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Discusses the mechanism and frequency of sustained monomorphic ventricular tachycardia in patients with nonischemic dilated cardiomyopathy compared to ischemic cardiomyopathy.
S ustained 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.
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Stevenson et al. (2011) studied this question.
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