Pulse wave analysis of the aortic pressure waveform in patients with vasovagal syncope

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Pulse wave analysis of the aortic pressure waveform in patients with vasovagal syncope. / Pecha, Simon; Hakmi, Samer; Wilke, Iris; Yildirim, Yalin; Hoffmann, Boris; Reichenspurner, Hermann; Willems, Stephan; von Kodolitsch, Yskert; Aydin, Ali.

In: HEART VESSELS, Vol. 31, No. 1, 01.2016, p. 74-79.

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@article{5259a6fafcb8496c935394f9e68ba21d,
title = "Pulse wave analysis of the aortic pressure waveform in patients with vasovagal syncope",
abstract = "Vascular reflex mechanisms contribute to vasovagal syncope. However, the alterations in central haemodynamics in patients with vasovagal syncope are unknown. 30 consecutive patients (36.5 ± 15 years, 14 females) with recurrent vasovagal syncope (VVS) and a positive tilt table test were compared to 39 age- and sex-matched controls (36.9 ± 16 years, 15 females) with a negative tilt table result and no history of syncope. Central aortic pressure parameters including augmentation index and central pulse pressure as markers of aortic stiffness were generated non-invasively by applanation tonometry of the radial artery and use of a validated mathematical transfer function. No difference in aortic augmentation index was observed between groups. (VVS 9 ± 2.6 vs. Control 11 ± 2.4, p = 0.8). However, in patients with vasovagal syncope the aortic pressure waveform significantly differed from healthy controls. A prolonged time to the peak of aortic pressure wave (aortic T2) was observed in patients with vasovagal syncope (226 ± 24 vs. 208 ± 21 ms, p = 0.001). Furthermore time to the first shoulder of the aortic pressure wave (aortic T1) was slightly shorter compared to healthy controls, but did not reach statistical significance (106 ± 22 vs. 110 ± 12 ms, p = 0.33). Patients with vasovagal syncope have an altered aortic pressure waveform at rest, but no signs of elevated aortic stiffness. The underlying mechanisms for these findings may potentially result from a complex imbalance of the autonomic nervous system with a continuous deregulation of the sympathetic and parasympathetic reflex arcs.",
keywords = "Adult, Arterial Pressure, Autonomic Nervous System/physiopathology, Blood Pressure, Case-Control Studies, Electrocardiography, Female, Germany, Heart Rate, Humans, Male, Middle Aged, Pulse Wave Analysis, Syncope, Vasovagal/physiopathology, Tilt-Table Test, Young Adult",
author = "Simon Pecha and Samer Hakmi and Iris Wilke and Yalin Yildirim and Boris Hoffmann and Hermann Reichenspurner and Stephan Willems and {von Kodolitsch}, Yskert and Ali Aydin",
year = "2016",
month = jan,
doi = "10.1007/s00380-014-0576-6",
language = "English",
volume = "31",
pages = "74--79",
journal = "HEART VESSELS",
issn = "0910-8327",
publisher = "Springer Japan",
number = "1",

}

RIS

TY - JOUR

T1 - Pulse wave analysis of the aortic pressure waveform in patients with vasovagal syncope

AU - Pecha, Simon

AU - Hakmi, Samer

AU - Wilke, Iris

AU - Yildirim, Yalin

AU - Hoffmann, Boris

AU - Reichenspurner, Hermann

AU - Willems, Stephan

AU - von Kodolitsch, Yskert

AU - Aydin, Ali

PY - 2016/1

Y1 - 2016/1

N2 - Vascular reflex mechanisms contribute to vasovagal syncope. However, the alterations in central haemodynamics in patients with vasovagal syncope are unknown. 30 consecutive patients (36.5 ± 15 years, 14 females) with recurrent vasovagal syncope (VVS) and a positive tilt table test were compared to 39 age- and sex-matched controls (36.9 ± 16 years, 15 females) with a negative tilt table result and no history of syncope. Central aortic pressure parameters including augmentation index and central pulse pressure as markers of aortic stiffness were generated non-invasively by applanation tonometry of the radial artery and use of a validated mathematical transfer function. No difference in aortic augmentation index was observed between groups. (VVS 9 ± 2.6 vs. Control 11 ± 2.4, p = 0.8). However, in patients with vasovagal syncope the aortic pressure waveform significantly differed from healthy controls. A prolonged time to the peak of aortic pressure wave (aortic T2) was observed in patients with vasovagal syncope (226 ± 24 vs. 208 ± 21 ms, p = 0.001). Furthermore time to the first shoulder of the aortic pressure wave (aortic T1) was slightly shorter compared to healthy controls, but did not reach statistical significance (106 ± 22 vs. 110 ± 12 ms, p = 0.33). Patients with vasovagal syncope have an altered aortic pressure waveform at rest, but no signs of elevated aortic stiffness. The underlying mechanisms for these findings may potentially result from a complex imbalance of the autonomic nervous system with a continuous deregulation of the sympathetic and parasympathetic reflex arcs.

AB - Vascular reflex mechanisms contribute to vasovagal syncope. However, the alterations in central haemodynamics in patients with vasovagal syncope are unknown. 30 consecutive patients (36.5 ± 15 years, 14 females) with recurrent vasovagal syncope (VVS) and a positive tilt table test were compared to 39 age- and sex-matched controls (36.9 ± 16 years, 15 females) with a negative tilt table result and no history of syncope. Central aortic pressure parameters including augmentation index and central pulse pressure as markers of aortic stiffness were generated non-invasively by applanation tonometry of the radial artery and use of a validated mathematical transfer function. No difference in aortic augmentation index was observed between groups. (VVS 9 ± 2.6 vs. Control 11 ± 2.4, p = 0.8). However, in patients with vasovagal syncope the aortic pressure waveform significantly differed from healthy controls. A prolonged time to the peak of aortic pressure wave (aortic T2) was observed in patients with vasovagal syncope (226 ± 24 vs. 208 ± 21 ms, p = 0.001). Furthermore time to the first shoulder of the aortic pressure wave (aortic T1) was slightly shorter compared to healthy controls, but did not reach statistical significance (106 ± 22 vs. 110 ± 12 ms, p = 0.33). Patients with vasovagal syncope have an altered aortic pressure waveform at rest, but no signs of elevated aortic stiffness. The underlying mechanisms for these findings may potentially result from a complex imbalance of the autonomic nervous system with a continuous deregulation of the sympathetic and parasympathetic reflex arcs.

KW - Adult

KW - Arterial Pressure

KW - Autonomic Nervous System/physiopathology

KW - Blood Pressure

KW - Case-Control Studies

KW - Electrocardiography

KW - Female

KW - Germany

KW - Heart Rate

KW - Humans

KW - Male

KW - Middle Aged

KW - Pulse Wave Analysis

KW - Syncope, Vasovagal/physiopathology

KW - Tilt-Table Test

KW - Young Adult

U2 - 10.1007/s00380-014-0576-6

DO - 10.1007/s00380-014-0576-6

M3 - SCORING: Journal article

C2 - 25164239

VL - 31

SP - 74

EP - 79

JO - HEART VESSELS

JF - HEART VESSELS

SN - 0910-8327

IS - 1

ER -