MR was defined as any MR not fulfilling the criteria for SMR) underestimated the number of SMR, particularly atrial SMR (ASMR). Although the original definition of ASMR was that MR improved significantly if sinus rhythm was restored, there is evidence that up to 40% of individuals with heart failure with preserved ejection fraction (HFpEF) may have ASMR with or without a history of AF. There is also evidence that the size of the LA may be less dilated in individuals with ASMR plus HFpEF but without AF than in those with HFpEF plus AF. Those with AF only and no HFpEF have been reported to have the largest LA size. Yet the survival was lowest in the two HFpEF groups with relatively smaller LA size and ASMR. LA function measured as LA work and strain was lowest in the two HFpEF groups with ASMR, especially in the HFpEF with ASMR plus AF. This perhaps highlights LA as an important mediator of the risk of AF and may be even reduced survival.3