Pathophysiology and clinical relevance of atrial myopathy.

Atrial myopathy is a condition that consists of electrical, structural, contractile, and autonomic remodeling of the atria and is the substrate for development of atrial fibrillation, the most common arrhythmia. Pathophysiologic mechanisms driving atrial myopathy are inflammation, oxidative stress, atrial stretch, and neurohormonal signals, e.g., angiotensin-II and aldosterone. These mechanisms initiate the structural and functional remodeling of the atrial myocardium. Novel therapeutic strategies are being developed that target the pathophysiologic mechanisms of atrial myopathy. In this review, we will discuss the pathophysiology of atrial myopathy, as well as diagnostic and therapeutic strategies.

Coronary sinus signal amplitude: A predictor of the atrial substrate and low voltage areas.

BACKGROUND: Low voltage areas (LVA) are pivotal in atrial fibrillation (AF) pathogenesis, influencing local left atrial LA excitation and perpetuating AF occurrences. While pulmonary vein isolation (PVI) with cryo-balloon (CB) ablation is effective for AF, it doesn't provide insights into the LA substrate or detect LVA, which affects ablation success rates. This study examines whether LA voltage and LVAs can be anticipated by analyzing the voltage signal amplitude at the coronary sinus (CS) catheter, which is standard in CB and radiofrequency ablation procedures. METHODS: A retrospective analysis of 284 patients with recurrent AF undergoing RF catheter ablation was conducted at a high-volume EP center in Germany. The correlation between LA voltage and LVA with the CS signal was explored. RESULTS: The signal amplitude in the CS significantly correlated with voltage in LA walls, particularly in the proximal CS (correlation coefficient ρ = 0.81, p < 0.001). A CS signal cut-off of 1.155 mV effectively predicted severe atrial LVAs (>40%) with a sensitivity of 90.7% and a specificity of 100%. While a threshold of 1.945 mV identified patients with no significant atrial LVAs (<5%) with a sensitivity of 88% and a specificity of 50% (AUC: 0.81, 95% CI: 0.71-0.89, p < 0.001). CONCLUSION: The CS signal amplitude is associated with the LA voltage. Due to its potential as a diagnostic tool for atrial LVAs, the signal amplitude in the CS could provide valuable information about the LA substrate, especially when 3D mapping is not feasible.

Dynamic changes of left atrial substrate over time following pulmonary vein isolation: the Progress-AF study.

AIMS: Little is known about dynamic changes of the left atrial (LA) substrate over time in patients with atrial fibrillation (AF). This study aims to evaluate substrate changes following pulmonary vein isolation (PVI). METHODS AND RESULTS: In our prospective observational study, consecutive patients undergoing first PVI-only and redo ablation were included. High-density maps of the two procedures were compared. Progression or regression was diagnosed if a significant concordant decrease or increase in bipolar voltages in ≥2 segments was observed, respectively. In 28 patients (61.2 ± 9.5 years, 39% female, 53.5% persistent AF), 111.013 voltage points from 56 high-density LA maps (1.982 points/patient) were analysed. Comparing the high-density maps of the first and second procedures, in the progression group (17 patients, 61%), there was a decrease in global (-35%, P < 0.001) and all regional voltages. In the regression group (11 patients, 39%), there was an increase in global (+43%, P < 0.001) and regional voltages. Comparing the progression with the regression group, the area of low-voltage zone (LVZ) increased (+3.5 vs. -4.5 cm2, P < 0.001) and LA activation time prolonged (+8.0 vs. -9.1 ms, P = 0.005). Baseline clinical parameters did not predict progression or regression. In patients with substrate progression, pulmonary veins (PVs) were more frequently isolated (P = 0.02) and the AF pattern at recurrence was more frequently persistent (P = 0.005). CONCLUSION: Our study describes bidirectional dynamic properties of the LA substrate with concordant either progressive or regressive changes. Regression occurs with reduced AF burden after the first procedure, while progression is associated with persistent AF recurrence despite durable PV isolation. The dynamic nature of LA substrate poses questions about LVZ-based ablation strategies.

