Dorsal vagal nucleus involvement relates to QTc‐prolongation after acute medullary infarction

Abstract

Background Infarction of the medulla has been associated with prolongation of the QTc, severe arrhythmia, and sudden cardiac death, yet the precise anatomical substrate remains uncertain. Aims We sought to determine the possible anatomical structures relating to QTc‐prolongation in patients with acute medullary infarction. Methods We included 12 subjects with acute ischemic medullary infarction on brain MRI, who presented within 4.5 h from the last known well time, with a 90‐day follow‐up. For an unbiased lesion analysis, medullary infarcts were manually outlined on diffusion weighted MRI and co‐registered with an anatomical atlas. Results Nine out of 12 had QTc‐prolongation. Qualitative and semi‐quantitative comparisons were made between infarct location and QTc‐prolongation. Among patients with QTc‐prolongation, the greatest degree of congruence of the infarct location was over the dorsal vagal nucleus (DVN, 8 out of 9). There was a significant correlation between the number of sections showing infarction of the DVN and presence of QTc‐prolongation (r = .582, p = .047). Among patients without QTc‐prolongation, the maximum lesion overlap included the medial aspect of the gigantocelluar reticular nucleus of the reticular formation. Conclusion We found that the DVN is a key anatomical substrate related to QTc‐prolongation. Further studies with more patients and high‐resolution, volumetric MRI are needed to confirm our findings.

Prolonged ventricular repolarization associated with mild cognitive impairment and white matter hyperintensities: a cross-sectional study

“…Fourth, altered ECG parameters may be related to autonomic dysfunction, which was common in patients with MCI 27 . Previous research reported a correlation between QT prolongation and dorsal vagal nucleus infarction 28 , which might affect the parasympathetic pathway and dysregulate the automatic neural control of cardiac function 29 . This indicates that prolonged ventricular repolarization may be cerebrogenic arrhythmia.…”

Single-nuclei transcriptome of brain-dead donor heart with long QT syndrome revealed neuronal modulation of cardiac immunity

“…al. suggested that long QT syndrome (LQTS, de ned by QT interval >500 milliseconds) in the donor heart was associated with accelerated development of cardiac allograft vasculopathy (CAV), a broproliferative disease causing intimal thickening of coronary vasculature in transplanted heart [16][17][18] . However the underlying molecular changes of LQTS donor myocardial and the molecular mechanisms contributing towards accelerated CAV post-transplant was not elucidated 3,19 .…”