Abstract
BackgroundT wave alternans (TWA) is an electrocardiographic marker of heightened sudden death risk from ventricular tachyarrhythmias in patients with cardiomyopathy. TWA is evaluated from the 12-lead electrocardiogram, Frank lead, or Holter lead recordings, however these clinical lead configurations will not record TWA from adjacent regions of the body torso.ObjectiveWe tested the hypothesis that changing heart rate or ventricular activation may alter the body surface distribution of TWA such that the clinical ECG leads fail to detect TWA in some patients; thereby producing a false-negative test.MethodsIn 28 cardiomyopathy patients (left ventricular ejection fraction 28±6%), 114 unipolar electrograms were recorded across the body torso during incremental atrial pacing, followed by atrioventricular pacing at 100, 110 and 120bpm. TWA was measured from each unipolar electrogram using the spectral method. A clinically positive TWA test was defined as TWA magnitude (Valt) ≥1.9 uV with k ≥3 at ≤110bpm.ResultsMaximum Valt (TWAmax) was greater from the body torso than clinical leads during atrial (p<0.005) and atrioventricular pacing (p<0.005). TWAmax was most prevalent in the right lower chest with atrial pacing 100 bpm and shifted to the left lower chest at 120 bpm. TWAmax was most prevalent in left lower chest with atrioventricular pacing at 100 bpm and shifted to the left upper chest at 120 bpm. Using the body torso as a gold standard, the false-negative rate for clinically positive TWA with clinical leads was 21% during atrial and 11% during atrioventricular pacing. Due to TWA signal migration outside the clinical leads, clinically positive TWA became false-negative when pacing mode was switched (atrial→atrioventricular pacing) in 21% of patients.ConclusionsThe body surface distribution of TWA is modulated by heart rate and the sequence of ventricular activation in patients with cardiomyopathy, which can give rise to modest false-negative TWA signal detection using standard clinical leads.
Highlights
Body surface microvolt T wave alternans (TWA) arises from beat-to-beat action potential alternans, and can presage ventricular tachyarrhythmias by increasing repolarization dispersion with subsequent conduction block and re-entry [1]
The body surface distribution of TWA is modulated by heart rate and the sequence of ventricular activation in patients with cardiomyopathy, which can give rise to modest false-negative TWA signal detection using standard clinical leads
In patients with moderate to severe left ventricular dysfunction, TWA magnitude measured from Holter recordings and implantable cardioverter defibrillator (ICD) electrograms increases before ventricular tachyarrhythmias [2,3]
Summary
Body surface microvolt T wave alternans (TWA) arises from beat-to-beat action potential alternans, and can presage ventricular tachyarrhythmias by increasing repolarization dispersion with subsequent conduction block and re-entry [1]. Several prospective clinical studies have shown a high negative predictive value (~97%/year) for sudden cardiac death with TWA testing in patients with cardiomyopathy [4] , while other studies [5,6] found no difference in adverse events between positive vs negative TWA patients, and a lower negative predictive accuracy of 93%/year In these clinical studies, TWA testing was performed during exercise or pacing to increase heart rates up to 110 bpm, and TWA was evaluated from a localized region of the body torso transcribed by the 12-lead ECG and Frank lead configuration [7,8]. TWA is evaluated from the 12-lead electrocardiogram, Frank lead, or Holter lead recordings, these clinical lead configurations will not record TWA from adjacent regions of the body torso
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