Tetralogy of Fallot

Pacing and Defibrillators in Complex Congenital Heart Disease

Device therapy is increasingly employed in the management of complex congenital heart disease (CHD). Bradycardias, most often related to sinus nodal dysfunction (SND) or atrioventricular nodal (AVN) block, may necessitate the implantation of pacing devices, while malignant arrhythmias may be treated by appropriate use of implantable cardioverter defibrillators (ICDs). However, there is a complex interplay between these classical device indications and associated supraventricular tachyarrhythmias, failure of ventricular function and ventricular dyssynchrony.

Long-term Outcomes of Ventricular Tachycardia Ablation in Different Types of Structural Heart Disease

Ventricular tachycardia (VT) is a significant cause of morbidity and mortality in patients with structural heart disease (SHD). While implantable cardioverter-defibrillators (ICDs) have been shown to be effective in preventing sudden death due to ventricular arrhythmias, they are not able to prevent recurrent VT episodes. Antiarrhythmic drugs (AADs) have some demonstrated efficacy in preventing VT episodes, although options remain limited in patients with SHD and the degree of benefit is suboptimal.

Approach to the Differentiation of Wide QRS Complex Tachycardias

The differentiation of wide QRS complex tachycardias presents a challenging diagnostic dilemma to many physicians despite multiple published algorithms and approaches.1 The differential diagnosis includes supraventricular tachycardia conducting over accessory pathways, supraventricular tachycardia with aberrant conduction, antidromic atrio-ventricular reentrant tachycardia, supraventricular tachycardia with QRS complex widening secondary to medication or electrolyte abnormalities, ventricular tachycardia (VT) or electrocardiographic artifacts.

Computed Tomography Angiography for Right Ventricular Function in an Adult with Complex Congenital Heart Disease

A 53-year-old with a history of surgically corrected tetralogy of Fallot (TOF) presented with dyspnea, fatigue, and increased abdominal girth. The patient was cyanotic as an infant and underwent a palliative left Blalock-Taussig (BT) shunt. At eight years of age he underwent corrective surgery with patch repair of a ventricular septal defect and resection of the infundibular region of the right ventricular (RV) outflow tract. The BT shunt was ligated at that time.