Body surface distribution of T wave alternans is modulated by heart rate and ventricular activation sequence in patients with cardiomyopathy

Fig 1. TWAmax is compared between clinical leads and body torso for atrial (A) and atrioventricular pacing (B). TWAmax is consistently greater when body torso is sampled vs. clinical leads, regardless of the pacing mode or rate. + indicates outliers.

Fig 2. TWAmax is compared between atrial and atrioventricular pacing for clinical leads (A) and body torso (B). TWAmax is similar between atrial and atrioventricular pacing, regardless of clinical leads or body torso sampling. + indicates outliers.

Fig 3. Body torso distribution of TWAmax during atrial and atrioventricular pacing. The body torso was divided into 6 regions (A). R1 indicates the location of the standard precordial leads, V1-V6. R6 is the posterior chest. With increasing atrial pacing rate, TWAmax shifted from R4 to R5 (B). With increasing atrioventricular pacing rate, TWAmax relocated from R5 to R2 (C).

Fig 4. Body torso maps of Valt (uV) in one patient during atrial and atrioventricular pacing. The anterior torso with V1-V6 is indicated by the bold circles and the V symbol depicts the sternal notch. The posterior torso is not shown for simplicity as there is virtually no TWA signal. With atrial pacing (A), TWA is detected outside the clinical leads at 100 and 110 bpm. This patient would be classified as clinically–TWA using clinical leads, but +TWA with body torso mapping (i.e. false negative). With atrioventricular pacing (B), TWA is detected in body torso as well as clinical leads at 110, but not 100 bpm. Thus atrioventricular pacing would classify this patient as clinically +TWA using clinical leads, while atrial pacing resulted in a clinically negative test (i.e. false negative).

Fig 5. Body torso maps of Valt (uV) in one patient during atrial and atrioventricular pacing. With atrial pacing (A), TWA is detected in body torso as well as clinical leads only at 110 bpm. With atrioventricular pacing (B), TWA is no longer detected in clinical leads, but remains detectible in body torso. Using clinical leads alone, this patient would be classified as clinically +TWA, but -TWA with atrioventricular pacing.

Fig 6. Body torso maps of Valt (uV) in one patient during atrial and atrioventricular pacing. With atrial pacing (A), TWA is detected in body torso as well as clinical leads at 110 bpm. However, TWA is no longer detected in clinical leads at 120 bpm, but still evident in body torso leads below the clinical leads. Using clinical leads alone, the clinical TWA classification would still remain positive because pacing rates above 110 bpm are not considered. With atrioventricular pacing (B), TWA is no longer detectible in the clinical leads at 110 or 120 bpm, but still present in the body torso. Although this patient would still be classified as clinically +TWA based on atrial pacing 110 bpm alone, changes in pacing rate or mode have altered the body surface distribution of TWA.

Fig 7. Illustration of TWA magnitude attenuation (lower panel) associated with increasing atrioventricular pacing rate (upper panel) in a precordial lead of a representative patient. The TWA magnitude decreases by ~1.5 uV with each subsequent 10 bpm increase in rate, causing TWA magnitude to fall below clinical significance at 120 bpm. The red shaded regions indicate Valt values with a k ≥3. The dotted black line denotes the clinical TWA Valt cutpoint of 1.9 uV.

Fig 8. (A) ECG depicting a premature ventricular ectopic beat during atrioventricular pacing at 110 bpm in a precordial lead of a representative patient. (B) Illustration of TWA nullification (lower panel) associated with the region surrounding the ectopic beat (upper panel) and the attenuation of TWA magnitude post ectopic. The red shaded regions indicate Valt values with a k ≥3.