BACKGROUND: The pathophysiology of neurocardiogenic syncope is heterogeneous. This study aim was to analyze whether extended monitoring during tilt-table testing provided additional information on the hemodynamic and vegetative state prior to neurocardiogenic syncope. METHODS: This retrospective analysis is based on data of head-up tilt-table testing of 40 unselected consecutive patients with a history of unexplained syncope. For optimized characterization of the type of syncope, monitoring included electrocardiogram (ECG), blood pressure measurements and cardiac output, peripheral vascular resistance and contractility index measurements by impedance cardiography, as well as epinephrine and norepinephrine plasma levels in supine position and every 5 min during tilting. RESULTS: Seven of 40 patients were unsuitable for analysis because of incomplete data sets. Tilt-table was positive in 26 patients, negative in 7. Groups did not differ in hemodynamic and catecholaminergic parameters at baseline. Responses to tilting were VASIS 1 (mix of cardioinhibitory and vasodepressor) in 5 patients, VASIS 2B (cardioinhibitory with asystole >3 sec) in 3, VASIS 3 (vasodepressor) in 16, orthostatic dysregulation in 2. In VASIS 1, the catecholamine measurement 4 min before syncope showed a proportionally larger increase of the epinephrine level than of norepinephrine. This disproportion was not observed in VASIS 2B and 3. In VASIS 2B, strong vasoconstriction and negative inotropy were evident in the presyncopal period. In VASIS 3, vascular resistance decreased continuously before syncope, while contractility index increased inadequately. Presyncopal epinephrine surge or norepinephrine loss was not observed in this group, suspecting other vasodilating factors. CONCLUSIONS: Extended monitoring by impedance cardiography and plasma catecholamine measurements during tilt-table testing gave further insight into different hemodynamic and neurohumoral presyncopal patterns among the various types of neurocardiogenic syncope and may thereby help to develop individualized therapeutic concepts.
BACKGROUND: The pathophysiology of neurocardiogenic syncope is heterogeneous. This study aim was to analyze whether extended monitoring during tilt-table testing provided additional information on the hemodynamic and vegetative state prior to neurocardiogenic syncope. METHODS: This retrospective analysis is based on data of head-up tilt-table testing of 40 unselected consecutive patients with a history of unexplained syncope. For optimized characterization of the type of syncope, monitoring included electrocardiogram (ECG), blood pressure measurements and cardiac output, peripheral vascular resistance and contractility index measurements by impedance cardiography, as well as epinephrine and norepinephrine plasma levels in supine position and every 5 min during tilting. RESULTS: Seven of 40 patients were unsuitable for analysis because of incomplete data sets. Tilt-table was positive in 26 patients, negative in 7. Groups did not differ in hemodynamic and catecholaminergic parameters at baseline. Responses to tilting were VASIS 1 (mix of cardioinhibitory and vasodepressor) in 5 patients, VASIS 2B (cardioinhibitory with asystole >3 sec) in 3, VASIS 3 (vasodepressor) in 16, orthostatic dysregulation in 2. In VASIS 1, the catecholamine measurement 4 min before syncope showed a proportionally larger increase of the epinephrine level than of norepinephrine. This disproportion was not observed in VASIS 2B and 3. In VASIS 2B, strong vasoconstriction and negative inotropy were evident in the presyncopal period. In VASIS 3, vascular resistance decreased continuously before syncope, while contractility index increased inadequately. Presyncopal epinephrine surge or norepinephrine loss was not observed in this group, suspecting other vasodilating factors. CONCLUSIONS: Extended monitoring by impedance cardiography and plasma catecholamine measurements during tilt-table testing gave further insight into different hemodynamic and neurohumoral presyncopal patterns among the various types of neurocardiogenic syncope and may thereby help to develop individualized therapeutic concepts.
Authors: Indu Taneja; Marvin S Medow; June L Glover; Neeraj K Raghunath; Julian M Stewart Journal: Am J Physiol Heart Circ Physiol Date: 2008-05-23 Impact factor: 4.733
Authors: Edward Koźluk; Gerard Cybulski; Agnieszka Piątkowska; Inga Zastawna; Wiktor Niewiadomski; Anna Strasz; Anna Gąsiorowska; Maciej Kempa; Dariusz Kozłowski; Grzegorz Opolski Journal: Arch Med Sci Date: 2014-12-22 Impact factor: 3.318
Authors: Parisa Torabi; Fabrizio Ricci; Viktor Hamrefors; Olle Melander; Richard Sutton; David G Benditt; Artur Fedorowski Journal: J Am Heart Assoc Date: 2019-06-18 Impact factor: 5.501