Key result
Patients with vasovagal syncope had a significantly lower cardiac index (1.47 vs 1.97 l/min/m2, p<0.001) and higher systemic vascular resistance index than those with vasodepressor syncope.
Why the study?
What are the hemodynamic differences between vasovagal and vasodepressor reactions during tilt-induced neurally mediated syncope?
Observational (n=35)
What are the hemodynamic differences between vasovagal and vasodepressor reactions during tilt-induced neurally mediated syncope?
Absolute Event Rate: 1.47% vs 1.97%
p-value: p=<0.001
Vasovagal and vasodepressor syncope exhibit distinct hemodynamic profiles during tilt testing, with heart rate playing a significant role in determining cardiac index.
These hemodynamic differences may aid syncope subtyping on tilt testing; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. HYPOTHESIS: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. METHODS: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). RESULTS: The baseline hemodynamic data (mean +/- standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 +/- 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 +/- 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 +/- 0.29 vs. 1.97 +/- 0.41 1/min/m2, p < 0.001 and 2098 +/- 615 vs. 1573 +/- 353 dynes x s x cm(-5) x m2, p < 0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. CONCLUSIONS: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope.
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Chan et al. (2004) conducted an observational in Neurally mediated syncope (n=35). Vasovagal reaction (bradycardia) vs. Vasodepressor reaction (no bradycardia) was evaluated on Cardiac index during syncope (l/min/m2) (p=<0.001). Patients with vasovagal syncope had a significantly lower cardiac index (1.47 vs 1.97 l/min/m2, p<0.001) and higher systemic vascular resistance index than those with vasodepressor syncope.
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