Abstract P130: QTc Prolongation in Acute Medullary Infarction Maps to the Dorsal Vagal Nucleus

Abstract

Objective: To determine the spatial relationship between acute medullary infarction and QTc prolongation. Background: Ischemic stroke has been associated with QTc-prolongation which increases the risk of cardiac arrhythmia and sudden cardiac death. In particular, pathological arrhythmia and unexpected sudden cardiac death has been described after acute medullary infarction (AMI). Nevertheless, it is not well understood why only as subset of patients with AMI develop significant cardiac arrhythmia. To gain insight into this issue, we sought to determine the possible anatomical structures relating to QTc-prolongation in patients. Methods: We retrospectively reviewed 1072 consecutive adult patients admitted for an acute ischemic stroke or a transient ischemic attack, who presented within 4.5 hours from the last known well time and had an admission ECG available. 724 patients had brain MRIs and among these, 13 (1.8 %) patients had an AMI and were included. For an unbiased lesion analyses, medullary infarcts were manually outlined on diffusion weighted MRI and manually co-registered with an anatomical atlas. Infarct lesions were then superimposed on each other as stratified by normal versus prolonged (men > 430 ms, women > 450 ms) QTc to determine the area of greatest degree of congruence. Results: 76.9 % of patients (10 out of 13, 9 men and 1 woman) had a prolonged QTc (476.9 ± 43.3 ms for men, 515 ms for women). There was no significant difference in electrolyte levels and preexisting comorbidities between subjects with normal and prolonged QTc. Among patients with QTc prolongation, the greatest degree of congruence of the infarct location was the dorsal vagal nucleus (DVN, 7 out of 10 patients). Conclusions: Our unbiased lesion segmentation approach identified the DVN a key anatomical substrate related to QTc-prolongation. Biological plausibility of our data and the presence of a causal link between the DVN and cardiac arrhythmia stems from the prior animal experimental data showing that selectively silencing the DVN via a pharmacogenetic approach caused QTc-prolongation in the rat. Further studies with more patients and high-resolution, volumetric MRI are needed to confirm our findings.