Key result
Cardiac deceleration capacity is ~47% higher in VVS patients versus controls, particularly cardioinhibitory subtypes.
Why the study?
While tilt-table testing categorizes vasovagal syncope into vasodepressor, cardioinhibitory, and mixed phenotypes, the characteristics of subtype-specific vagal activity assessed with cardiac deceleration capacity remained unclear.
Does cardiac deceleration capacity differentiate between subtypes of vasovagal syncope?
Does cardiac deceleration capacity differentiate between subtypes of vasovagal syncope?
Cardiac deceleration capacity is significantly higher in cardioinhibitory and mixed VVS compared to vasodepressor VVS, offering a potential non-invasive tool for VVS subtyping without requiring syncopal episodes.
DC independently associated with VVS subtypes; extends autonomic observations but leaves open clinical utility pending prospective validation.
Background Vasovagal syncope (VVS), one of the most common reasons for transient loss of consciousness, is linked to autonomic dysregulation. Cardiac deceleration capacity (DC), a novel index related to vagal tone, has potential diagnostic value for VVS. While tilt-table testing (TTT) categorizes VVS into vasodepressor, cardioinhibitory, and mixed phenotypes, the characteristics of subtype-specific vagal activity assessed with DC remain unclear. Purpose This study aimed to investigate the relationship between DC and VVS subtypes, elucidating the discrepancy in vagal activity among VVS patients with different phenotypes. Methods In this prospective observational study, 226 TTT-positive VVS patients (58 vasodepressor, 66 cardioinhibitory, and 102 mixed phenotypes), with 127 asymptomatic individuals as controls, underwent 24-hour Holter monitoring. DC was calculated based on phased-rectified signal averaging algorithm. Multiple multivariate logistic regression analysis adjusted for potential confounders was performed between VVS patients with different subtypes and controls. Restricted cubic spline (RCS) and receiver operating characteristic (ROC) curves were performed for DC between VVS patients with and without vasodepressor phenotype. Results A significant increase in DC was observed in VVS patients compared to controls (8.33 ± 2.72 ms vs. 5.65 ± 1.07 ms, P < 0.001). Among VVS patients, cardioinhibitory (8.79 ± 2.48 ms) and mixed (9.04 ± 2.77 ms) subtypes exhibited higher DC than vasodepressor phenotype (6.55 ± 2.03 ms, P < 0.001). After comprehensive adjustment, increased DC was independently associated with VVS (OR, 2.78; 95% CI, 2.12-3.64), with stronger associations observed in cardioinhibitory (OR, 3.31; 95% CI, 2.41-4.54) and mixed (OR, 3.53; 95% CI, 2.59-4.82) subtypes compared to vasodepressor phenotype (OR, 1.97; 95% CI, 1.44-2.70). In the RCS analysis, lower DC was associated with vasodepressor VVS without nonlinearity observed. DC demonstrated subtype-discriminative value in VVS patients (AUC, 0.779; 95% CI, 0.708-0.850), and DC < 7.8 ms could be utilized to detect vasodepressor VVS with 82.8% sensitivity and 64.3% specificity. Conclusion Cardioinhibitory and mixed VVS patients exhibited more enhanced vagal tone than vasodepressor cases during the non-syncopal period, indicative of the discrepancy in autonomic dysregulation. DC could serve as a practical indicator for VVS subtyping without syncopal episodes, offering a potential tool to guide subtype-specific therapeutic strategies for VVS.RCS for DC among TTT-pos VVS patients ROC for DC to identify vasodepressor VVS
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Maimaitijiang et al. (2025) studied this question. Cardiac deceleration capacity was significantly higher in VVS patients (8.33 ms vs 5.65 ms controls), particularly cardioinhibitory and mixed subtypes, and DC <7.8 ms detects vasodepressor VVS with 82.
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