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Many asymptomatic patients with a Wolff–Parkinson–White pattern on the electrocardiogram are at low risk for arrhythmias. However, younger asymptomatic patients with inducible arrhythmias may be at higher risk. This study found that prophylactic catheter ablation of accessory pathways in such patients greatly reduced the risk of arrhythmias. Prophylactic ablation in asymptomatic patients. Sudden death from cardiac causes in a healthy young person is a tragic event. Although ventricular fibrillation can be the presenting arrhythmia in asymptomatic patients with a Wolff–Parkinson–White electrocardiographic pattern, invasive electrophysiological testing for risk stratification and catheter ablation are not routinely recommended. 1 We recently reported that a particular subgroup of asymptomatic patients may be at risk for an arrhythmic event during follow-up. 2 We also demonstrated the value of electrophysiological testing for stratifying asymptomatic patients into high- and low-risk groups. In the present trial, we tested the hypothesis that prophylactic accessory-pathway ablation performed at the time of the initial electrophysiological . . .

Arrhythmia induction and identifying the functional characteristics of accessory pathways in Wolff‐Parkinson‐White (WPW) syndrome typically requires an invasive electrophysiological study. This case reports a 13‐year‐old boy with a five‐year history of paroxysmal palpitations, where transesophageal atrial pacing (TEAP) was used to identify accessory pathways. TEAP revealed multiple tachycardia forms, differentiating orthodromic atrioventricular reentrant tachycardia with narrow and wide QRS complexes. EPS confirmed two pathways, diagnosing WPW syndrome. TEAP effectively assessed accessory pathways' functional characteristics and their roles in tachycardia, showcasing its potential as a minimally invasive diagnostic tool for this condition. A 13‐year‐old boy has experienced intermittent paroxysmal palpitations for 5 years. Finally, tachycardia was induced through transesophageal atrial pacing, and an in‐depth analysis of the mechanism of tachycardia was conducted. The diagnostic results from transesophageal atrial pacing were fully consistent with those from intracardiac electrophysiological examination.

Background Wolff-Parkinson-White (WPW) syndrome is a congenital abnormality of the cardiac conduction system characterized by the presence of an accessory pathway, which can predispose affected individuals to supraventricular tachycardia (SVT), atrial fibrillation, ventricular fibrillation, and sudden cardiac death. Despite its clinical significance, WPW syndrome is often underdiagnosed, particularly in resource-limited settings where cardiac arrhythmias may be misattributed to other conditions. Case presentation We report an eight-year-old Nigerian girl with WPW syndrome who was repeatedly misdiagnosed and managed for malaria over four years before an accurate diagnosis was established. She presented with recurrent episodes of chest discomfort, generalized weakness, nausea, and near-syncope. Each episode was treated as malaria, and symptoms resolved following treatment. During the most recent episode of the symptoms, she received care in a tertiary centre where SVT was identified following an electrocardiogram (ECG), heart rate was persistently about 250 beats per minute. Initial pharmacologic intervention with intravenous amiodarone was ineffective, necessitating external cardioversion to restore normal sinus rhythm. A post-recovery ECG confirmed a Wolf Parkinson White pattern. Conclusion WPW syndrome remains a diagnostic challenge in paediatric populations, where it can masquerade varying diseases, resulting in misdiagnosis. This case underscores the importance of a high index of suspicion for cardiac arrhythmias in children presenting with unexplained recurrent symptoms. Early recognition and appropriate intervention are crucial in preventing life-threatening complications associated with WPW syndrome. Increased awareness among healthcare providers can lead to improved diagnostic accuracy and better patient outcomes.