Atrial substrate characterization based on bipolar voltage electrograms acquired with multipolar, focal and mini-electrode catheters.

BACKGROUND: Bipolar voltage (BV) electrograms for left atrial (LA) substrate characterization depend on catheter design and electrode configuration. AIMS: The aim of the study was to investigate the relationship between the BV amplitude (BVA) using four catheters with different electrode design and to identify their specific LA cutoffs for scar and healthy tissue. METHODS AND RESULTS: Consecutive high-resolution electroanatomic mapping was performed using a multipolar-minielectrode Orion catheter (Orion-map), a duo-decapolar circular mapping catheter (Lasso-map), and an irrigated focal ablation catheter with minielectrodes (Mifi-map). Virtual remapping using the Mifi-map was performed with a 4.5 mm tip-size electrode configuration (Nav-map). BVAs were compared in voxels of 3 × 3 × 3 mm3. The equivalent BVA cutoff for every catheter was calculated for established reference cutoff values of 0.1, 0.2, 0.5, 1.0, and 1.5 mV. We analyzed 25 patients (72% men, age 68 ± 15 years). For scar tissue, a 0.5 mV cutoff using the Nav corresponds to a lower cutoff of 0.35 mV for the Orion and of 0.48 mV for the Lasso. Accordingly, a 0.2 mV cutoff corresponds to a cutoff of 0.09 mV for the Orion and of 0.14 mV for the Lasso. For healthy tissue cutoff at 1.5 mV, a larger BVA cutoff for the small electrodes of the Orion and the Lasso was determined of 1.68 and 2.21 mV, respectively. CONCLUSION: When measuring LA BVA, significant differences were seen between focal, multielectrode, and minielectrode catheters. Adapted cutoffs for scar and healthy tissue are required for different catheters.

Uric acid significantly correlates with the presence of low-voltage areas at the endocardial mapping in patients with non-valvular atrial fibrillation.

BACKGROUND AND AIMS: Interest in the role of atrial substrate in maintaining Atrial Fibrillation (AF) is growing. Fibrosis is the culprit in the electrical derangement of the myocytes. Many cardiovascular risk factors are known to be linked to atrial scarring; among them Uric Acid (UA) is emerging. The purpose of our study is to find whether UA is associated with Left Atrium (LA) with pathological substrate. METHODS AND RESULTS: 81 patients who underwent radiofrequency transcatheter ablation for nonvalvular AF at the cardiological department of the Niguarda Hospital were enrolled in an observational, cross-sectional, single-center study. UA levels were analysed before the procedure. High density electroanatomic mapping of the LA was performed and patients were divided according to the presence or not of areas of pathological substrate (bipolar voltage <0.5 mV in sinus rhythm). 19 patients showed a LA with pathological substrate. These subjects showed a significant higher prevalence of persistent phenotype of AF (84.2 vs. 25.8%, p < 0.001). UA levels were significantly higher in the group of patients with LA with pathological substrate (6.8 ± 1.9 vs 5.3 ± 1.4 mg/dL, p < 0.001) as well as the prevalence of hyperuricemia (26.5 vs. 6.5%, p = 0.021). The association between uric acid LA with pathological substrate remains significant even after correction for confounding factors (age, left ventricular dysfunction, valvular disease, arrythmia phenotype and furosemide use) and also when the ratio UA/creatinine was evaluated. CONCLUSIONS: In a population of patients who underwent AF ablation, higher UA levels were significantly associated with pathological LA substrate at electro-anatomical mapping.

Left atrial conduction times and regional velocities in persistent atrial fibrillation patients with and without fibrotic atrial cardiomyopathy.

