V. Yu. Tcivkovskii

Aim . To evaluate the impact of the extent of left atrial (LA) low-voltage areas on the risk of atrial arrhythmia recurrence after radiofrequency ablation (RFA) in patients with atrial fibrillation (AF). Methods . The study included 159 patients (mean age 65.36±9.33 years; 61.6% male) undergoing first-time RFA for AF (68.6% paroxysmal, 31.4% persistent). High-density LA voltage mapping was performed using a multielectrode catheter and CARTO 3 system. Areas with bipolar amplitude Results . Arrhythmia recurrence occurred in 40% of patients with persistent AF and 18.3% with paroxysmal AF. LVA% was significantly higher in patients with recurrence (40.40% vs. 4.80%; p < 0.001). In the Cox model, each 1% increase in LVA% was associated with a 3.6% higher recurrence risk (HR 1.036; p < 0.001). After adjustment for AF type and LA volume, LVA% remained an independent predictor (adjusted HR 1.034; p < 0.001). ROC analysis identified an optimal threshold of 22.4% (AUC=0.746). Patients with LVA% ≥22,4% had more than six-fold higher recurrence risk (adjusted HR 6.478; p < 0.001). LVA% measured during AF showed even stronger discrimination (AUC=0.786 for any arrhythmia; AUC=0.790 for atypical flutter/atrial tachycardia recurrence). Conclusions . The extent of low-voltage substrate in the left atrium is a strong and independent predictor of arrhythmia recurrence after RFA. Thresholds of ≥22,4% (or ≥24,7% for mapping during atrial fibrillation) allow reliable risk stratification and may guide individualized ablation strategies.

Aim . To identify predictors of sinus rhythm restoration during radiofrequency ablation (RFA) in patients with persistent atrial fibrillation (AF). Methods . The study included 51 patients with persistent AF who underwent primary RFA. All patients underwent left atrial (LA) voltage mapping. The percentage of low-voltage areas (LVA%) was calculated, with a low-voltage threshold 0.5 mV. After pulmonary vein isolation (PVI), if AF persist, posterior wall isolation and mitral isthmus ablation were performed. In cases of persistent AF, LA electrophysiological mapping was performed using a multielectrode catheter to identify areas of fractionated signals and local re-entry, followed by ablation of these areas. If AF transformed into atrial flutter, activation mapping was performed to verify the arrhythmia mechanism and ablate the critical isthmus. If the AF rhythm persisted, electrical cardioversion was performed. Results . Sinus rhythm was restored during RFA in 29 patients (56.8%) and by electrical cardioversion in 22 patients (43.2%). Statistically significant differences between rhythm restoration types were found in AF duration (p=0.013; AUC=0.705) and LA appendage flow velocity (p=0.021; AUC=0.697). Patients who achieved rhythm restoration at the PVI stage had significantly smaller LA volume (p=0.004; AUC=0.796) and LVA% (p=0.002; AUC=0.792). In the group of patients in whom AF was eliminated by direct restoration to sinus rhythm during RFA, LVA% was significantly lower (p=0.039; AUC=0.738) compared with those in whom AF was eliminated via transformation into atrial flutter. Conclusions . AF duration and LA appendage flow velocity are predictors of rhythm restoration during RFA. Among patients who achieved sinus rhythm restoration during ablation, those who converted at the PVI stage had smaller LA volume and LVA%. An LVA% greater than 28.5% was identified as a predictor of AF transformation into atypical atrial flutter during RFA of persistent AF.

Background: Meta-analyses suggest an association between patent foramen ovale (PFO) and white-matter hyperintensities (WMH), but pooled effect sizes do not clarify applicability to routine transthoracic echocardiography (TTE) or provide patient-level risk estimates. Objective: The objective of this study was to evaluate the association between TTE-detected PFO and MRI-defined WMH in routine practice and to develop a practice-anchored framework (PAMAP) that translates literature-derived evidence into individualized risk. Methods: We performed a retrospective, single-center, propensity-matched analysis of 149 adults undergoing TTE and brain MRI (37 PFO-positive, 112 controls). The primary endpoint was WMH (Fazekas ≥ 1). PAMAP synthesized 12 studies; 4 eligible studies were pooled using random-effects meta-analysis to derive a locked shunt coefficient (OR 3.65). The locked model used age and shunt (H); embolic context (E), and atrial stress (A) were neutral until refit. Transportability was assessed at the cohort level (expected vs. observed prevalence) and patient level (calibration, discrimination), followed by a minimal prespecified refit. Results: WMH was more frequent in PFO-positive versus control participants (54% vs. 32%). Literature-based expected prevalence approximated observed prevalence, supporting transportability. The locked model showed acceptable performance (calibration intercept 0.106; slope 0.912; Brier 0.188; AUC 0.756). A parsimonious refit improved performance (Brier 0.176; AUC 0.783), with the shunt term remaining significant (OR 2.45, 95% CI 1.23–4.88). Conclusions: PAMAP translates meta-analytic associations into a transportable patient-level risk framework. In routine TTE-defined PFO populations, the WMH association is preserved, suggesting that incidental PFO may mark early subclinical cerebral injury and enabling calibrated, individualized risk assessment.

