Why the study?
Do MRI and SAECG detect early or localized forms of ARVD in patients with RMVT and otherwise normal ECG?
Do MRI and SAECG detect early or localized forms of ARVD in patients with RMVT and otherwise normal ECG?
Normal MRI and SAECG findings in the vast majority of patients with RMVT and normal ECG suggest that early or localized ARVD is not the primary arrhythmogenic substrate in this population.
Answers are grounded in this paper and cite their sources.
Normal MRI/SAECG in most RMVT patients with normal ECG supports early ARVD as unlikely substrate; hypothesis-generating and requires prospective validation.
Early or localized forms of arrhythmogenic right ventricular dysplasia (ARVD) have been proposed as the arrhythmogenic substrate of repetitive monomorphic ventricular tachycardia (RMVT) originating in the right ventricular outflow tract in patients without any underlying cardiac abnormality on clinical examination and echocardiography. To further examine this hypothesis, magnetic resonance imaging (MRI) and signal-averaged electrocardiography (SAECG) were performed on 23 patients with RMVT and normal 12-lead standard ECG of conducted sinus beats. MRI was performed using ECG-gated turbo spin-echo images of the heart in order to detect signs of early or localized forms of ARVD, such as localized wall thickness reductions, signal intensity increase indicating adipose tissue infiltrates, and regional bulgings or aneurysms. MRI was normal in 22 (96%) of 23 study patients. In the remaining patient (4%), MRI demonstrated signal intensity increase in the intraventricular septum but not in the right ventricular outflow tract. Time-domain analysis of the SAECG was normal in 21 (91%) of 23 patients and revealed ventricular late potentials in 2 study patients (9%). Frequency-domain analysis of the SAECG was normal in 22 (96%) of 23 patients and revealed ventricular late potentials in one study patient (4%). We conclude that normal MRI findings of the heart and absence of ventricular late potentials in the SAECG in most patients with RMVT and otherwise normal ECG do not support the hypothesis that early or localized forms of ARVD create the arrhythmogenic substrate in the majority of these patients.
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Grimm et al. (1997) studied this question.
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