Key result
Patients developing syncope during head-up tilt test had lower systemic vascular resistance index than those who did not (122.7 vs 185.6 dyn sec cm(-5)/m2, P=0.002), with no difference in contractility.
Why the study?
Do increased myocardial contractility and decreased cardiac filling trigger vasovagal syncope during head-up tilt testing?
Observational (n=46)
Do increased myocardial contractility and decreased cardiac filling trigger vasovagal syncope during head-up tilt testing?
Absolute Event Rate: 122.7% vs 185.6%
p-value: p=0.002
The study does not support the hypothesis that increased myocardial contractility and decreased cardiac filling are the primary triggering mechanisms for vasovagal syncope.
Lower SVR without contractility differences in tilt syncope; challenges contractility hypothesis and leaves open vasodepressor mechanisms for confirmation.
OBJECTIVE: Increased myocardial contractility and inadequate cardiac filling leading to activation of the Bezold-Jarisch reflex were proposed as possible triggering mechanisms of vasovagal syncope (VVS). In the present study noninvasive hemodynamic measurements were performed in order to examine the role of myocardial contractility and cardiac filling in pathogenesis of VVS. METHODS: Hemodynamic parameters were measured during head-up tilt test (HUT) by impedance cardiography in 46 patients with unexplained syncope. Myocardial contractility was measured as index of contractility (IC), acceleration index (ACI), and ejection fraction (EF). Afterload was measured as systemic vascular resistance index (SVRI) and preload was expressed as end-diastolic index (EDI). Serial measurements were done 1 minute before HUT, during HUT at 1-minute intervals, and 1 minute after completion of HUT. RESULTS: HUT was positive in 30 patients (10 men, 20 women, mean age 36 +/- 16 years) and negative in 16 patients (8 men, 8 women, mean age 31 +/- 14 years). No significant differences were observed between HUT(+) and HUT(-) groups in hemodynamic parameters at supine rest and during HUT until the development of syncope. SVRI was lower in HUT(+) than in HUT(-) group at syncope (122.7 + 66.3 vs 185.6 + 51.4 dyn sec cm(-5)/m2, P = 0.002) and after syncope (117.0 + 61.1 vs 198.0 + 95.7 dyn sec cm(-5)/m2, P = 0.007). ACI, IC, EF, and EDI did not differ between groups at syncope. After syncope EF was higher in HUT(+) group compared to HUT(-) group (59.2 + 6.1 vs 52.7 + 9.4%, P = 0.02). CONCLUSION: The role of increased myocardial contractility and decreased cardiac filling is not confirmed in the present study.
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Mitro et al. (2006) conducted an observational in Unexplained syncope (n=46). Positive head-up tilt test (development of syncope) vs. Negative head-up tilt test (no syncope) was evaluated on Systemic vascular resistance index (SVRI) at syncope (p=0.002). Patients developing syncope during head-up tilt test had lower systemic vascular resistance index than those who did not (122.7 vs 185.6 dyn sec cm(-5)/m2, P=0.002), with no difference in contractility.
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