Despite the progress in understanding left atrial substrate and arrhythmogenesis, only little is known about conduction characteristics in atrial fibrillation patients with various stages of fibrotic atrial cardiomyopathy (FACM). This study evaluates left atrial conduction times and conduction velocities based on high-density voltage and activation maps in sinus rhythm (CARTO®3 V7) of 53 patients with persistent atrial fibrillation (LVEF 60% (55-60 IQR), LAVI 39 ml/m2 (31-47 IQR), LApa 24 ± 6 cm2). Measurements were made in low voltage areas (LVA ≤ 0.5 mV) and normal voltage areas (NVA ≥ 1.5 mV) at the left atrial anterior and posterior walls. Maps of 28 FACM and 25 no FACM patients were analyzed (19 FACM I/II, 9 FACM III/IV, LVA 14 ± 11 cm2). Left atrial conduction time averaged to 110 ± 24 ms but was shown to be prolonged in FACM (119 ms, + 17%) when compared to no FACM patients (101 ms, p = 0.005). This finding was pronounced in high-grade FACM (III/IV) (133 ms, + 31.2%, p = 0.001). In addition, the LVA extension correlated significantly with the left atrial conduction time (r = 0.56, p = 0.002). Conduction velocities were overall slower in LVA than in NVA (0.6 ± 0.3 vs. 1.3 ± 0.5 m/s, -51%, p < 0.001). Anterior conduction appeared slower than posterior, which was significant in NVA (1 vs. 1.4 m/s, -29%, p < 0.001) but not in LVA (0.6 vs. 0.8 m/s, p = 0.096). FACM has a significant influence on left atrial conduction characteristics in patients with persistent atrial fibrillation. Left atrial conduction time prolongs with the grade of FACM and the quantitative expanse of LVA up to 31%. LVAs show a 51% conduction velocity reduction compared to NVA. Moreover, regional conduction velocity differences are present in the left atrium when comparing anterior to posterior walls. Our data may influence individualized ablation strategies.

Bi-atrial characterization of the electrical substrate in patients with atrial fibrillation.

BACKGROUND: Little is known regarding the characterization of electrical substrate in both atria in patients with atrial fibrillation (AF). METHODS: Eight consecutive patients undergoing AF ablation (five paroxysmal, three persistent) underwent electrical substrate characterization during sinus rhythm. Mapping of the left (LA) and right atrium (RA) was performed with the use of the HD Grid catheter (Abbott). Bipolar voltage maps were analyzed to search for low voltage areas (LVA), the following electrophysiological phenomena were assessed: (1) slow conduction corridors, and (2) lines of block. EGMs were characterized to search for fractionation. Electrical characteristics were compared between atria and between paroxysmal versus persistent AF patients. RESULTS: In the RA, LVAs were present in 60% of patients with paroxysmal AF and 100% of patients with persistent AF. In the LA, LVAs were present in 40% of patients with paroxysmal AF and 66% of patients with persistent AF. The areas of LVA in the RA and LA were 4.8±7.3 cm2 and 7.8±13.6 cm2 in patients with paroxysmal AF versus 11.7±3.0 cm2 and 2.1±1.8 cm2 in patients with persistent AF. In the RA, slow conduction corridors were present in 40.0% (paroxysmal AF) versus 66.7% (persistent AF) whereas in the LA, slow conduction corridors occurred in 20.0% versus 33.3% respectively (p = ns). EGM analysis showed more fractionation in persistent AF patients than paroxysmal (RA: persistent AF 10.8 vs. paroxysmal AF 4.7%, p = .036, LA: 10.3 vs. 4.1%, p = .108). CONCLUSION: Bi-atrial involvement is present in patients with paroxysmal and persistent AF. This is expressed by low voltage areas and slow conduction corridors whose extension progresses as the arrhythmia becomes persistent. This electrophysiological substrate demonstrates the important interplay with the pulmonary vein triggers to constitute the substrate for persistent arrhythmia.

Sleep apnoea has a dose-dependent effect on atrial remodelling in paroxysmal but not persistent atrial fibrillation: a high-density mapping study.

