Atrial arrhythmias and heart failure: A "modern view" of an old paradox.

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. About 150 titles/abstracts were excluded for the following reasons: no original available data, no mention of atrial arrhythmias and heart failure crosstalk, very low quality analysis or evidence. We excluded also non-English articles. When multiple articles were published on the same topic, the articles with the most complete set of data were considered. We preferentially included all papers that could provide the best evidence in the field. As a result, the present review article is based on a final number of 104 references. RESULTS: While the pathophysiology of AACM and Heart Failure with reduced ejection fraction (HFrEF) has been studied in detail over the years, the causal link between atrial arrhythmias and heart failure with Preserved Ejection Fraction (HFpEF) has been often subject of interest. HFpEF is strictly related to AAs, which has always been considered significant risk factor. In this review we described the pathophysiological links between atrial fibrillation and heart failure. Furthermore, we illustrated and discussed the preclinical and clinical predicting factors of AF and HFpEF, and the corresponding targets of the available therapeutic agents. Finally, we outlined the patient phenotype at risk of developing AF and HFpEF (Central Illustration). CONCLUSIONS: In this review, we underline how these two clinical conditions (AF and HFpEF) represent a "unicum" and, therefore, should be considered as a single disease that can manifest itself in the same phenotype of patients but at different times. Furthermore, considering that today we have few therapeutic strategies to treat these patients, it would be good to make an early diagnosis in the initial stages of the disease or intervene even before the development of signs and symptoms of HF. This is possible only by paying greater attention to patients with predisposing factors and carrying out a targeted screening with the correct diagnostic methods. A systemic approach aimed at improving the immuno-metabolic profile of these patients by lowering the body mass index, threatening the predisposing factors, lowering the mean heart rate and reducing the sympathetic nervous system activation is the key strategy to reduce the clinical impact of this disease.

Right atrial appendage firing in atrial fibrillation.

Background: The role of atrial fibrillation (AF) drivers located at the left atrium, superior vena cava, crista terminalis and coronary sinus (CS) is well established. While these regions are classically targeted during catheter ablation, the role of right atrial appendage (RAA) drivers has been incompletely investigated. Objective: To determine the prevalence and electrophysiological characteristics of AF driver's arising from the RAA. Materials and methods: We conducted a retrospective analysis of clinical and procedural data of 317 consecutive patients who underwent an AF ablation procedure after bi-atrial mapping (multipolar catheter). We selected patients who presented with a per-procedural RAA firing (RAAF). RAAF was defined as the recording of a sustained RAA EGM with a cycle length shorter than 120 ms or 120 < RAAF CL ≤ 130 ms and ratio RAA CL/CS CL ≤ 0.75. Results: Right atrial/atrium appendage firing was found in 22 patients. The prevalence was estimated at 7% (95% CI, 4-10). These patients were mostly men (72%), median age: 66 yo ± 8 without structural heart disease (77%). RAAFs were predominantly found in paroxysmal AF patients (63%, 32%, and 5% for paroxysmal, short standing and long-standing AF, respectively, p > 0.05). RAAF median cycle length was 117 ms ± 7 while CS cycle length was 180 ms ± 10 (p < 0.01). Conclusion: In 317 consecutive AF ablation patients (22 patients, 7%) the presence of a high-voltage short-cycle-length right atrial appendage driver (RAAF) may conclusively be associated with AF termination. This case series exemplifies the not-so-uncommon role of the RAA in the perpetuation of AF.

Localized Atrial Tachycardia and Dispersion Regions in Atrial Fibrillation: Evidence of Spatial Concordance.

INTRODUCTION: During atrial fibrillation (AF) ablation, it is generally considered that atrial tachycardia (AT) episodes are a consequence of ablation. Objective: To investigate the spatial relationship between localized AT episodes and dispersion/ablation regions during persistent AF ablation procedures. Methods: We analyzed 72 consecutive patients who presented for an index persistent AF ablation procedure guided by the presence of spatiotemporal dispersion of multipolar electrograms. We characterized spontaneous or post-ablation ATs' mechanism and location in regard to dispersion regions and ablation lesions. RESULTS: In 72 consecutive patients admitted for persistent AF ablation, 128 ATs occurred in 62 patients (1.9 ± 1.1/patient). Seventeen ATs were recorded before any ablation. In a total of 100 ATs with elucidated mechanism, there were 58 localized sources and 42 macro-reentries. A large number of localized ATs arose from regions exhibiting dispersion during AF (n = 49, 84%). Importantly, these ATs' locations were generally remote from the closest ablation lesion (n = 42, 72%). CONCLUSIONS: In patients undergoing a persistent AF ablation procedure guided by the presence of spatiotemporal dispersion of multipolar electrograms, localized ATs originate within dispersion regions but remotely from the closest ablation lesion. These results suggest that ATs represent a stabilized manifestation of co-existing AF drivers rather than ablation-induced arrhythmias.

Phrenic nerve displacement by intrapericardial balloon inflation during epicardial ablation of ventricular tachycardia: Four case reports.

BACKGROUND: Phrenic nerve (PN) injury is one of the recognized possible complications following epicardial ablation of ventricular tachycardia (VT). High-output pacing is a widely used maneuver to establish a relationship between the PN and the ablation catheter tip. An absence of PN capture is usually considered an indication that it is safe to ablate, and that successful ablation may be performed at adjacent sites. However, PN capture may impact the procedural outcome. Only a few cases have been reported in the literature that avoid PN injury by using different techniques. CASE SUMMARY: Three patients with a previous history of myocarditis and one patient with ischemic cardiomyopathy underwent epicardial ablation for drug-refractory VT. Before the procedure, transthoracic echocardiogram, coronary angiogram, and cardiac magnetic resonance imaging were performed on all patients. Under general anesthesia, endo/epicardial three-dimensional anatomical and substrate maps of the left ventricle were accomplished. Before radiofrequency delivery, the course of the PN was identified by provoking diaphragmatic stimulation with high-output pacing from the distal electrode of the ablation catheter. In every case, a scar region with late potentials was mapped along the PN course. After obtaining another epicardial access, a second introducer sheath was placed, and a vascular balloon catheter was inserted into the epicardial space and inflated with saline solution to separate the PN from the epicardium. Once the absence of PN capture had been proven, radiofrequency was applied to aim for complete late potential elimination and avoid VT induction. CONCLUSION: PN injury can occur as one of the complications following epicardial VT ablation procedures, and may prevent successful ablation of these arrhythmias. PN displacement by using large balloon catheters into the epicardial space seems to be feasible and reproducible, avoid procedure-related morbidity, and improve ablation success when performed in selected centers and by experienced operators.

Use of wearable cardioverter-defibrillator in association with catheter ablation for atrial fibrillation-related tachycardiomyopathy.

Implantable cardioverter-defibrillator (ICD) is an effective therapy in patients known to be at high risk for sudden cardiac death (SCD). Nevertheless, ICD implantation is not indicated in transient or reversible causes of SCD. Wearable cardioverter-defibrillator is increasingly used for SCD prevention in patients with a transient risk of ventricular arrhythmia.