PRKAG2 cardiac syndrome is an autosomal dominant inherited disease resulted from mutations in the PRK- AG2 gene that encodes γ2 regulatory subunit of AMP-activated protein kinase. Affected patients usually develop ventricular tachyarrhythmia and experience progressive heart failure that is refractory to medical treatment and requires cardiac transplantation. In this study, we identify a H530R mutation in PRKAG2 from patients with familial Wolff-Parkinson-White syndrome. By generating H530R PRKAG2 transgenic and knock-in mice, we show that both models recapitulate human symptoms including cardiac hypertrophy and glycogen storage, confirming that the H530R mutation is causally related to PRKAG2 cardiac syndrome. We further combine adeno-associated virus-9 （AAV9） and the CRISPR/Cas9 gene-editing system to disrupt the mutant PRKAG2 allele encoding H530R while leav- ing the wild-type allele intact. A single systemic injection of AAV9-Cas9/sgRNA at postnatal day 4 or day 42 substantially restores the morphology and function of the heart in H530R PRKAG2 transgenic and knock-in mice. Together, our work suggests that in vivo CRISPR/Cas9 genome editing is an effective tool in the treatment of PRKAG2 cardiac syndrome and other dominant inherited cardiac diseases by selectively disrupting disease-causing mutations.

Purpose of Review With increased electrocardiogram screening, asymptomatic preexcitation has become more prevalent. Historically, the asymptomatic-symptomatic dichotomy has directed management. This approach warrants scrutiny, as asymptomatic Wolff-Parkinson-White (WPW) syndrome is not without risk. Children may be unreliable symptom reporters, have atypical arrhythmia symptoms, yet have years to become symptomatic. Recent Findings In a large WPW study, symptomatic patients were more likely to undergo ablation than asymptomatic patients, yet, except for symptoms, there were no differences in clinical or electrophysiology study (EPS) characteristics. Present data confirm real risk in asymptomatic WPW—sudden death can be the first symptom. Although malignant arrhythmias correlate better with EPS risk stratification than with symptoms, EPS data are imperfect predictors. Summary Unlike adults with WPW, children have yet to prove survivorship. Asymptomatic children must be treated differently than adults. Sudden death risk is low but front-loaded in the young. An aggressive approach to asymptomatic WPW is warranted in this era of highly successful, low-risk catheter ablations.

Background Wolf–Parkinson–White syndrome predisposes patients to tachyarrhythmias and sudden cardiac death, with pregnancy further exacerbating arrhythmia risk due to hemodynamic, hormonal, and autonomic changes. We present a rare case of a pregnant woman with Wolf–Parkinson–White syndrome, which was unmasked after successful cardioversion of unstable ventricular tachycardia. Case Presentation A 40-year-old Black Ethiopian pregnant woman in her 35th week of gestation presented with unstable ventricular tachycardia, requiring multiple cardioversions, along with treatment with amiodarone and magnesium sulfate. She had a similar episode of unstable ventricular tachycardia 2 years earlier that was managed with cardioversion and subsequent pharmacotherapy, including amiodarone and metoprolol. After stabilization during the current episode, the electrocardiogram showed a short PR interval, delta waves, and wide QRS complexes, indicating previously undiagnosed type A Wolf–Parkinson–White syndrome. Laboratory investigations and echocardiography were unremarkable. The patient received optimal multidisciplinary care except for the absence of an electrophysiology study, which was not available locally. Finally, she delivered a healthy neonate at term via cesarean section with favorable maternal and neonatal outcomes. Conclusion This case underscores a rare instance of undiagnosed Wolf–Parkinson–White syndrome presenting as a life-threatening ventricular arrhythmia in pregnancy. It highlights how vigilant post-cardioversion electrocardiogram review can unmask concealed pre-excitation, the necessity of a coordinated multidisciplinary team for prompt stabilization, and the profound impact that limited access to electrophysiology services has on patient care in resource-constrained settings.

We report a 68-year-old man who presented with heart failure and atrial fibrillation (AF) with rapid ventricular response and wide QRS complexes. Tachycardia-induced cardiomyopathy (TIC) due to persistent AF developing on the basis of Wolff-Parkinson-White (WPW) syndrome was considered. Signs and symptoms of heart failure improved with restoration of sinus rhythm. This case suggested that persistent AF in a patient with WPW syndrome is one of the rare causes of TIC.

