Association between deceleration capacity-quantified vagal tone and vasovagal syncope patients with different responses to head-up tilt test

Figure 1. Study flowchart of subject selection. ∗Structural cardiac disease was identified and confirmed based on electrocardiogram findings and echocardiography. During the initial clinical evaluation, the admission diagnosis of VVS was considered with strict adherence to the 2018 syncope guidelines. Based on detailed history taking, VVS was highly probable if syncope was precipitated by pain, fear, or standing, and was associated with a typical progressive prodrome (pallor, sweating, and/or nausea), highly suggestive of a reflex mechanism. Furthermore, competing diagnoses, such as cardiac syncope, syncope caused by classical or initial OH, and syncope caused by POTS, were systematically ruled out. Classical OH was defined as a sustained decrease in systolic BP of ≥20 mm Hg, diastolic BP of ≥10 mm Hg, or a sustained decrease in systolic BP to an absolute value of <90 mm Hg within 3 minutes of HUT. Initial OH was defined as a BP decrease on standing of >40 mm Hg for systolic BP and/or >20 mm Hg for diastolic BP within 15 seconds of standing. POTS was considered when there was a marked orthostatic heart rate increase (>30 bpm or to >120 bpm within 10 minutes of HUT) in the absence of OH.…

Figure 2. Cardiac DC in patients with VVS with different responses to the head-up tilt test (HUT). A: DC was calculated as per the phase-rectified signal averaging (PRSA) algorithm for a patient with VVS and an asymptomatic individual. B: 1-way analysis of variance and post hoc analysis with the Bonferroni correction revealed that patients with VVS with a VD response had significantly lower DC than those with a CI, mixed, or Neg response to HUT. CI = cardioinhibitory; DC = deceleration capacity; Neg = negative; VD = vasodepressor; VVS = vasovagal syncope; X(i) = index of PRSA signal.

Figure 3. Association between deceleration capacity (DC) and VVS subtypes. In multinomial logistic regression analysis adjusted for age, gender, body mass index, mean blood pressure, comorbid hypertension, and mean heart rate, (A) enhanced DC-quantified vagal tone was differentially associated with VVS subtypes compared with controls. B: Higher DC was significantly associated with cardioinhibitory, mixed, and HUT-negative VVS when referring to vasodepressor VVS. CI = confidence interval; HUT = head-up tilt test; OR = odds ratio; Ref = reference; VVS = vasovagal syncope.

Figure 4. Subgroup analysis for the relationship between deceleration capacity (DC) and vasodepressor vasovagal syncope (VVS). There was no significant difference in the relationship between DC and vasodepressor VVS by age, gender, BMI, course, syncopal episode, mean BP, comorbid hypertension, and mean heart rate. BMI = body mass index; BP = blood pressure; CI = confidence interval; HR = heart rate; OR = odds ratio.

Figure 5. Association between DC and vasodepressor vasovagal syncope (VVS). A: Restricted cubic spline (RCS) analysis for DC’s association with vasodepressor VVS. The RCS analysis was based on multivariable logistic regression models with full adjustment for potential confounders (including age, gender, body mass index, course, syncopal episode, mean blood pressure, comorbid hypertension, and mean heart rate). We used 3 knots, placed at the 10th, 50th (median), and 90th percentiles of the DC distribution, as was commonly recommended to balance flexibility and avoid overfitting. B: The receiver operating characteristic curve showing the discriminative value of DC for vasodepressor VVS. AUC = area under the curve; DC = deceleration capacity; OR = odds ratio.