Abstract
Abstract 4669: Does Long-QT Syndrome Involve the Sinus Node?
Circulation (New York, N.Y.), Vol.118(suppl_18)
10/28/2008
DOI: 10.1161/circ.118.suppl_18.S_928-b
Abstract
Background:
The hallmark of Long QT Syndrome (LQTS) is a prolongation of the ventricular electrical action potential caused by mutations involving key cardiac ion channels on the surface membrane of ventricular myocytes. Different mutations are associated with specific modes of arrhythmia initiation and distinct changes in cardiac rhythm prior to these events. We hypothesized that some LQTS-causing mutations might involve the sinus node, leading to aberrations in cardiac rhythm. To test this hypothesis, we examined the features of cardiac rhythm in 23 genotyped patients with LQTS and 14 matched controls (C) using Holter ECG data (6hrs).
Methods:
QRS-complexes were identified using custom software and verified by an experienced ECG reader; series of sinus beats were extracted and gaps in time series were linearly interpolated. The mean, max, and min heart rate (HR), the time (SD, SDNN, SDANN, RMSSD, pNN50) and frequency-domain (Total (TP), Very low (VLF), Low (LF), High (HF) frequency powers, and LF/HF) indices of heart rate variability (HRV) were calculated in each 5-min interval and over the entire recording. The short-long-short irregularity was examined using the novel multiscale rhythmogenetic analysis (MRA), which quantifies changes in the HRV indices during the transition from one time-scale window to another.
Results:
The maximum heart rate was slower in LQTS than in C (101±13 and 119±19bpm, p=0.001). The high-frequency power (HF) was lower in LQTS than in C (80±76 and 113±58ms
2
, p<0.05). However, the short-term irregularity (quantified by the difference in RMSSD between the 75ms and 2000ms time scales) was 4 times greater in LQTS compared to C (p=0.003). Inclusion or exclusion of two patents who were on β-blockers did not change the results.
Conclusions:
LQTS is associated with specific changes in cardiac rhythm, including:
diminished acceleration capacity,
decreased high-frequency power, and
enhanced short-long-short irregularity.
This suggests that LQTS involves channel modifications in the sinus node, which might contribute to arrhythmogenesis. Rhythm characterization in genetic sub-types of LQTS might improve arrhythmia risk stratification in this heterogeneous patient population.
Details
- Title: Subtitle
- Abstract 4669: Does Long-QT Syndrome Involve the Sinus Node?
- Creators
- Vladimir Shusterman - University of PittsburghJan Nemec - University of PittsburghMarie Buncova - IKEM, Prague, Czech RepublicBruce Winter - Mayo Clinic, Rochester, MNWin-Kuang Shen - Mayo Clinic, Rochester, MNMichael J Ackerman - Mayo Clinic, Rochester, MN
- Resource Type
- Abstract
- Publication Details
- Circulation (New York, N.Y.), Vol.118(suppl_18)
- DOI
- 10.1161/circ.118.suppl_18.S_928-b
- ISSN
- 0009-7322
- eISSN
- 1524-4539
- Language
- English
- Date published
- 10/28/2008
- Academic Unit
- Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984363460302771
Metrics
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