Falsely detected atrial tachycardia episode in a patient with CRT-P due to FFRW oversensing resulting in ventricular sensed response triggered BiV pacing and auto adjusting sensitivity phenomenon.
Falsely detected atrial tachycardia episode in a patient with CRT-P due to FFRW oversensing resulting in ventricular sensed response triggered BiV pacing and auto adjusting sensitivity phenomenon.
Right ventricular (RV) dysfunction is independently predictive of sudden cardiac death. This study aimed to compare the performance of different risk stratification methods for death and appropriate implantable cardioverter-defibrillator (ICD) therapy using echocardiography and cardiac magnetic resonance imaging (CMR) to quantify RV function.
Consecutive patients undergoing ICD implantations who had completed both preprocedural echocardiography and CMR were retrospectively enrolled. Patients with channelopathies or arrhythmogenic right ventricular disease were excluded. The RV fractional area change (RVFAC) and estimated pulmonary artery pressure (EPAP) were calculated from echocardiography. The contraction pressure index (CPI) was defined as the quotient of the RVFAC divided by the EPAP. Both metrics were used to predict the composite endpoint of death and an appropriate ICD therapy. RV dysfunction was defined by either RVFAC < 35% or RV ejection fraction (RVEF) < 45%.
In total, 88 patients (60.4 ± 14.7 years, 61 males) including 15 with ischemic cardiomyopathy were retrospectively enrolled. Forty-two patients received ICDs as secondary prevention. The mean RVFAC, CPI, and RVEF were 35.9% ± 9.22%, 1.4% ± 0.7%/mmHg, and 39.5% ± 14.4%, respectively. Regarding the composite endpoint, the best cut-off value of the CPI was 1.59 (specificity 0.45, sensitivity 0.96, ROC-AUC 0.68). The hazard ratio of a low RVFAC was 3.28 (95% CI: 1.39–7.77, p = 0.007, concordance = 0.622), a low CPI, 14.2 (95% CI: 1.91–104.9, p = 0.010, c = 0.665), and a low RVEF, 3.44 (95% CI: 1.17–10.1, p = 0.003, c = 0.620).
Both CMR-derived RVEF and the echocardiographic CPI predicted appropriate ICD therapy and death. The CPI may provide superior risk stratification.
Research regarding the adverse outcomes of atrial fibrillation (AF) in patients with acute pancreatitis (AP) is limited. We hypothesize that the presence of AF is associated with worse inpatient outcomes, including increased mortality and complications in patients admitted with AP.
In this cohort study, de-identified patient data from the US Collaborative Network in TriNetX was used to assess the risk of all-cause mortality and adverse events in patients with AP having AF compared to those without AF within 30 days of the index event from January 1, 2010 to July 6, 2024. Analyses were performed before and after propensity score matching, with risks expressed as odds ratios (OR) with 95% confidence intervals (95% CI), and Kaplan–Meier curves were generated for outcomes.
A total of 267 429 patients with AP were identified, of whom 44 621 had a diagnosis of AF. Patients with AP having AF presented with higher comorbidity burdens compared to the non-AF cohort before propensity score matching. After matching, patients with AF exhibited increased risks of all-cause mortality (OR, 1.24; 95% CI, 1.18–1.3), acute kidney injury (OR, 1.17; 95% CI, 1.14–1.2), deep venous thrombosis (OR, 1.33; 95% CI, 1.27–1.39), hemorrhage (OR, 1.06; 95% CI, 1.01–1.11), severe sepsis (OR, 1.3; 95% CI, 1.25–1.35), and requiring critical care services (OR, 1.19; 95% CI, 1.16–1.23).
Our results suggest that AF significantly increases the risk of mortality in patients with AP, even after accounting for confounding etiological, comorbid, and pharmacological factors.
Implantable cardioverter-defibrillator undersensing may delay therapy in ventricular fibrillation with low-amplitude signals. Ventricular fibrillation therapy assurance (VFTA) detected persistent VF after initial shock failure, enabling timely shock delivery and successful resuscitation. VFTA may help optimize device programming by preventing misclassification and treatment delay in life-threatening arrhythmias.
This case illustrates both termination and re-initiation of repetitive non-reentrant ventriculoatrial synchrony (RNRVAS) visualized on a standard 12-lead ECG. It highlights how pacemaker algorithms such as VIP and PVC response, together with abnormal atrial refractoriness, can trigger or terminate RNRVAS.
Pulsed-field ablation (PFA) is increasingly used for catheter ablation of atrial fibrillation (AF), but older patients remain underrepresented in clinical trials. This study aimed to compare procedural outcomes and mid-term effectiveness of PFA in patients aged ≤ 75 and > 75 years.
In this retrospective single-center cohort, 479 consecutive patients underwent PFA for AF between January 2022 and April 2024. Patients were grouped by age (≤ 75 vs. > 75 years at ablation). Procedural parameters and acute complications were compared. Arrhythmia-free survival was assessed with Kaplan–Meier analysis after an 8-weeks blanking period, and predictors of recurrence were evaluated using Cox regressions.