AIMS: Obstructive sleep apnoea (OSA) associates with atrial fibrillation (AF), but the relationship of OSA severity and AF phenotype with the atrial substrate remains poorly defined. We sought to define the atrial substrate across the spectrum of OSA severity utilizing high-density mapping. METHODS AND RESULTS: Sixty-six consecutive patients (male 71%, age 61 ± 9) having AF ablation (paroxysmal AF 36, persistent AF 30) were recruited. All patents underwent formal overnight polysomnography and high-density left atrial (LA) mapping (mean 2351 ± 1244 points) in paced rhythm. Apnoea-hypopnoea index (AHI) (mean 21 ± 18) associated with lower voltage (-0.34, P = 0.005), increased complex points (r = 0.43, P < 0.001), more low-voltage areas (r = 0.42, P < 0.001), and greater voltage heterogeneity (r = 0.39, P = 0.001), and persisted after multivariable adjustment. Atrial conduction heterogeneity (r = 0.24, P = 0.025) but not conduction velocity (r = -0.09, P = 0.50) associated with AHI. Patchy regions of low voltage that co-localized with slowed conduction defined the atrial substrate in paroxysmal AF, while a diffuse atrial substrate predominated in persistent AF. The association of AHI with remodelling was most apparent among paroxysmal AF [LA voltage: paroxysmal AF -0.015 (-0.025, -0.005), P = 0.004 vs. persistent AF -0.006 (-0.017, 0.005), P = 0.30]. Furthermore, in paroxysmal AF an AHI ≥ 30 defined a threshold at which atrial remodelling became most evident (nil-mild vs. moderate vs. severe: 1.92 ± 0.42 mV vs. 1.84 ± 0.28 mV vs. 1.34 ± 0.41 mV, P = 0.006). In contrast, significant remodelling was observed across all OSA categories in persistent AF (1.67 ± 0.55 mV vs. 1.50 ± 0.66 mV vs. 1.55 ± 0.67 mV, P = 0.82). CONCLUSION: High-density mapping observed that OSA associates with marked atrial remodelling, predominantly among paroxysmal AF cohorts with severe OSA. This may facilitate the identification of AF patients that stand to derive the greatest benefit from OSA management.

Splitting the P-Wave: Improved Evaluation of Left Atrial Substrate Modification after Pulmonary Vein Isolation of Paroxysmal Atrial Fibrillation.

Atrial substrate modification after pulmonary vein isolation (PVI) of paroxysmal atrial fibrillation (pAF) can be assessed non-invasively by analyzing P-wave duration in the electrocardiogram (ECG). However, whether right (RA) and left atrium (LA) contribute equally to this phenomenon remains unknown. The present study splits fundamental P-wave features to investigate the different RA and LA contributions to P-wave duration. Recordings of 29 pAF patients undergoing first-ever PVI were acquired before and after PVI. P-wave features were calculated: P-wave duration (PWD), duration of the first (PWDon-peak) and second (PWDpeak-off) P-wave halves, estimating RA and LA conduction, respectively. P-wave onset (PWon-R) or offset (PWoff-R) to R-peak interval, measuring combined atrial/atrioventricular and single atrioventricular conduction, respectively. Heart-rate fluctuation was corrected by scaling. Pre- and post-PVI results were compared with Mann-Whitney U-test. PWD was correlated with the remaining features. Only PWD (non-scaling: Δ=-9.84%, p=0.0085, scaling: Δ=-17.96%, p=0.0442) and PWDpeak-off (non-scaling: Δ=-22.03%, p=0.0250, scaling: Δ=-27.77%, p=0.0268) were decreased. Correlation of all features with PWD was significant before/after PVI (p<0.0001), showing the highest value between PWD and PWon-R (ρmax=0.855). PWD correlated more with PWDon-peak (ρ= 0.540-0.805) than PWDpeak-off (ρ= 0.419-0.710). PWD shortening after PVI of pAF stems mainly from the second half of the P-wave. Therefore, noninvasive estimation of LA conduction time is critical for the study of atrial substrate modification after PVI and should be addressed by splitting the P-wave in order to achieve improved estimations.

Clinical and echocardiographic characteristics of cardioembolic stroke.

