Electrophysiology of T-wave alternans: mechanisms and pharmacologic influences.
Extensive experimental evidence indicates a fundamental link between T-wave alternans (TWA) and arrhythmogenesis. Diverse physiologic and pathophysiologic influences alter TWA magnitude in parallel with their effects on vulnerability to ventricular tachyarrhythmias. Specifically, interventions that impede intracellular calcium handling, such as elevated heart rate, heightened adrenergic activity, myocardial ischemia, and heart failure, predispose to greater levels of TWA, reflecting heightened risk for arrhythmias. Conversely, vagus nerve stimulation, blockade of beta-adrenergic receptors and late sodium and L-type calcium channels, and sympathetic denervation decrease TWA magnitude, reflecting the potential of these interventions to reduce risk for ventricular tachycardia and fibrillation. TWA thus appears able to detect the influence of pathophysiologically relevant triggers as well as the efficacy of antiarrhythmic drugs without reducing the predictive capacity of the phenomenon.
Beth Israel Deaconess Medical Center, Division of Cardiovascular Medicine, Boston, MA, USA. Electronic address: rverrier@bidmc.harvard.edu.
Richard L
RL
Verrier
Marek
M
Malik
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D053840:Brugada Syndrome; D000075224:Cardiac Conduction System Disease; D002317:Cardiovascular Agents / Q000494:pharmacology*; D006329:Heart Conduction System / Q000002:abnormalities* / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular
D002317:Cardiovascular Agents
Arrhythmia trigger; Heterogeneity of repolarization; T-wave alternans