Dear Editor, We read with interest the study by Robles et al. examining intermittent ventricular pre-excitation in patients with Wolff-Parkinson-White syndrome (1). This registry contributes valuable data to an underexplored area, however, we have observed methodological concerns that constrain the clinical applicability of their findings. First, the study’s most significant limitation lies in the imbalance between symptomatic and asymptomatic patients within the intermittent pre-excitation group. With only 9 asymptomatic patients among 79 with intermittent pre-excitation, the statistical power to detect meaningful differences is compromised (1). This sample size cannot reliably exclude clinically important differences in electrophysiological parameters between symptomatic and asymptomatic intermittent patients, rendering the study’s conclusions about risk equivalence statistically unsupported. Power calculations would likely require 50-100 asymptomatic patients per group to detect moderate effect sizes in accessory pathway properties (2). Second, the heterogeneous use of isoproterenol across centers, along with varying sedation practices and equipment preferences creates systematic variability that could obscure the true differences between groups (1). Isoproterenol is a powerful heart stimulant that can make accessory pathways conduct electricity faster and trigger arrhythmias more easily than would occur naturally in patients’ daily lives (3). Studies comparing provoked versus baseline electrophysiological parameters show that catecholamine stimulation can dramatically alter pathway characteristics, potentially masking important differences between intermittent and persistent pre-excitation groups (4). Third, the definition used for symptomatic patients in this study as those reporting palpitations regardless of documented arrhythmias, accounts for another methodological weakness. This broad categorization does not distinguish between patients with confirmed tachyarrhythmias and those with non-specific symptoms, potentially misclassifying patients and obscuring true risk differences (1). Considering that symptom perception can be influenced by awareness of the cardiac condition, this classification bias could systematically inflate the apparent similarity between groups. Finally, the study’s international, retrospective, multicenter design introduces selection bias and heterogeneity in patient populations, referral practices and electrophysiological techniques. The unmeasured confounders could account for the observed similarities between groups given the relatively small effect sizes being studied. The 20-year data collection period spans through evolutions in clinical practice, diagnostic criteria and risk assessment approaches and this introduces temporal bias which could confound contemporary relevance. Exclusion of patients with central sleep apnea or inadequate monitoring may also have systematically excluded important subgroups. Future studies should prioritize standardized protocols, adequate sample sizes and prospective data collection to address these limitations. In conclusion, the study’s deduction that intermittent pre-excitation requires invasive assessment does align with evolving clinical evidence which suggests that non-invasive risk stratification has limited negative predictive value in excluding high-risk pathways. However, we believe this recommendation should be based on the established limitations of non-invasive testing rather than the equivalence of risk parameters demonstrated in this study.