caa a22 4500 463157796 CHVBK 20180406164739.0 cr unu---uuuuu 170326e20070201xx s 000 0 eng 10.1007/s10286-006-0386-8 doi (NATIONALLICENCE)springer-10.1007/s10286-006-0386-8 Vasovagal syncope in patients with reduced left ventricular function [Elektronische Daten] [Christopher Stanton, Phillip Low, David Hodge, Win-Kuang Shen] Vasovagal syncope (VVS) is mediated by arterial mechanoreceptors, resulting in reflexive changes in heart rate and vascular tone. The Bezold-Jarisch reflex was originally described as enhanced contraction and activation of left ventricular mechanoreceptors, but later studies implicated other triggers, including coronary, carotid, and cerebral arterial mechanoreceptors. VVS is uncommon in patients with left ventricular dysfunction. We hypothesized that VVS could occur in this subset and examined patient characteristics and hemodynamic responses during tilt table testing. From 1996 through 1998, 128 consecutive patients with ejection fraction <40% underwent tilt table testing (70°, 45min). A total of 15 patients (11.7%) had a positive neurocardiogenic response thought to be the cause of syncope. Clinical data and hemodynamic responses were reviewed. Mean patient age (±SEM) was 70.1±12.2 years. Nine patients were male. Mean ejection fraction was 27.7%±7.1%. Thirteen had electrophysiologic studies with normal findings or abnormal findings insufficient to account for syncope. Hemodynamic analysis of 14 patients who had a vasovagal response during passive tilt table testing showed a mean time to positive response of 17.6± 12.7 min. Cardioinhibitory responses (pauses >3sec or heart rate < 40 beats/min for ≥10sec) were not observed. Five responses were classified as mixed type (>10% decrease in heart rate without a cardioinhibitory response) and 9 as vasodepressor type (≤10% decrease in heart rate). VVS occurs in patients who have clinically significant left ventricular dysfunction. Although this study had a small cohort size, the predominantly vasodepressor response without a cardioinhibitory component warrants further investigation into mechanisms of VVS in these patients. Steinkopff Verlag Darmstadt, 2007 autonomic nervous system nationallicence heart failure nationallicence hemodynamics nationallicence reflexes nationallicence syncope nationallicence Stanton Christopher Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, 55905, Rochester, MN, USA aut Low Phillip Dept. of Neurology, Mayo Clinic, Rochester, MN, USA aut Hodge David Division of Biostatistics, Mayo Clinic, Rochester, MN, USA aut Shen Win-Kuang Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, 55905, Rochester, MN, USA aut Clinical Autonomic Research Steinkopff-Verlag; www.steinkopff.springer.de 17/1(2007-02-01), 33-38 0959-9851 17:1<33 2007 17 10286 https://doi.org/10.1007/s10286-006-0386-8 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10286-006-0386-8 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Stanton Christopher Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, 55905, Rochester, MN, USA aut NATIONALLICENCE 700 1- Low Phillip Dept. of Neurology, Mayo Clinic, Rochester, MN, USA aut NATIONALLICENCE 700 1- Hodge David Division of Biostatistics, Mayo Clinic, Rochester, MN, USA aut NATIONALLICENCE 700 1- Shen Win-Kuang Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, 55905, Rochester, MN, USA aut NATIONALLICENCE 773 0- Clinical Autonomic Research Steinkopff-Verlag; www.steinkopff.springer.de 17/1(2007-02-01), 33-38 0959-9851 17:1<33 2007 17 10286 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer