Key result
Vasovagal syncope causes ~28 mmHg greater tilt-test systolic BP drop than non-vasovagal causes.
Why the study?
Diagnosing vasovagal syncope remains challenging because its manifestations overlap with cardiac, neurological, and functional disorders. This study evaluated diagnostic approaches, haemodynamic characteristics, and preventive strategies in patients with suspected VVS.
Does integrated clinical and haemodynamic assessment differentiate vasovagal syncope from other causes of transient loss of consciousness in patients with recurrent syncope?
Observational (n=78)
Does integrated clinical and haemodynamic assessment differentiate vasovagal syncope from other causes of transient loss of consciousness in patients with recurrent syncope?
In patients presenting with suspected vasovagal syncope, integrated clinical and haemodynamic evaluation confirmed VVS in 73.1% of cases while identifying potentially serious cardiac (9.0%) and neurological (3.8%) causes in a clinically important minority.
Answers are grounded in this paper and cite their sources.
May aid differentiation of vasovagal syncope via tilt testing; leaves open prospective validation of diagnostic accuracy.
Background: Vasovagal syncope (VVS) is a common cause of transient loss of consciousness, particularly among young adults. Its diagnosis remains challenging because of overlapping manifestations with cardiac, neurological and functional disorders. This study aimed to evaluate diagnostic approaches, haemodynamic characteristics and preventive strategies in patients with suspected VVS. Materials and Methods: Clinical and instrumental findings were analysed in 78 patients with recurrent transient loss of consciousness, including 69 women (88.5%). Assessment comprised clinical history, neurological and cardiovascular examinations, electrocardiography, orthostatic testing and, where indicated, head-up tilt testing, ambulatory ECG monitoring, echocardiography and electroencephalography. Recurrence frequency, precipitating factors and preventive interventions were evaluated. Results: VVS was confirmed in 57 patients (73.1%), functional disorders in 8 (10.3%), epilepsy in 3 (3.8%) and cardiac causes in 7 (9.0%); the aetiology remained undetermined in 3 (3.8%). Annual syncope frequency was 3 [2; 5] episodes in VVS versus 2 [1; 4] in other diagnostic groups (p = 0.13). During active standing, heart rate increased by 18 [12; 25] versus 12 [8; 18] beats/min (p = 0.028), while systolic blood pressure decreased by 16 [10; 23] versus 8 [5; 14] mmHg (p = 0.005). Head-up tilt testing demonstrated greater hypotensive responses in VVS (p < 0.001). Coughing was identified as a potential situational trigger requiring separate diagnostic consideration. Conclusions: Accurate VVS diagnosis requires integrated clinical and haemodynamic assessment and exclusion of potentially serious alternative causes. Individualised trigger management, physical counter-pressure manoeuvres and appropriate preventive interventions are important components of patient care.
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Khubetova et al. (2026) conducted an observational in Recurrent transient loss of consciousness (suspected vasovagal syncope) (n=78). Confirmed vasovagal syncope vs. Other established causes of loss of consciousness (functional disorders, cardiac causes, epilepsy) was evaluated on Median systolic blood pressure reduction during head-up tilt testing (mmHg) (p=<0.001). Confirmed vasovagal syncope accounted for 73.1% of recurrent transient loss of consciousness cases and showed greater tilt-test systolic BP reductions than other causes (42 vs 14 mmHg, p<0.001).
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