A.Z. Pietrucha, T. Wójcik, J. Jedrzejczyk-Spaho, I. Bzukala, M. Wnuk, D. Mroczek-Czernecka, E. Konduracka, S. Ch?opicki, J. Nessler

1. Syncope Unit, Department of Coronary Disease and Heart Failure, Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Cracow, Poland; 2. Jagiellonian Centre for Experimental Therapeutics, Cracow, Poland


Introduction: Pronounced vasodilatation and thrombotic activation during vasovagal syncope indicate the role of endothelium in its patomechanism.The aim of study was evaluation of Thromboxan B2 (TXB2) serum changes during head-up tilt-test in patients with vasovagal syncope (VVS).Study population: 25pts (11 men, 14 women) aged 18-42 years (median of age: 21yrs) with VVS referred to HUTT. Cardio- and neurological causes of syncope were previously excluded in all studied pts.
Methods: In all pts HUTT according Westminetr protocol was done with sublingual nitroglycerine (NTG) provocation, in the case of negative result of passive tilting.During HUTT continuous, noninvasive beat-to-beat monitoring of heart rate and blood pressure were performed using NEXFIN (Bmeye) monitor. Before the test, after completion of both – passive and active phases (after NTG provocation) and 15 minutes after finishing the test (syncope induction or protocol completion) the blood samples were taken, to evaluation of serum concentration of TXB2. Changes of TXB2 serum concentrations during HUTT were analyzed in relation to the type of vasovagal response during the test.
Results: HUTT was positive in 21 pts (84%) – in 5 pts there were cardioinhibitory response, in 14 pts. – mixed and in 2 - vasodepressive. Serum TXB2 concentration before the test in pts with negative HUTT was significantly lower in relation to pts with positive HUTT (674,7 vs 1212,3 pg/ml p < 0,03). After completion of passive phase of HUTT significant increase of TXB2 concentration was noticed in HUTT-positive pts. (3195,5 vs 1212,3 pg/ml; p,0,04), whereas pts with negative HUTT revealed no significant changes. (909,7 vs 674,7 pg/ml). After sublingual NTG administration, increase of NO concentration was observed in HUTT negative pts (2741,2 vs 909,4 pg/ml, p < 0,02 ) whereas in HUTT positive pts. The significant decrease was observed (1923,7 vs 3195,5 pg/ml;p < 0,02). After the test, NO concentration decreased to about the value observed prior to HUTT in HUTT negative pts. But in syncope induced pts increased of TXB2 was noticed (2955,1 vs 1923,7 pg/ml; p < 0,04) There were no relation between serum NO concentration and type of vasovagal response to the orthostatic stress.
Conclusions: 1. Syncope induction during HUTT was related to significantly higher values of serum Thromboxan B2 concentration after passive phase of HUTT as well as reduce of the concentration after NTG provocation in relation to the HUTT-negative patients.2. Changes of Thromboxan B2 concentrations seems to important role in the pathomechanism of vasovagal response to orthostatic stress in patients with vasovagal syncope.