A surgical option for ventricular tachycardia caused by nonischemic cardiomyopathy.
نویسندگان
چکیده
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.4
منابع مشابه
Perivalvular fibrosis and monomorphic ventricular tachycardia: toward a unifying hypothesis in nonischemic cardiomyopathy.
The basis for arrhythmogenesis in patients with nonischemic cardiomyopathy and ventricular tachycardia (VT) needs further elucidation. Cardiac arrest and/or nonsustained VT are common arrhythmia presentations in the setting of nonischemic cardiomyopathy, with sustained monomorphic VT being relatively uncommon.1,2 Importantly, bundlebranch reentrant VT is identified as the VT mechanism in a sign...
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ورودعنوان ژورنال:
- Circulation. Arrhythmia and electrophysiology
دوره 4 4 شماره
صفحات -
تاریخ انتشار 2011