title: Assessment of left ventricular volume by an ambulatory radionuclide monitoring system during head-up tilt in patients with unexplained syncope: relation to autonomic activity assessed by heart rate variability.
abstract: BACKGROUND
  Decreased left ventricular volume during head-up tilt plays an important role in triggering syncope in patients with neurally mediated syncope. However, precise changes in left ventricular volume during head-up tilt have not been well investigated. This study was conducted to test the hypothesis that the decline in left ventricular volume during tilt could trigger ventricular mechanoreceptor activation.
  
  
  RESULTS
  To investigate the mechanisms of tilt-induced syncope, we measured the temporal changes in left ventricular volume, ejection fraction, cardiac output, and heart rate variability indices during head-up tilt in 25 patients with syncope of undetermined etiology. Eleven patients had a cardioinhibitory response (CI group), 7 patients showed a vasodepressor response (VD group), and 7 patients demonstrated a negative response (NG group). Before syncope, ejection fraction increased most in the CI group, the left ventricular end-diastolic volume declined most in the VD group (VD group, -11.0% +/- 3.3%; CI group, -2.8% +/- 4.8%; NG group, -3.4% +/- 2.2%; P <.005), and the high-frequency spectra increased most in the CI group (CI group, 25.0% +/- 21.0%; VD group, -4.1% +/- 11.7%; NG group, -5.3% +/- 12.7%; P <.01). The vasodepressor response was dependent on left ventricular volume, whereas the cardioinhibitory response was related to the vagal activity reflected by high-frequency spectra.
  
  
  CONCLUSIONS
  The precise evaluation of left ventricular volume by an ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered useful for clarifying the pathophysiology of neurally mediated syncope.
authors.affiliation: Internal Medicine-1, Radiology, and Research Center, National Defense Medical College, Saitama, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hosaka
authors.forename: B
authors.initials: B
authors.lastname: Takase
authors.forename: K
authors.initials: K
authors.lastname: Kitamura
authors.forename: A
authors.initials: A
authors.lastname: Uehata
authors.forename: K
authors.initials: K
authors.lastname: Satomura
authors.forename: K
authors.initials: K
authors.lastname: Isojima
authors.forename: S
authors.initials: S
authors.lastname: Kosuda
authors.forename: S
authors.initials: S
authors.lastname: Kusano
authors.forename: A
authors.initials: A
authors.lastname: Kurita
authors.forename: F
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001342:Autonomic Nervous System Diseases / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002302:Cardiac Output / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology*; D004562:Electrocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D015637:Gated Blood-Pool Imaging; D006257:Head / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008465:Mechanoreceptors / Q000000981:diagnostic imaging / Q000503:physiopathology; D011187:Posture / Q000502:physiology*; D013318:Stroke Volume / Q000502:physiology; D013575:Syncope / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*