Ventricular tachycardia in structurally normal hearts.
This review focuses on four distinct syndromes of ventricular tachycardia that occur in the structurally normal heart. Recent advances in the fields of molecular biology and genetics, along with intracardiac mapping techniques, have led to a greater understanding of the underlying mechanisms of and therapeutic options for these syndromes. The cyclic AMP-mediated triggered activity tachycardias, including exercise-induced right ventricular outflow track tachycardia and repetitive monomorphic ventricular tachycardia, are the most common of these syndromes. Idiopathic left ventricular tachycardia, for which there is significant evidence for re-entry within the Purkinje network, is largely curable with catheter ablation. The long QT syndrome comprises a heterogeneous group of ion channel defects leading to prolongation of myocyte repolarization and Torsade de Pointes ventricular tachycardia. Brugada syndrome, a familial disorder of transmembrane ion transport, is felt to be the result of a group of sodium channel defects leading to characteristic electrocardiographic abnormalities, and syncope and sudden death. Primary focus is given to recent advances in our understanding of the underlying mechanism and current therapeutic approaches.
Wall
T Scott
TS
University of Utah Medical Center, Division of Cardiology, 50 North Medical Drive, Salt Lake City, UT 84132, USA.
Freedman
Roger A
RA
D018780:Body Surface Potential Mapping; D002037:Bundle-Branch Block / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D022062:Electrophysiologic Techniques, Cardiac; D006352:Heart Ventricles / Q000473:pathology*; D006801:Humans; D008133:Long QT Syndrome / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D013577:Syndrome; D017180:Tachycardia, Ventricular / Q000175:diagnosis* / Q000209:etiology / Q000628:therapy*; D014694:Ventricular Outflow Obstruction / Q000175:diagnosis / Q000209:etiology / Q000628:therapy