BACKGROUND AND PURPOSE: Ischaemic stroke frequently has a cardioembolic (CE) source. Clinical and echocardiographic parameters associated with CE stroke were evaluated. METHODS: In all, 93 consecutive ischaemic stroke patients who underwent a transthoracic echocardiogram were retrospectively analysed; strokes were classified by TOAST (Trial of Org 10172 in Acute Stroke Treatment) criteria. Echocardiographic parameters related to CE stroke, including left atrial volumes and function, were compared to 73 healthy controls. RESULTS: Of 93 patients (mean age 66.1 years, 56% male), nine (10%) had large artery atherosclerosis, 38 (41%) CE stroke, two (2%) small vessel disease, two (2%) other and 42 (45%) undetermined aetiology. Left atrial (LA) maximum volumes (LAVImax ) and minimum volumes (LAVImin ) were larger in the CE group than the non-CE group (45 vs. 32 ml/m2 , 32 vs. 13 ml/m2 , respectively, P < 0.001), whilst LA function indices including LA emptying fraction and LA function index (LAFI) were lower in the CE group (34% vs. 55%, and 0.12 vs. 0.35, respectively, P < 0.001). Adjusting for clinical characteristics, LAFI ≤0.3 was an independent predictor of CE stroke (adjusted odds ratio 5.3, P = 0.001). Additionally, LAVImax and LAVImin were larger (61 vs. 44 and 32 vs. 24 ml/m2 respectively, P < 0.01) and LAFI significantly lower (0.34 vs. 0.52, P < 0.001) in the undetermined aetiology group versus healthy controls. CONCLUSIONS: Left atrial enlargement with reduced LA function was associated with CE stroke and LAFI was the best independent predictor. LA parameters were also altered in the undetermined aetiology group, suggesting an underlying LA myopathy in this subset.

Comparison between linear and focal ablation of complex fractionated atrial electrograms in patients with non-paroxysmal atrial fibrillation: a prospective randomized trial.

AIMS: Findings regarding efficacy of substrate modification for non-paroxysmal atrial fibrillation (AF) are inconsistent. We prospectively compared clinical outcomes of complex fractionated atrial electrogram (CFAE)-guided focal ablation (CFA) and CFAE-guided linear ablation (CLA) in patients with non-paroxysmal AF. METHODS AND RESULTS: We randomized 150 patients with non-paroxysmal AF into CFA and CLA groups in a 1:1 ratio. Complex fractionated atrial electrogram distribution was evaluated using an automated algorithm of a three-dimensional mapping system. After pulmonary vein isolation (PVI), CFAE-guided ablation was performed in the left atrium and then in the right atrium (RA). When compared with conventional CFA, CLA was performed based on conventional lines, with additional lines. Atrial fibrillation was not induced after PVI alone or with cavotricuspid isthmus ablation in 20.7% of patients. To achieve the endpoint, additional CFAE-guided RA ablation was required in 42.7% and 36.0% of patients undergoing CFA and CLA, respectively (P = 0.403). Atrial fibrillation was terminated during CFAE-guided ablation in 72.9% and 75.0% of patients undergoing CFA and CLA, respectively (P = 0.792). Termination of atrial tachycardia (AT) or non-inducibility of AF/AT was achieved in 61.3% and 68.0% of patients undergoing CFA and CLA, respectively (P = 0.393). The CLA group showed decreased 1-year freedom from AF/AT recurrence (60.0%, CFA vs. 47.3%, CLA; log rank P = 0.085), but no significant difference throughout the follow-up (22.2 ± 21.0 months) (67.1%, CFA vs. 68.9%, CLA; log rank P = 0.298). CONCLUSION: Long-term efficacy of CFAE-guided ablation was unaffected by the ablation technique in patients with non-paroxysmal AF.

Cigarette smoking causes a worse long-term outcome in persistent atrial fibrillation following catheter ablation.