The approach to pediatric asymptomatic Wolff–Parkinson–White (WPW) patients is controversial. The objective of this review is to update the last consensus of specialists of the Pediatric and Congenital Electrophysiology Society/Heart Rhythm Society on this subject in order to summarize the most recent evidence on the management of young patients with asymptomatic WPW pattern. A systematic review of the literature published between 2008 and 2018 was performed taking into account the protocol of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) in PubMed (including Cochrane), Embase, and Web of Science. Observational, experimental, and multicentric studies were included. Out of a total of 37 articles selected, 4 were considered eligible. Most studies considered a cutoff age of 8 or greater as recommended in the 2012 consensus. The identification of a shortest pre-excitatory RR interval (SPERRI) ≤ 250 ms seems to be the best predictor for risk stratification. The importance of routine isoprenaline use to improve the sensitivity of the electrophysiological study to identify patients at high risk of sudden death was consensual. Prophylactic ablative therapy has been indicated in asymptomatic children with an accessory pathway (AP) who have a low SPERRI and/or a low effective anterograde period of the AP and/or multiple APs. Despite the evidence found in the most recent studies, more studies are warranted in this setting.

To assess the mid-term mortality and risk of atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HC) and Wolff-Parkinson-White (WPW) syndrome, 40 patients with HC and WPW were enrolled in our center between 2010 and 2017. An age- and gender-matched comparison cohort of patients with HC without WPW (n = 160) was generated from the same center. The clinical profile and outcomes were assessed. Of 40 patients with WPW, 28 underwent accessory pathway (AP) elimination. Two patients (7%) had failed in AP elimination. During mid-term follow-up, 1 patient had an implantable cardioverter-defibrillator intervention. Fourteen patients had AF. A previous history of AF (hazard ratio [HR]: 4.69; 95% confidence interval [CI] 1.51 to 14.63) and left atrial dimension (HR: 1.12; 95% CI 1.03 to 1.23) at baseline were risk factors for AF occurrence during follow-up. The AP elimination significantly reduced risk for the incidence of AF (HR: 0.22; 95% CI 0.06 to 0.83). Compared with the control group, the prevalence of syncope and AF were significantly higher in the WPW group. During follow-up, no difference was identified in outcome measures consisting of all-cause death, cardiac transplantation, and implantable cardioverter-defibrillator intervention. A previous history of AF (HR: 5.20; 95% CI 2.63 to 10.30, p <0.001) and persistent existing WPW (HR: 3.64; 95% CI 1.63 to 8.11, p = 0.002) were independent risk factors for AF occurrence during follow-up in the entire cohort. In conclusion, although WPW was uncommon and might not be correlated with mid-term mortality in HC patients, WPW might increase the risk of AF occurrence. Additionally, AP elimination may reduce the risk of AF occurrence.

A 54-year-old man with a 20-year history of recurrent paroxysmal tachycardia was admitted to hospital because of chest pain. The electrocardiogram (ECG) on admission (Figure 1A) showed signs suggestive of an antero septal accessory pathway, as well as ST segment elevation in leads V1 through V4, aVL and aVR, with elevated levels of cardiac enzymes. This was consistent with a diagnosis of Wolff-Parkinson-White syndrome with acute myocardial infarction (MI).1 The patient's chest pain persisted for two hours after coronary thrombolytic therapy. A subsequent ECG showed right bundle branch block, leftanterior fascicular block and no evidence of preexcitation changes. Pathologic Q waves in leads V1 through V3 with persistent ST segment elevation were also noted. A coronary angiogram showed a proximal leftanterior descending artery occlusion, which was successfully stented. Following this procedure, the patient became asymptomatic and a subsequent ECG (Figure 1B) showed complete resolution of the right bundle branch block and the preexcitation changes, with persistent anterior Q waves.