Features of changes in volume-impedance hemodynamic indicators during the tilt test in young males with a history of vasovagal syncopes

Abstract

Background. The direction of changes in hemodynamic parameters during the tilt test (TT) nin individuals with history of vasovagal syncope (VVS) is a subject of discussion. Objective: to study changes of volume-impedance hemodynamic indicators in the process of tilt test in somatically healthy young men with history of VVS. Materials and methods. A total of 102 men aged 18–30 years were divided into 4 groups, taking into account the specific features of fainting history and response to TT. Persons of group 1 (n=14) had history of VVS and positive response to TT (syncope). Subjects of group 2 (n=14) had history of VVS and a pattern of postural tachycardia without fainting during TT. Persons of group 3 (n=42) had history of VVS and negative response to TT. Subjects of group 4 (n=32) had no history of VVS and negative response to TT. During TT, we studied dynamics of some indicators, including cardiac output (CO) and total peripheral vascular resistance (TPVR). Results. In individuals of all groups in the initial horizontal phase of TT values of CO and TPVR corresponded to the norm. Subjects of group 1 had significantly lower CO compared with subjects of groups 2, 3, 4 (p<0.05, p<0.01, p<0.05, respectively). Values of TPVR in subjects of group 1 were significantly higher than in subjects of groups 2, 3, 4 (p<0.05; p<0.05; p<0.05, respectively). In response to orthostasis CO values increased in groups 1, 2, 4 (by 18%, 10%, 5%, respectively) and did not change in group 3; TPVR values decreased in groups 1, 2 (by 8%, 0.5%, respectively), and increased in groups 3, 4 (by 8%, 4% respectively). In the final horizontal phase of TT, CO values in group 1 were significantly lower than in groups 3, 4 (p<0.05), while TPVR values did not significantly differ between all groups (p>0.05). Conclusions. In tilt-positive and tilt-negative subjects with history of VVS, standardized postural stress leads to unidirectional changes in cardiac output, but to multidirectional changes in total peripheral vascular resistance.