A Surgical Option for Ventricular Tachycardia Caused by Nonischemic Cardiomyopathy

Sustained monomorphic ventricular tachycardia (VT) in patients with heart disease is usually due to reentry involving a region of myocardial scar. Most commonly, the scar is due to prior myocardial infarction and associated with significantly depressed left ventricular function. Scars create a very stable substrate for VT, such that up to 70% of patients who present with sustained monomorphic VT late after myocardial infarction will have another episode within the next 2 years.1,2 Scars also occur in patients with nonischemic dilated cardiomyopathies (NICM) but are generally small, averaging less than 4% of the ventricular myocardium in one study using MRI.3 Replacement fibrosis is a likely mechanism. Consistent with the less frequent and smaller areas of confluent scar in nonischemic cardiomyopathies, sustained monomorphic VT is relatively infrequent. In patients with depressed left ventricular function who received an implantable cardioverter-defibrillator (ICD) for primary prevention, 15% had spontaneous VT or ventricular fibrillation detected by the ICD during a follow-up of 29 months, and approximately half of these arrhythmias were monomorphic VT.4Article see p 494Because large scars are not common in NICM, the possibility of bundle-branch reentry, which may occur without large scars, is an important consideration when sustained VT is encountered but accounts for fewer than 10% of VTs in this patient population.5 It has become increasingly clear that ventricular scars are a major factor causing sustained monomorphic VT in patients with NICM.6,7 Of patients who have recurrent episodes of VT, who are considered for catheter ablation, the vast majority have evidence of ventricular scars, based on voltage mapping or late Gd enhancement (LGE) on MRI.8 …