Key result
Non-prodromal VVS linked to ~8% lower baseline cerebral blood flow velocity versus prodromal VVS.
Why the study?
Vasovagal syncope without aura carries a high fall risk and misdiagnosis rate, but its cardio-cerebral hemodynamic characteristics remain unclear.
What are the cardio-cerebral hemodynamic differences between non-prodromal and prodromal vasovagal syncope during head-up tilt testing?
Observational (n=221)
What are the cardio-cerebral hemodynamic differences between non-prodromal and prodromal vasovagal syncope during head-up tilt testing?
Absolute Event Rate: 55% vs 60%
p-value: p=0.009
Non-prodromal vasovagal syncope is characterized by early cerebral hypoperfusion and impaired central compensatory mechanisms, distinguishing it hemodynamically from prodromal VVS.
Hemodynamic subtyping in non-prodromal VVS may refine diagnosis; leaves open whether it improves risk stratification or targeted therapy.
BACKGROUND: Vasovagal syncope (VVS) without aura is characterized by a high fall risk and misdiagnosis rate. However, its hemodynamic characteristics remain unclear. In this study, we aimed to analyze the cardio-cerebral hemodynamic changes in patients with non-prodromal VVS, to generate a scientific basis for its management. METHODS: A total of 221 participants were prospectively and consecutively enrolled, including 34 patients with non-prodromal VVS, 118 patients with prodromal VVS, and 69 non-syncope controls. All participants completed the head-up tilt test (HUTT) combined with transcranial Doppler (TCD). Blood pressure, heart rate, and cerebral hemodynamic parameters were monitored dynamically during the test. Data were statistically analyzed. RESULTS: ), and was older (median 47 vs. 37 years) (all P < 0.05). The baseline cerebral blood flow velocity (CBFV) in the non-prodromal VVS group was significantly lower than that in the prodromal VVS group (55 vs. 60 cm/s, P = 0.009), and the decrease of CBFV during the tilt test preceded the change of blood pressure. During the return to the supine position after HUTT, systolic blood pressure was significantly higher in the non-prodromal VVS group than in the prodromal VVS group (117.19 vs. 111.95 mmHg, P = 0.019), and the heart rate increment was greater during the drug-induced phase (11.35 vs. 8.38 beats per minute). CONCLUSIONS: Non-prodromal VVS, with its unique hemodynamic profile involving early cerebral hypoperfusion and impaired central compensatory mechanisms, represents a high-risk subtype associated with higher fall risk. The identified hemodynamic differences may serve as objective biomarkers for its diagnosis. This study highlights the need for tailored management strategies, including comprehensive fall prevention measures and targeted interventions.
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Yu et al. (2026) conducted an observational in Vasovagal syncope (n=221). Non-prodromal VVS vs. Prodromal VVS was evaluated on Baseline cerebral blood flow velocity (CBFV) (p=0.009). Non-prodromal VVS was associated with significantly lower baseline cerebral blood flow velocity compared to prodromal VVS (55 vs. 60 cm/s, P=0.009).
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