INTRODUCTION: Cigarette smoking contributes to the development of atrial fibrosis via nicotine. The impact of smoking on ablation results in persistent atrial fibrillation (AF) is unknown. We aimed to investigate the triggers and long-term outcome between smokers and nonsmokers in the patients with persistent AF after catheter ablation. METHODS: This study included 201 (177 males, 53 ± 10 years old) patients who received index catheter ablation, including pulmonary vein isolation (PVI) and complex fractionated atrial electrograms (CFAEs) ablation for persistent AF, retrospectively. Electrophysiological characteristics at the index procedure and long-term outcome were investigated to determine the differences between smokers and nonsmokers. RESULTS: Baseline characteristics were similar between two groups. Pulmonary vein (PV) triggers were found in all patients in the two groups. There was a higher incidence of nonpulmonary vein (NPV) triggers in smokers than in nonsmokers (61% vs. 31%, P < 0.05). There were no differences of the long-term ablation outcomes between smokers and nonsmokers in Kaplan-Meier analysis. Smokers with PV plus right atrial NPV (RA-NPV) triggers had a higher incidence of recurrence (log-rank P < 0.05) than those without RA-NPV triggers, but not in nonsmokers, after a mean follow-up of 31 ± 25 months. CONCLUSIONS: Smoking increases the incidence of NPV triggers in patients with persistent AF. Smokers who have RA-NPV triggers during index procedure do have a worse outcome after catheter ablation, indicating the harmful effects of nicotine to right atrium.

A prospective and randomized comparison of limited versus extensive atrial substrate modification after circumferential pulmonary vein isolation in nonparoxysmal atrial fibrillation.

INTRODUCTION: The optimal substrate ablation approach in patients with persistent atrial fibrillation (Per AF) remains unclear. This was a prospective randomized study comparing the efficacy of limited (continuous complex fractionated atrial electrogram, CFAE: <60 milliseconds) versus extensive (continuous CFAE plus variable CFAE: <120 milliseconds) atrial substrate modification in Per AF patients. METHODS AND RESULTS: We enrolled 120 Per AF patients in the study, and 30 patients with AF termination after pulmonary vein isolation (PVI) were excluded. In the remaining 90 patients, 45 were treated with limited approach (Group 1) and 45 with an extensive approach (Group 2). The end point of the study was the incidence of an atrial arrhythmia recurrence postblanking period. The patients were followed up for 15 months with 3-month clinical reviews, electrograms (ECGs), Holter recordings, and echocardiographic monitoring. Procedural AF termination and the single procedural efficacy were statistically comparable between the 2 groups (48.9% vs. 63.4% in Groups 1 and 2, respectively, P = 0.289). During the follow-up, patients who received limited ablation had a lower incidence of recurrent AFL (P = 0.04), and better reverse remodeling of the left atrium (LA, P = 0.04). After 2 procedures, the freedom from any atrial arrhythmia was better in Group 2 (62.2% vs. 87.8%, P = 0.009). Those with longstanding AF and a larger baseline LA size responded better to the extensive ablation. CONCLUSIONS: In the Per AF patients who failed to achieve AF termination after PVI alone, a specific atrial substrate modification approach targeting only continuous CFAEs could be considered as an initial ablation strategy.

Clinical correlates of echocardiographic tissue velocity imaging abnormalities of the left atrial wall during atrial fibrillation.

AIMS: In patients with atrial fibrillation (AF), echocardiographic tissue velocity imaging (TVI) enables assessment of electrical and structural remodelling by measuring, respectively, the AF cycle length (AFCL-TVI) and the atrial fibrillatory wall motion velocity (AFV-TVI). We investigated the clinical and echocardiographic correlates of atrial remodelling assessed by TVI. METHODS AND RESULTS: We studied 215 patients presenting with AF. In all patients, we measured the AFCL-TVI and the AFV-TVI in the left atrium. Standard baseline characteristics were recorded. We divided patients by median value of AFV-TVI and AFCL-TVI to evaluate the determinants of atrial remodelling. A low AFV-TVI was related with a longer median duration of the current AF episode, a higher prevalence of significant mitral regurgitation and a thicker left ventricle (LV). Multivariate analysis revealed that a low AFV-TVI was independently associated with a longer median duration of the current AF episode [OR 0.09 (95% CI 0.03-0.027); P < 0.001]. Univariately, a short AFCL-TVI was associated with a long median duration of the current AF episode, the use of anti-arrhythmic drugs, a lower LV ejection fraction (LVEF) and a smaller left atrial volume index (LAVI). Multivariate analysis revealed that LVEF [OR 1.48 (95% CI 1.09-2.01); P = 0.013] and LAVI [OR 1.37 (95% CI 1.08-1.74); P = 0.010] were independently associated with AFCL-TVI. CONCLUSION: This study investigated the clinical and echocardiographic correlates of atrial remodelling assessed by TVI. The AFV-TVI is reduced in patients with a long AF duration and who have mitral regurgitation. In addition, the AFCL is long if LAVI is high and LVEF preserved. Tissue velocity imaging parameters measured during AF may be helpful to characterize the degree of atrial remodelling and optimize treatment.