Aim. To identify predictors of atrial tachyarrhythmias inducibility after pulmonary vein isolation in patients with paroxysmal atrial fibrillation (AF). Methods. The study included 82 patients (63,65±9,21 years, 45 men (54,9%)) with paroxysmal AF referred for primary radiofrequency ablation. All patients underwent voltage mapping of the left atrium, with areas exhibiting bipolar signal amplitudes less than 0.5 mV identified as low-voltage areas (LVA). After pulmonary vein isolation, arrhythmia induction was performed by pacing with a cycle length of 180 milliseconds sequentially from the left atrial appendage, anterior wall, roof, posterior wall, and mitral isthmus area. When sustained tachycardia was induced, electrophysiological mapping of the left atrium was performed to verify the tachycardia mechanism. Results. Tachyarrhythmias were not induced in 25 patients (30,48%), while 57 patients experienced induced tachyarrhythmias of varying durations (69,52%). The arrhythmia mechanisms in patients with induced sustained tachycardias were macro re-entry in 12 cases (38,7%), atrial fibrillation in 12 cases (38,7%), and a combination of macro re-entry and atrial fibrillation in 7 cases (22,6%). We found a statistically significant correlation between the induction of any type of arrhythmia and body mass index (p=0.014) and left atrial volume (p=0.024). A correlation was also found between AF induction and left atrial volume (p=0.016) and the percentage of LVA (p=0.014). The threshold value of the percentage of LVA indicating the probability of AF induction was 2.2%. No correlation was found between macro re-entry induction and any of the investigated factors. Conclusions. Independent predictors of sustained arrhythmia induction were left atrial volume and body mass index. Atrial fibrillation induction was associated with left atrial volume and LVA percentage with a threshold of ≥2.2%. No significant associations with the investigated parameters were found for macro re-entry.

Aim. The aim of the study was to assess the impact of comorbidities and duration of arrhythmic anamnesis on the results of left atrium voltage mapping in patients with persistent atrial fibrillation (AF).Methods. The study enrolled 50 patients who underwent the first radiofrequency ablation of persistent AF. Left atrium endocardial voltage maps were obtained using a 3D electroanatomical mapping system during AF. The voltage maps consisted of at least 2,000 points, with an average of 2,128±104 points. Low-voltage areas (LVA) were defined as Methods. The study enrolled 50 patients who underwent the first radiofrequency ablation of persistent AF. Left atrium endocardial voltage maps were obtained using a 3D electroanatomical mapping system during AF. The voltage maps consisted of at least 2,000 points, with an average of 2,128±104 points. Low-voltage areas (LVA) were defined as Results. We found a statistically significant correlation of LVA% with age (p<0.001, r=0.720), female sex (p=0.016), and the duration of arrhythmic history at the time of the start of persistence (p<0.001, r=0.503). Based on the data obtained, an original scale was developed to predict LVA%. The scale includes age, female sex, and the duration of arrhyth

Background: Cardiac laminopathies, associated with mutations in the LMNA gene, are a rare inherited disorder characterized by a broad range of clinical manifestations. There are currently no data on the association between supraventricular re-entrant tachycardias and LMNA-related cardiomyopathy. Case summary: A 26-year-old male presented with either wide-QRS tachycardia with a left bundle branch block (LBBB) pattern or narrow QRS tachycardia, as well as a history of palpitations since age 15. Echocardiography showed no overt structural heart disease. Electrophysiological studies confirmed the diagnosis of orthodromic atrioventricular re-entrant tachycardia mediated by a concealed left posterolateral accessory pathway (AP), with transient LBBB and dual AV-node physiology, characterized by single echo beats. A short-run, asymptomatic episode of atrial fibrillation was induced. Cardiac magnetic resonance (CMR) imaging demonstrated myocardial hyperaemia, subepicardial late gadolinium enhancement, and a small pericardial effusion, initially interpreted as myocarditis according to the modified Lake Louise criteria. A family history of pacemaker implantation and cardiac death at age 65 of the patient’s grandfather, a history of re-entrant arrhythmia recurrence following ablation, and further CMR deteriorations led to genetic counselling. Genetic testing identified a heterozygous pathogenic variant in the LMNA gene (NM_170707.3.456_457insTCTC, NP_733821.1.Glu154GlnfsX2), classified as likely pathogenic and associated with laminopathy. Discussion: This case raises the question of whether the combination of re-entrant arrhythmias is coincidental or an early indicator of LMNA-related cardiomyopathy.