Sustained Monomorphic Ventricular Tachycardia

Abstract

The clinical significance, evaluation and management, and pathophysiology of sustained monomorphic ventricular tachycardia (VT) is very much dependent upon the presence or absence and type of underlying organic heart disease [1]. Sustained monomorphic VT usually occurs in the presence of organic heart disease, most often ischemic heart disease with prior myocardial infarction in this country, although almost any type of organic heart disease can be associated with sustained monomorphic VT. In patients with ischemic heart disease, Buxton et al. [2] recently evaluated the role of clinical variables to predict inducible sustained VT in patients with coronary artery disease and clinical nonsustained VT. Although the number of variables was significantly associated with inducible VT, they had limited utility to guide clinical decisions regarding the use of electrophysiologic testing. In patients with acute myocardial infarction treated with lytic therapy, VT alone or VT with VF early ( two days) after myocardial infarction conferred a negative impact on one year mortality [3]. Additional research in patients with ischemic heart disease has demonstrated that sustained monomorphic VT is unusual in the recovery period following coronary artery bypass surgery but a recent study has demonstrated that the placement of a bypass graft across a noncollateralized totally occluded vessel supplying an infarct zone was associated with the development of VT [4]. Several recent studies have highlighted the importance of bundle branch reentrant VT in patients with or without organic heart disease. Five of six patients with myotonic dystrophy had no apparent organic heart disease and bundle branch reentrant VT was presumably related to the known frequent involvement of the conduction system in patients with myotonic dystrophy [5]. Although bundle branch reentrant VT most often does occur in patients with organic heart disease, it has previously been reported in patients with His-Purkinje system disease in the absence of identifiable organic heart disease [6]. Of 31 patients with sustained monomorphic VT after valve surgery, the mechanism of VT was bundle branch reentrant in 9, myocardial reentry in 20 and both in 2 patients [7]. Bundle branch reentrant VT occurred much earlier after surgery (median 10 days compared to 72 months) compared to myocardial VT and 40% of patients with bundle branch reentrant VT had normal left ventricular function suggesting that post-operative conduction system abnormalities alone may create the appropriate electrophysiologic milieu for the development of bundle branch reentrant VT. In these patients with bundle branch reentrant VT, 40% had right bundle branch block morphology VT, which is generally much less common than left bundle branch block morphology.