Adenosine-Sensitive Ventricular Tachycardia: Right Ventricular Abnormalities by
Adenosine-Sensitive Ventricular Tachycardia: Right Ventricular Abnormalities by MRI
ABSTRACT & COMMENTARY
Synopsis: Minor structural abnormalities can be commonly identified in patients with adenosine-sensitive VT, but, based on present information, they were unable to define a relationship between these abnormalities and the patient’s arrhythmia.
Source: Markowitz SM, et al. Circulation 1997;96: 1192-1200.
Markowitz and colleagues performed mag- netic resonance imaging (MRI) in 14 patients with a sustained ventricular tachycardia (VT) that was shown at electrophysiologic study to be sensitive to adenosine. Previous work from Markowitz et al and others has suggested that this particular form of ventricular tachycardia is due to catecholamine-mediated triggered activity. Most patients with this arrhythmia in prior reports have been described as having no identifiable structural heart disease. The 14 patients in this study presented clinically with either sustained monomorphic VT, repetitive bursts of nonsustained monomorphic VT, or both. All manifest sustained VT during electrophysiologic study in response to isoproterenol infusion and/or programmed stimulation. In 11 of the 14 patients, the VT had the left bundle branch block inferior axis QRS morphology most commonly described for this arrhythmia, but VT in two patients had a right bundle branch block QRS morphology. One patient had two VT morphologies. In all patients, termination of VT was reproducibly demonstrated in response to adenosine infusion. Twelve of the 14 patients underwent catheter ablation. The ablation sites were in the right ventricular outflow tract (8 patients), the right ventricular apex (1 patient), and the left ventricle (3 patients). The remaining two patients did not undergo ablation, but mapping identified a probable site of origin in the right ventricular outflow tract. Other tests for structural heart disease including two dimensional echocardiograms (14 patients), signal averaged electrocardiograms (9 patients), and cardiac catheterization (7 patients) were either normal or showed only minor abnormalities. MRI images were obtained at variable times ranging from just before to five years after the patient’s electrophysiologic study.
Ten of the 14 patients demonstrated abnormal findings on the MRI images. Abnormal findings included thinning of the right ventricular free wall in six patients, fatty infiltration of the RV in four patients, and focal hypokinesis in four patients. Four patients had multiple abnormalities. Interestingly, only three patients had abnormal MRI findings in the right ventricular outflow tract, and there was no apparent correlation between the location of the MRI abnormalities and the site of VT origin identified by intracardiac mapping. Abnormal findings were seen in seven of the 11 patients who had their MRI after an ablation procedure and in all three patients who either did not undergo ablation or had their scan before the procedure. Markowitz et al conclude that minor structural abnormalities can be commonly identified in patients with adenosine-sensitive VT, but, based on present information, they were unable to define a relationship between these abnormalities and the patient’s arrhythmia.
COMMENT BY JOHN P. DiMARCO, MD, PhD
A number of different types of so-called "idiopathic" VT have been described. Adenosine-sensitive VT usually but not always has a site of origin in the right ventricular outflow tract and manifests electrophysiologic characteristics most consistent with a mechanism of triggered automaticity. The postulated cellular mechanism has been that beta adrenergic stimulation increases intracellular cyclic AMP generation, which results in increased intracellular calcium and delayed afterdepolarizations (DADs). Adenosine, by inhibiting cyclic AMP production, blocks the development of the DADs and terminates the arrhythmia. Because of this dependence on adrenergic stimulation and the usual absence of anatomic abnormalities, most prior speculation about the cause of the arrhythmia has involved changes in either the innervation of the right ventricular outflow tract or the sensitivity of the cells themselves. This paper raises significant questions about the validity of these hypotheses.
Focal thinning and fatty infiltration have been long considered to be characteristic findings for another form of right ventricular tachycardia (seen in patients with arrhythmogenic right ventricular dysplasia [ARVD]). The electrophysiologic characteristics of the tachycardia in the latter group are much different than those in patients with adenosine-sensitive VT. In patients with ARVD, VT does not typically respond to adenosine or verapamil; extrastimuli, in contrast to rapid pacing, are more effective for initiating VT; and entrainment, a finding of reentry, can usually be demonstrated. The observations in this paper suggest that there may not be as definite a difference in the etiology of the two syndromes as has previously been thought. In patients with adenosine-sensitive VT, the structural changes described in this report are minor, but it might be speculated that enough tissue change occurs to permit catecholamine stimulation to cause VT. In patients with ARVD, structural changes are prominent and are associated with enough scarring to permit large reentrant circuits to become established. If the results of this are confirmed by others, the paradox of VT in a normal heart may be resolved by the finding that the heart was not quite so normal after all.
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