Quantitative analysis of fractionated electrogram area of left atrium during right atrial pacing as an indicator of left atrial electrical remodeling in patients with atrial fibrillation.

Background: The clinical significance of left atrial local electrogram fractionation after restoration of sinus rhythm in patients with atrial fibrillation (AF) has not been elucidated. Methods: We evaluated ultrahigh-resolution maps of the left atrium (LA) during RA pacing acquired after pulmonary vein isolation in 40 patients with AF. The association between low-voltage area (LVA, <0.5 mV), fractionated electrogram area (FEA, the highlighted area with LUMIPOINT™ Complex Activation), the interval from onset of LA activation to wavefront collision at the mitral isthmus (LA activation time), and wave propagation velocity (WPV) was evaluated quantitatively. Results: The total LVA, total FEA with ≥5.0 peaks or ≥7.0 peaks were 7.0 ± 7.9 cm2, 15.9 ± 12.9 cm2, and 5.2 ± 7.5 cm2, respectively. These areas were predominantly observed in the anteroseptal region. Total LVA, total FEA with ≥5.0 peaks, and total FEA with ≥5.0 peaks in the normal voltage area (NVA: ≥0.5 mV) correlated with LA activation time (R = 0.69, 0.75, and 0.71; each p < .0001). In the anterior wall, these areas correlated with regional mean WPV (R = -0.75, -0.83, and - 0.55; each p < .0001) and the extent of slow conduction area (SCA) with WPV <0.3 m/s (R = 0.89, 0.84, 0.33; p < .0001 for LVA and FEA, p < .05 for FEA located in NVA). The anterior wall FEA with ≥7.0 peaks and that in the NVA showed a better correlation in predicting anterior wall SCA (R = 0.92 and 0.86, each p < .0001). Conclusion: Quantitative analysis of FEA together with LVA may facilitate the assessment of LA electrical remodeling.

Practical approach for atrial cardiomyopathy characterization in patients with atrial fibrillation.

Atrial fibrillation (AF) causes progressive structural and electrical changes in the atria that can be summarized within the general concept of atrial remodeling. In parallel, other clinical characteristics and comorbidities may also affect atrial tissue properties and make the atria susceptible to AF initiation and its long-term persistence. Overall, pathological atrial changes lead to atrial cardiomyopathy with important implications for rhythm control. Although there is general agreement on the role of the atrial substrate for successful rhythm control in AF, the current classification oversimplifies clinical management. The classification uses temporal criteria and does not establish a well-defined strategy to characterize the individual-specific degree of atrial cardiomyopathy. Better characterization of atrial cardiomyopathy may improve the decision-making process on the most appropriate therapeutic option. We review current scientific evidence and propose a practical characterization of the atrial substrate based on 3 evaluation steps starting with a clinical evaluation (step 1), then assess outpatient complementary data (step 2), and finally include information from advanced diagnostic tools (step 3). The information from each of the steps or a combination thereof can be used to classify AF patients in 4 stages of atrial cardiomyopathy, which we also use to estimate the success on effective rhythm control.

Unraveling the interplay: early-stage atrial functional mitral regurgitation and left atrial electrical substrate in atrial fibrillation patients.

