INTRODUCTION
Postural orthostatic tachycardia syndrome (POTS) is characterized by excessive increase in heart rate (HR) when moving from horizontal to vertical body position with relatively stable blood pressure (BP). Among numerous symptoms in patients suffering from POTS, such as increased heart rate, dizziness, chest discomfort, nausea, sweating, there is also syncope. The mechanisms of syncope are currently not fully understood.
OBJECTIVE. T
O analyze hemodynamic and autonomic regulation parameters during tilt tests in patients with POTS who have previous syncope, and to identify their possible mechanisms.
MATERIAL AND METHODS
The study included 28 patients (median age 31 years, 57% women) with POTS confirmed by tilt tests. In all cases, secondary causes of POTS, such as anemia, thyrotoxicosis, medication intake, etc., were excluded. All patients had previous syncope, whose provoking factors and clinical manifestations indicated vasovagal nature. We excluded cardiac, including arrhythmic causes of syncope, as well as neurological diseases. Tilt tests were performed according to the protocol adopted at the Chazov National Medical Research Center of Cardiology. HR, BP, central hemodynamics and autonomic parameters were continuously recorded.
RESULTS
According to tilt tests, 21 (75%) patients demonstrated early excessive HR response, and 7 (25%) patients showed delayed (by 2.8 minutes) excessive HR increase. In the first group, patients were significantly younger (20 versus 38 years, p=0.014). In the first group, more pronounced decrease in high-frequency component of R-R interval oscillation spectrum was observed upon transition to orthostasis compared to the second group (752 [ms2] lying — 227 standing, p=0.008 versus 484 lying — 267 standing, NS). After transition to orthostatic position, patients in both groups showed increase in total peripheral vascular resistance by the first minute of tilt test (1310 [dyn.s.cm-5] lying — 1783 standing in the 1-st group, p=0.0009 and 1331 lying — 1898 standing in the 2-nd group, NS). In patients with delayed HR response, systolic blood pressure decreased more significantly than in patients with early HR increase (117 [mm Hg] lying down — 106 standing, p=0.023 versus 111 lying down — 110 standing, NS). In all cases, systolic blood pressure decrease did not reach criteria of orthostatic hypotension. Induction of vasovagal syncope during tilt tests occurred in 5 patients (24%) of the first group and 2 patients (28.5%) of the second group.
CONCLUSION
Tilt tests in patients with POTS may be followed by “early” and “delayed” (by 2.8 minutes) reactions of excessive HR increase. “Early” reactions are more common (75%) and typical for younger patients. A more pronounced decrease in parasympathetic influences on sinus node during transition to orthostasis can explain early excessive reactions of increased heart rate. In patients with POTS, vasoconstrictor mechanisms of blood pressure regulation are preserved at the early stage of tilt test. Syncope is caused by vasovagal reactions. Despite obvious anamnestic data indicating syncope of this type, vasovagal reactions are induced in only 25% of patients in tilt tests.
