Very Low QRS Voltage in Single Frontal Lead Predicts Recurrence of Neurally Mediated Syncope
Key findings
- In a prospective study of 205 patients suspected of neurally mediated syncope (formerly called vasovagal syncope), 45% had very low QRS voltage (=0.3 mV) in one frontal plane lead
- Isolated very low QRS voltage was associated with a threefold increased risk of syncope recurrence, independent of any history of presyncope or syncope and independent of left ventricular end-diastolic diameter
- Isolated very low QRS voltage in the frontal leads may reflect abnormalities in ventricular geometry and electrical activation
- This phenomenon may help generate new prognostic tools and insights into the pathogenesis of neurally mediated syncope
Jeremy N. Ruskin, MD, founder and director emeritus of the Telemachus & Irene Demoulas Family Foundation Center for Cardiac Arrhythmias at the Corrigan Minehan Heart Center at Massachusetts General Hospital, Dan Blendea, MD, PhD, FHRS, and colleagues have observed an interesting phenomenon. Some patients with neurally mediated syncope have a QRS complex of very low voltage in just one frontal lead on 12-lead electrocardiography (ECG).
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In a prospective study, they found that this ECG finding predicts recurrence of syncope independently of clinical risk factors. Their report appears in Heart Rhythm.
Diagnostic Testing
The study involved 205 consecutive patients with suspected neurally mediated syncope (NMS) who had a tilt table test as part of their diagnostic evaluation. The test was positive in 87 patients (42%).
Twelve-lead resting ECG was performed within three days of the tilt table test. The results were reviewed by a single investigator, in a blinded fashion, on two occasions, four weeks apart. For QRS amplitude, ≤0.3 mV proved to be the best cutoff for very low voltage.
ECG Findings
Very low voltage (≤0.3 mV) in one frontal plane lead was present in 92 patients (45%).
- In most of those patients (55%), the lead that displayed very low voltage was aVL
- Other leads that displayed very low voltage were aVF (14% of patients), lead I (14%), lead III (12%), lead II (4%) and aVR (1%)
Recurrence of Syncope
All patients visited the clinic every three to six months, and the median follow-up period was 14 months (range, 3–70 months). During that period, 60 patients experienced recurrence of syncope. The actuarial recurrence rate was 22% at one year and 38% at two years.
Patients with syncope recurrence had a higher prevalence of history of presyncope, a significantly higher chance of a positive tilt table test and smaller left ventricular (LV) end-diastolic and end-systolic dimensions, compared with those who had no recurrence.
Predictors of Syncope Recurrence
On multivariate analysis, very low voltage in one frontal lead predicted a threefold increased risk of syncope recurrence (RR, 3.02; 95% CI, 1.67–5.45; P < .001). The increase was independent of any history of presyncope or syncope and independent of the LV end-diastolic diameter during the follow-up period.
A history of >3 syncopal episodes predicted recurrence of syncope in a bivariate analysis that included a history of presyncope. However, it did not retain predictive value when included in a multivariate model together with very low voltage in frontal leads.
Clues for Better Prognostication
The isolated very-low-amplitude QRS complexes found in this study don't fit the typical criteria for low voltage because they were not present in all frontal leads. There is no clear explanation for this finding.
In all patients, the lead with very low voltage was nearly perpendicular to the QRS axis. Opposing LV walls may be in closer proximity in patients with neurally mediated syncope because of ventricular underfilling and the smaller ventricular dimensions found in this syndrome. This could result in greater cancellation of forces along an axis that is perpendicular to the long axis of the ventricle, resulting in low voltage in some frontal leads and not others.
Further investigation of this phenomenon may help generate new prognostic tools and insights into the pathogenesis of neurally mediated syncope.
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