In latent Wolff–Parkinson–White syndrome, ventricular pre-excitation is inapparent during sinus rhythm but carries the same possibility of sudden cardiac death and palpitations as overt Wolff–Parkinson–White syndrome. It is difficult to diagnose latent Wolff–Parkinson–White syndrome when a patient does not have syncope or palpitations. We report the case of an asymptomatic patient with latent Wolff–Parkinson–White syndrome detected on school heart screening using subtle electrocardiography findings.

Tuberous sclerosis complex is a rare multisystem genetic disorder characterised by the growth of numerous tumour-like malformations in many parts of the body including skin, kidneys, brain, lung, eyes, liver, and heart. Mutations in the TSC1 or TSC2 genes have been reported to cause disruption in the TSC1–TSC2 intracellular protein complex, causing over-activation of the mammalian target of rapamycin protein complex. In this study, we present a 3-month-old male infant diagnosed with tuberous sclerosis, bilateral neurosensorial hearing loss, Wolff–Parkinson–White syndrome on electrocardiography, multiple cardiac rhabdomyomas with severe stenosis in the left ventricular outflow tract, who responded well to the Everolimus therapy.

We present a young soldier presenting with aborted sudden cardiac death, who was found to have concomitant hypertrophic cardiomyopathy and Wolff–Parkinson–White syndrome. Along with pathological haemodynamic features of hypertrophic cardiomyopathy, an easily-inducible re-entrant tachycardia was clearly documented in our patient. Given the fatal potential of supraventricular tachycardia in hypertrophic cardiomyopathy, we postulated that his tachyarrhythmia could potentially trigger the event. Upon his refusal to receive implantable cardioverter/defibrillator therapy, we ablated anatomical arrhythmogenic substrate instead, and he remained uneventfully over 3 years on β-blocker.

Some asymptomatic patients with Wolff–Parkinson–White syndrome have severe left ventricular dyssynchrony and dysfunction. We describe a patient who was given a diagnosis of Wolff–Parkinson–White syndrome in infancy and had a complete response to pharmacologic therapy with flecainide. Our findings suggest that flecainide is a suitable resynchronisation therapy for such infants.

Wolff–Parkinson–White (WPW) syndrome with atrial fibrillation (AF) is a potentially life-threatening problem requiring rapid conversion to sinus rhythm. The most recent American Heart Association guidelines for the treatment of patients with WPW, published in conjunction with the 2000 Advanced Cardiac Life Support (ACLS) guidelines, suggests that intravenous amiodarone is a first-line therapy for AF–WPW; however the evidence suggests this is a potentially dangerous myth.

Radiofrequency lesions can, theoretically, be the substrate for new persistent arrhythmias. As far as we know, this has never previously been encountered after transcatheter ablation of accessory pathways. A child with Wolff–Parkinson–White syndrome was referred for radiofrequency catheter ablation of a left-sided accessory pathway. After successful ablation of the accessory pathway using a retrograde transaortic approach, the child developed an incessant wide QRS complex tachycardia at slow rate that was resistant to pharmacologic interventions. The focus of the tachycardia was identical to the ventricular site of insertion of the eliminated accessory pathway.

Over a six year period, we identified four children with dilated cardiomyopathy associated with ventricular preexcitation, three in the absence of any documented tachyarrhythmias, and one with but a solitary episode of tachyarrhythmia. None of them had another identifiable aetiology for the cardiomyopathy. Based on the 12 lead electrocardiogram, and/or invasive electrophysiologic studies, we localised the accessory pathways to the right atrioventricular groove in all patients. We commenced antifailure medications in two of the four patients, but did not produce any measurable improvement in ventricular function. Catheter ablation was performed in two patients, with resolution of the cardiomyopathy. The ventricular preexcitation disappeared spontaneously in one child during follow-up, again with resolution of cardiomyopathy. The youngest patient continues to receive antifailure medications, albeit without improvement. We suggest, therefore, that dilated cardiomyopathy of reversible nature is associated with manifest ventricular preexcitation, even in the absence of sustained arrhythmias.