Herzschrittmachertherapie und Elektrophysiologie最新文献

Background: Catheter-assisted ablation of supraventricular tachycardia, especially of atrial fibrillation, often results in atrial tachycardia (AT) in the further course. ATs are favored by incomplete linear lesions, scarring of the atria or persistent pulmonary vein connections, and vary in incidence depending on the type of the preceding procedure.

Objectives: This article discusses different forms of postablation AT in terms of diagnosis, treatment options, and perspectives for prevention and effective treatment.

Materials and methods: Overview-based review of the literature and case-based experiences from our own center on incidence, mapping methods, and ablation strategies as well as emerging technologies.

Results and conclusion: The reported incidence of postablation ATs varies widely (4-36%), depending on patient selection and procedural complexity. Invasive diagnostics are mainly based on ultra-high-resolution mapping methods, while classical electrophysiological maneuvers are less reliable in this patient population. The therapy of choice is reablation, as drug options are less effective. Depending on the mechanism of AT, focal or linear ablation strategies are preferred, with variable success and more frequent recurrences than with initial ablations. Newer catheter designs and improved lesion control are gaining importance. A technically precise and completely transmural initial ablation remains a central predictor of long-term rhythm stability. Multimodal approaches and individualized strategies are key to the future to sustainably reduce the incidence and recurrence of postablation AT.

Recent advances in technology and clinical electrophysiology have led to precise characterization of re-entry circuits and effective ablation strategies of atypical atrial flutter. Combination of activation and entrainment mapping is the key to identifying the re-entry circuit. The presence of a slow-conducting isthmus, localized re-entry, dual-loop re-entry or bystander loops may lead to misleading activation maps but can be identified by electrogram analysis and entrainment mapping. The ECG pattern of atypical atrial flutter is poorly predictive of circuit anatomy but may still provide mechanistic insight. Long-term ablation success requires the creation of a transmural continuous lesion across a critical component of the re-entry circuit. Procedural endpoints include bidirectional conduction block across linear lesions and non-inducibility of atrial tachycardia.

The analysis of atrial rhythm is a fundamental step in the interpretation of a resting electrocardiogram. Careful identification of P waves is essential; however, their presence alone does not necessarily indicate sinus rhythm. A systematic assessment of P-wave morphology and axis, as well as a focused search for non-conducted P waves, is crucial for accurate classification of the underlying cardiac rhythm. Ectopic atrial rhythms, atrial tachycardias, and atrial flutter typically exhibit P-wave patterns that differ from those seen in normal sinus rhythm. Normal sinus rhythm originates in the region of the superior vena cava and propagates from right to left and from cranial to caudal across both atria. The present case highlights common diagnostic pitfalls in a patient with clearly discernible P waves.

Narrow QRS complex tachycardias originating from the atrioventricular (AV) node region primarily include atrioventricular nodal reentrant tachycardia (AVNRT) and junctional ectopic tachycardia (JET). While AVNRT, the most common paroxysmal supraventricular tachycardia, is based on a reentrant mechanism involving dual AV nodal physiology, JET predominantly arises from enhanced automaticity or triggered activity and frequently occurs either congenitally or postoperatively. Electrophysiological studies allow for a differentiated diagnosis of both entities, with maneuvers such as ventricular stimulation and analysis of retrograde activation patterns being particularly helpful in distinguishing AVNRT from other supraventricular tachycardias. In terms of therapy, modified vagal maneuvers, adenosine, and especially catheter ablation in long-term management are central for AVNRT, whereas in JET, pharmacological therapy, treatment of underlying causes, and ablation in selected cases are employed. A thorough understanding of the anatomical and electrophysiological foundations is essential for targeted diagnosis and therapy of these tachycardias.

Background: Wolff-Parkinson-White (WPW) syndrome is characterised by accessory pathways that bypass the normal atrioventricular conduction system. Precise preprocedural localisation is pivotal for optimising ablation strategy, minimising complications, and reducing radiation exposure.

Methods: This review systematically analyses ECG-based algorithms for accessory pathway localisation, including classical and recent rule-based approaches, as well as modern deep learning models.

Results: Classical algorithms showed variable accuracy ranging from 72% (Milstein) to 92% (D'Avila, St. George). Modern rule-based algorithms demonstrate significantly improved performance: EASY-WPW achieved 93% accuracy (sensitivity 92%, specificity 99%), and SMART-WPW reached 97% (sensitivity 96%, specificity 100%) using a 12-location clock-face model. DL approaches achieved an 84% accuracy with AUROC 0.92, significantly outperforming classical algorithms (Milstein AUROC 0.81, Arruda AUROC 0.80). The DL model enables automatic analysis, reduces interobserver variability, and identifies parahisian pathways and locations requiring transseptal puncture. Both EASY-WPW and SMART-WPW showed excellent results in pediatric populations.

Conclusions: Both validated ECG algorithms and deep learning models represent valuable tools for preinterventional planning in patients with WPW syndrome. Modern rule-based algorithms offer excellent diagnostic accuracy with sensitivities and specificities exceeding 90%. The integration of artificial intelligence (AI) and multimodal approaches promises further improvements in accessory pathway localisation.

With the growing number of adults with congenital heart disease (ACHD), the incidence of arrhythmias as a late complication is also increasing. Narrow QRS tachycardias are the most common form of supraventricular arrhythmias in this population, typically arising from postoperative scarring, anatomical reconstruction, and altered conduction pathways. The 12-lead surface ECG remains a key tool for mechanism diagnosis, distinguishing between typical and atypical atrial flutter circuits, focal atrial tachycardias, and atrioventricular (AV) reentrant tachycardias, as well as for guiding interventional therapy planning. Following complex atrial surgeries such as Mustard, Senning, Fontan procedures, or biatrial heart transplantation, conventional ECG interpretation reaches its limits: atypical electrical activation, an abnormal heart axis, multiple reentry substrates, and altered P‑wave morphologies complicate classification. In such cases, the combination of ECG findings, detailed knowledge of the individual postoperative anatomy, three-dimensional electroanatomical mapping, and complementary imaging is essential. Catheter ablation in this patient group achieves high acute success rates with acceptable safety, yet remains prone to recurrences. Structured ECG analysis, modern imaging, and treatment in specialized centers are key to improving long-term outcomes and prognosis.

Supraventricular tachyarrhythmias are a clinical finding that is seen to a varying extent in patients with ion channel diseases depending on the underlying genetic disease. In addition to the classical symptoms that they cause, they may trigger ventricular tachyarrhythmias or induce inappropriate implantable cardioverter-defibrillator (ICD) therapies and, thus, cause psychological harm. Antiarrhythmic drugs can be used in some diseases, but are contraindicated in a number of genetic conditions. In these patients, catheter ablation is a good alternative and sometimes the only treatment choice. In young individuals with atrial fibrillation, ion channel diseases should be excluded, especially when there is familial disease or early onset of atrial fibrillation, in particular below 30 years of age.