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The left atrium (LA) plays an important role in cardiovascular homeostasis through the modulation of cardiac filling and output, as well as the regulation of circulatory volume and tone. LA remodelling is characterised by dynamic alterations in atrial structure, function and electrophysiology. Most frequently, it occurs in association with ageing, hypertension, ischaemia, metabolic and pulmonary disorders (central illustration, figure 1). LA dilatation, the hallmark of atrial remodelling, has been increasingly recognised as a prognostic biomarker of thromboembolic and cardiovascular events, in particular in patients with atrial fibrillation (AF). However, cardiovascular risk attributable to atrial dilatation also appears to be increased in individuals without AF and is incompletely explained by the associated comorbidities and risk factors. The clarification of this issue was attempted by putting forward the concept of atrial cardiomyopathy, as a primary form of atrial abnormality, in which atrial fibrosis, hypercoagulability, contractile and endothelial dysfunction may lead to incident AF, heart failure (HF) and thromboembolism, independent of other causes (central illustration, figure 1).1 However, evidence from human studies supporting this concept is inconclusive. Also, a comparison of cardiovascular risk associated with LA dilatation in patients with and without AF has not been systematically conducted.
The study by Froehlich et al,2 published in Heart, provides a new insight into this important subject. This study presents a systematic review and a meta-analysis of 91 observational studies exploring the association between several indices of LA dilatation and outcomes in patients with AF (23 studies with a total of 14 936 participants) and those without AF (68 studies with a total of 50 720 patients). The studies included in the meta-analysis integrated data on a wide array of background cardiovascular pathology, including hypertension, ischaemic …
Contributors All the coauthors have participated in the drafting, writing and final revision of the editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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