Key result
Exercise testing reveals greater ventricular activation heterogeneity in idiopathic VF survivors versus other groups.
Why the study?
Idiopathic VF is a diagnosis of exclusion after normal cardiac investigations, and it was unknown whether exercise-induced electrical substrate changes could distinguish different ventricular arrhythmic conditions and identify VF susceptibility.
Does noninvasive mapping of ventricular conduction stability during exercise identify an arrhythmic substrate in survivors of idiopathic ventricular fibrillation?
Observational (n=46)
Does noninvasive mapping of ventricular conduction stability during exercise identify an arrhythmic substrate in survivors of idiopathic ventricular fibrillation?
Noninvasive mapping of ventricular conduction stability during exercise reveals increased activation heterogeneity in idiopathic VF survivors, identifying a previously silent arrhythmic substrate.
May support noninvasive detection of arrhythmic substrate in idiopathic VF; leaves open prospective validation before clinical use.
Background Idiopathic ventricular fibrillation (VF) is a diagnosis of exclusion following normal cardiac investigations. We sought to determine if exercise‐induced changes in electrical substrate could distinguish patient groups with various ventricular arrhythmic pathophysiological conditions and identify patients susceptible to VF. Methods and Results Computed tomography and exercise testing in patients wearing a 252‐electrode vest were combined to determine ventricular conduction stability between rest and peak exercise, as previously described. Using ventricular conduction stability, conduction heterogeneity in idiopathic VF survivors (n=14) was compared with those surviving VF during acute ischemia with preserved ventricular function following full revascularization (n=10), patients with benign ventricular ectopy (n=11), and patients with normal hearts, no arrhythmic history, and negative Ajmaline challenge during Brugada family screening (Brugada syndrome relatives; n=11). Activation patterns in normal subjects (Brugada syndrome relatives) are preserved following exercise, with mean ventricular conduction stability of 99.2±0.9%. Increased heterogeneity of activation occurred in the idiopathic VF survivors (ventricular conduction stability: 96.9±2.3%) compared with the other groups combined (versus 98.8±1.6%; P =0.001). All groups demonstrated periodic variation in activation heterogeneity (frequency, 0.3–1 Hz), but magnitude was greater in idiopathic VF survivors than Brugada syndrome relatives or patients with ventricular ectopy (7.6±4.1%, 2.9±2.9%, and 2.8±1.2%, respectively). The cause of this periodicity is unknown and was not replicable by introducing exercise‐induced noise at comparable frequencies. Conclusions In normal subjects, ventricular activation patterns change little with exercise. In contrast, patients with susceptibility to VF experience activation heterogeneity following exercise that requires further investigation as a testable manifestation of underlying myocardial abnormalities otherwise silent during routine testing.
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Chow et al. (2023) conducted an observational in Idiopathic ventricular fibrillation (n=46). Exercise testing with 252-electrode vest vs. Other groups combined (ischemia VF, benign ectopy, normal hearts) was evaluated on Ventricular conduction stability between rest and peak exercise (p=0.001). Exercise-induced ventricular conduction stability assessment revealed increased activation heterogeneity in idiopathic VF survivors (96.9±2.3%) compared with other groups combined (98.8±1.6%; P=0.001).
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