Of 479 patients (mean age 65.0 ± 12.1 years; 73.6% males), 104 (21.7%) were > 75 years at ablation. Patients > 75 years had more comorbidities, including hypertension and impaired renal function. Pulmonary vein isolation was achieved in 99.8% of cases. Acute complication rates were similar between groups (7.7% in > 75 vs. 8.5% in ≤ 75, p = 1.00), with low rates of tamponade (1.5%) and stroke (1.3%). Kaplan–Meier analysis showed no difference in arrhythmia-free survival. At 6 months, freedom from atrial arrhythmia was 81.4% in the > 75 group and 83.8% in the ≤ 75 group (p = 0.57); corresponding rates at 12 months were 60.1% and 68.6%. Age was not an independent predictor of recurrence. At last follow-up, 75.7% of patients were off antiarrhythmic drugs.
PFA in patients > 75 years is associated with low complication rates and favorable rhythm outcomes, comparable to those in younger patients. These findings support the use of PFA in elderly patients with AF.
E. Aydin, M. M. Öğütveren, G. Ö. Mert, et al., “Clinical Profiles and In-Hospital Outcomes of Pre-Existing Versus Newly Diagnosed Atrial Fibrillation in Coronary Care Units: Insights From the MORCOR-TURK National Registry,” Journal of Arrhythmia 41, no. 6 (2025): e70238, https://doi.org/10.1002/joa3.70238.
The name of the last author is corrected from “Aymet Seyda Yilmaz” to “Ahmet Seyda Yılmaz.” The online version of this article has been corrected accordingly.
We apologize for this error.
We read with interest the article titled “Impact of anisotropic conduction and premature atrial contraction on the fractionated atrial potentials” [1]. They report that premature atrial contractions (PACs) shift fractionated atrial potentials (FAPs) away from the right and mid anterior walls toward the left anterior, left inferior, and lateral walls, emphasizing the impact of extrastimuli direction on atrial substrate characterization.
In contrast, Heida et al., using intraoperative high-resolution epicardial mapping during spontaneous PACs in 228 patients, found no clear increase in conduction heterogeneity or fractionation in regions like Bachmann's bundle or pulmonary vein area that would support a substantial PAC-induced FAP burden [2]. Their quantification of local directional heterogeneity revealed that while PACs modestly increased LDH, they did so uniformly and did not reproduce the dramatic regional redistribution seen by Toyama and Kumagai. This raises the question of whether PACs truly alter FAP distribution in the manner proposed by the recent study.
Moreover, Hirokami et al. studied fractionated signal areas in the atrial muscle during pacing and premature extrasystoles and concluded that the effect of premature stimuli direction on fractionation patterns was minimal, suggesting that the directionality emphasized by Toyama and Kumagai may be overinterpreted [3].
A further layer of contradiction comes from two additional studies. Teuwen et al. [4] used high-resolution epicardial mapping to compare conduction during sinus rhythm and atrial extrasystoles (AES) in over 160 patients; they found that decreases in conduction velocity and increases in delay occurred primarily in cases of aberrant wavefronts or breakthrough AES, but the degree of prematurity itself did not consistently correlate with increased conduction block or fractionation, indicating that not all PACs cause enhanced FAP burden [4]. Additionally, modeling and optical mapping work in canine atria by Roberts-Thomson et al. demonstrated that anisotropic conduction properties and resulting fractionated electrograms were highly dependent on tissue structural geometry and pacing rate rather than PAC direction per se—suggesting a more complex interplay than Toyama and Kumagai's direction-based hypothesis allows [5].
Taken together, these contradictory findings highlight that while Toyama and Kumagai's work provides valuable insight into how anisotropic conduction and extrastimuli may affect FAP distribution, other clinical and modeling data challenge the magnitude and regional specificity of those effects—emphasizing the need for standardized high-density mapping and controlled comparisons between spontaneous and paced PACs to resolve these discrepancies.
The authors declare no conflicts of interest.
Dual-chamber pacemakers equipped with anti-reflex syncope algorithms are an established therapeutic option for preventing recurrent syncope in selected patients with reflex syncope. However, their efficacy in patients under 40 years old and in non-type 2B syncope remains uncertain and clinical predictors of recurrent syncope post-implantation are not well established.
To identify clinical factors associated with early recurrence of syncope in patients with reflex syncope who received dual-chamber pacemakers with anti-syncope functionality.
This retrospective cohort study included 117 patients (65% female) with reflex syncope confirmed by a positive tilt-table test. All received dual-chamber pacemakers. The primary endpoint was syncope recurrence within 6 months.
Among 117 paced patients, 15 (12.8%) had recurrent syncope by 6 months. In the reduced Cox model, all three prespecified variables independently predicted recurrence: female sex (HR: 5.386; 95% CI: 1.689–17.175; p = 0.004), systolic blood pressure differential between the end of the passive phase and the syncope onset (HR: 1.036; 95% CI: 1.008–1.064; p = 0.011), number of prior syncope episodes (HR: 2.950; 95% CI: 1.565–5.561; p = 0.001). ROC-based cutoffs supported descriptive separation (e.g., ≥ 2.5 prior episodes; ΔSBP ≥ 87.5 mmHg; asystole ≥ 13.5 s), but continuous coding was used for modeling to avoid information loss.
Within 6 months of dual-chamber pacemaker implantation, recurrent syncope was more likely in female sex, a larger systolic blood pressure differential between the end of the passive phase and syncope onset, and greater pre-implantation syncope burdens.
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