Background: Heart failure (HF) and atrial arrhythmias (AAs) are two clinical conditions that characterize the daily clinical practice of cardiologists. In this perspective review, we analyze the shared etiopathogenetic pathways of atrial arrhythmias, which are the most common cause of atrial arrhythmias-induced cardiomyopathy (AACM) and HF. Hypothesis:The aim is to explore the pathophysiology of these two conditions considering them as a "unicum", allowing the definition of a cardiovascular continuum where it is possible to predict the factors and to identify the patient phenotype most at risk to develop HF due to atrial arrhythmias.Methods: Potentially eligible articles, identified from the Electronic database (PubMed), and related references were used for a literature search that was conducted between January 2022 and January 2023. Search strategies were designed to identify articles that reported atrial arrhythmias in association with heart failure and vice versa. For the search we used the following keywords: atrial arrhythmias, atrial fibrillation, heart failure, arrhythmia-induced cardiomyopathy, tachycardiomyopathy. We identified 620 articles through the electronic database search. Out of the 620 total articles we removed 320 duplicates, thus selecting 300 eligible articles.
Introduction Little is known about progression of atrial fibrillation (AF) from paroxysmal to persistent form. Electrical remodeling may play a pivotal role in the arrhythmia transition. The aim of the study was the characterization of the atrial electrical substrate in patients suffering from AF. Methods Twenty-seven patients were included in the study (14 with paroxysmal AF and 13 with persistent AF). Two simultaneous electroanatomical maps of the left atrium were collected using PentaRay catheter using the parallel mapping feature [first map during sinus rhythm and a second one with an extrastimulus from coronary sinus (CS)]. We analyzed the propagation of the wavefront and we identified zones of abnormal conduction: slow conduction (SC) corridors and pivot points (PP). SC corridors were defined by the slowing of conduction velocity; pivot points were zones in which propagation pattern changed the direction of 90° or more. Maximum delay between the recording dipoles located at the extremities of the PentaRay splines was calculated. At each of these sites, EGMs were collected and analyzed in terms of amplitude and duration. We checked if areas of abnormal conduction during sinus rhythm were present or they disappeared by delivering an extrastimulus from the coronary sinus. Results The average number of collected EGMs per map was 4790 ± 1333 (PAF 4829 ± 1407; PsAF 4745 ± 1402). Total abnormal conduction areas in the 27 patients were 62, 65% of which were slow conduction. Pivot points and slow conduction manifested a trend to cluster in some areas: both of them were mostly present at the ostia of pulmonary veins, in a specific segment between LAA ostium and mitral annulus and in the posterior wall. During sinus rhythm, pivot points were 29, while pacing from distal CS catheter the same zones showed normal conduction in 14 cases: they were still present in 60% in PAF group and 50% in PsAF. Slow conduction corridors, instead, show a trend to remain while pacing from CS: 76% in the first group and 78% in the second one. Conclusions SC corridors are fixed alterations of atrial substrate, while pivot sites may be more dynamic entities: both of them may have a key role in remodeling atrial structures and atrial fibrillation progression and maintenance. These may represent future targets for AF therapy and prevention.
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