@entity943 remain a major cause of late mortality following @entity583 . They arise due to @entity82 within the @entity1188 , which creates the conditions of slow conduction necessary for re-entry. In individual @entity1 who have already manifested a malignant @entity943 , antiarrhythmic drug therapy, guided by invasive electrophysiological testing, is of proven benefit in prolonging survival. By contrast, when used on a population basis, antiarrhythmic drug therapy has proved singularly ineffective. This is illustrated by the recent @entity943 Suppression Trial (CAST) study--far from improving survival, antiarrhythmic therapy increased mortality. The use of antiarrhythmic drugs on a population basis is therefore fundamentally flawed. Hemodynamic intervention provides an alternative strategy in @entity943 prevention. Hemodynamic changes may influence electrophysiological parameters and arrhythmogenesis in a number of ways. First, myocardial stretch may contribute to arrhythmogenesis through contraction-excitation feedback. Second, hemodynamic changes can influence ventricular remodeling following @entity1188 , which may be an important determinant of subsequent arrhythmogenesis. Hemodynamic intervention, therefore, represents a promising new approach to @entity943 prevention following @entity583 .

Antiarrhythmic therapy and survival following XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity1188 :: ('MESH:D007238', 'Disease') :: ['infarct', 'infarction'] @entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarction'] @entity943 :: ('MESH:D001145', 'Disease') :: ['Arrhythmias', 'arrhythmia', 'Cardiac Arrhythmia']
@entity583 :: (MESH:D009203,Disease) :: ['myocardial infarction']