Background: Atrial fibrillation (AF) triggers atrial remodeling, impacting atrial function and ablation efficacy. This remodeling leads to atrial cardiomyopathy and dilatation, linked to mitral regurgitation, forming atrial functional mitral regurgitation (aFMR). Our study explores the relationship between early-stage-aFMR and the atrial electrical architecture, focusing on left atrial bipolar voltage and low-voltage areas (LVAs) in AF patients. Methods: We enrolled 282 patients undergoing redo-PVI after AF recurrence post-PVI. Echocardiography was performed prior to ablation, and only patients with no, mild, or mild-to-moderate aFMR were included. Ablation used radiofrequency and a 3D mapping system, with atrial voltage documented on each atrial wall. LVAs were calculated using high-density maps, and patients were followed for 15 months. Results: Significant differences in left atrial voltage and LVA extent were observed based on aFMR severity. Patients with aFMR 1 + had significantly lower atrial voltage compared to no-aFMR, but no significant increase in LVAs. Patients with aFMR 2 + showed lower voltage amplitudes in all atrial regions and larger LVAs compared to no-aFMR patients. AF recurrence was significantly higher in the aFMR group (62.9% vs. 48.3%, p = 0.027) within 1 year. aFMR was associated with AF recurrence after adjusting for sex, age, and AF types (HR: 1.517, 95% CI: 1.057-2.184, p = 0.025). Conclusion: aFMR in AF patients may indicate progressive atrial remodeling and left atrial cardiomyopathy, characterized by reduced atrial voltage and increased LVAs. aFMR is linked to PVI outcomes, suggesting its consideration in AF therapy decision-making.

COVID-19 HEART unveiling as atrial fibrillation: pathophysiology, management and future directions for research.

BACKGROUND: COVID-19 infections are known to cause numerous systemic complications including cardiovascular disorders. In this regard, clinicians recently noticed that patients recovering from COVID-19 infections presented with diverse set of cardiovascular disorders in addition to those admitted to ICU (intensive care unit). COVID-19 heart has multifaceted presentation ranging from dysrhythmias, myocarditis, stroke, coronary artery disease, thromboembolism to heart failure. Atrial fibrillation is the most common cardiac arrhythmia among COVID-19 patients. In the background section, we briefly discussed epidemiology and spectrum of cardiac arrhythmias in COVID-19 patients. MAIN BODY: In this state-of-the-art review we present here, we present the information regarding COVID-19-induced A-fib in sections, namely mechanism of action, clinical presentation, diagnosis and treatment. Unfortunately, its occurrence significantly increases the mortality and morbidity with a potential risk of complications such as cardiac arrest and sudden death. We included separate sections on complications including thromboembolism and ventricular arrhythmias. Since its mechanism is currently a gray area, we included a separate section on basic science research studies that are warranted in the future to comprehend its underlying pathogenic mechanisms. CONCLUSIONS: Taken together, this review builds upon the current literature of COVID-19-induced A-fib, including pathophysiology, clinical presentation, treatment and complications. Furthermore, it provides recommendations for future research moving forward that can open avenues for developing novel remedies that can prevent as well as hasten clinical recovery of atrial fibrillation in COVID-19 patients.

The Atrium in Atrial Fibrillation - A Clinical Review on How to Manage Atrial Fibrotic Substrates.

Atrial fibrillation (AF) is the most common sustained arrhythmia in the population and is associated with a significant clinical and economic burden. Rigorous assessment of the presence and degree of an atrial arrhythmic substrate is essential for determining treatment options, predicting long-term success after catheter ablation, and as a substrate critical in the pathophysiology of atrial thrombogenesis. Catheter ablation of AF has developed into an essential rhythm-control strategy. Nowadays is one of the most common cardiac ablation procedures performed worldwide, with its success inversely related to the extent of atrial structural disease. Although atrial substrate evaluation remains complex, several diagnostic resources allow for a more comprehensive assessment and quantification of the extent of left atrial structural remodeling and the presence of atrial fibrosis. In this review, we summarize the current knowledge on the pathophysiology, etiology, and electrophysiological aspects of atrial substrates promoting the development of AF. We also describe the risk factors for its development and how to diagnose its presence using imaging, electrocardiograms, and electroanatomic voltage mapping. Finally, we discuss recent data regarding fibrosis biomarkers that could help diagnose atrial fibrotic substrates.