Comment on “The Relationship Between Tumor Size and Electrocardiographic Findings in Carotid Body Paragangliomas: A Retrospective Observational Study”

Dear Editor,

We read with great interest the study by Baki et al investigating the association between carotid body tumor (CBT) size and electrocardiographic changes, particularly corrected QT interval (QTc) prolongation. ¹ The authors present an intriguing correlation suggesting that tumor burden may modulate autonomic cardiac regulation. While this observation adds novelty to the field of head and neck paragangliomas, several methodological and interpretative issues require closer consideration before firm clinical inferences can be drawn.

First, the retrospective design and very limited cohort of 21 patients present challenges for robust inference. Although a statistically strong correlation (r = .94) was reported, the small sample size markedly increases the risk of model instability, exaggerated effect sizes, and type I error. ² A correlation coefficient of this magnitude in a biological context is unusual and may reflect overfitting. Future prospective studies with larger sample sizes and power calculations are essential to confirm whether the observed effect is reproducible and clinically meaningful.

Second, QTc measurement was performed using Bazett’s correction, which is known to overestimate QTc at higher heart rates and underestimate it at lower ones. ³ Given the potential confounding influence of autonomic variation on both RR interval and QT duration, reliance on Bazett’s formula may have distorted the association. ⁴ Alternative correction methods (eg, Fridericia and Framingham) or direct QT/RR regression modeling would provide a more reliable assessment of repolarization in this context. ⁵

Third, the exclusion of patients with comorbidities or medications affecting cardiac conduction, while methodologically intended to reduce confounding, may limit generalizability. In real-world surgical populations, patients frequently present with hypertension, diabetes, or pharmacologic exposures that influence QT dynamics. ⁶ The current sample, therefore, represents a highly selected subgroup, which reduces the external validity of proposing QTc as a perioperative risk marker.

Fourth, the authors hypothesize vagal hyperactivity as the mechanism linking tumor size to QTc prolongation. However, no direct measures of autonomic tone (eg, heart rate variability and baroreflex sensitivity) were included. Without physiological corroboration, attributing causality to vagal pathways remains speculative. Incorporating mechanistic assessments, or at minimum perioperative outcome correlations, would strengthen the biological plausibility of QTc as a surrogate marker.

Finally, although the study suggests perioperative relevance, no data were presented regarding arrhythmic events, hemodynamic instability, or surgical outcomes in relation to QTc prolongation. Without evidence linking the observed electrophysiological changes to adverse clinical endpoints, the prognostic value of QTc in CBT remains uncertain. ⁷ Bridging this gap will require longitudinal follow-up assessing arrhythmia incidence and perioperative cardiac events.

In summary, this study provides an innovative starting point for exploring the electrophysiological consequences of CBTs. However, the small sample, methodological limitations in QTc correction, and lack of mechanistic or outcome data caution against premature translation into perioperative risk stratification. Larger prospective cohorts integrating autonomic assessments and clinical endpoints will be crucial to determine whether QTc can serve as a valid biomarker of cardiovascular risk in patients with CBT.

Shyam Sundar Sah, MDDr. D. Y. Patil Medical College Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth (Deemed-to-be-University), Pimpri, Pune, Maharashtra, India Abhishek Kumbhalwar, PhDDr. D. Y. Patil Medical College Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth (Deemed-to-be-University), Pimpri, Pune, Maharashtra, India