title: Altered autonomic regulation as a cardiovascular risk marker for patients with sudden sensorineural hearing loss.
abstract: OBJECTIVE
  To measure autonomic nervous system function after idiopathic sudden sensorineural hearing loss (ISSHL).
  
  
  METHODS
  Diagnostic prospective cohort single-center study.
  
  
  METHODS
  Tertiary referral university hospital.
  
  
  METHODS
  Twenty-three adult patients with ISSHL and 10 normal-hearing control patients without ISSHL (CON) matched with respect to age, sex, hypertension, and medication.
  
  
  METHODS
  Bivariate analysis of autonomic regulation (ISSHL versus CON) using 30-minute heart rate (HR) and systolic and diastolic blood pressure (BP) time series at baseline, based on cardiovascular coupling, HR and BP regulatory patterns, high-resolution coupling analysis based on joint symbolic dynamics (High-Resolution Joint Symbolic Dynamics).
  
  
  METHODS
  No intervention.
  
  
  RESULTS
  Multivariate discrimination between ISSHL and CON achieved values of area under the receiver operator characteristic curve = 95.5, sensitivity = 90.9%, and specificity = 88.9%. Independent from medication and hypertension increased the complexity of nonlinear HR regulation and reduced cardiovascular coupling of ISSHL patients and independent from hypertension altered nonlinear systolic and diastolic BP regulation. Coupling patterns are characterized by a less pronounced strong and fast decrease of systolic BP when HR increases and rapidly changes in ISSHL patients. Disturbed BP modulation and complexity by impaired baroreflex activities resulting in short-term BP fluctuations, altered peripheral resistance, and reduced cochlear blood flow. Increased values for the pulse wave velocity in the aorta and carotid-femoral were early indicators that the elasticity of the arteries might be restricted in ISSHL patients.
  
  
  CONCLUSIONS
  ISSHL patients show an altered autonomic regulation. At least a subgroup of ISSHL patients seems to exist where a vascular impairment might play an important role in the pathogenesis of this disease.
authors.affiliation: *Department of Medical Engineering and Biotechnology, University of Applied Sciences; and †Departments of Otorhinolaryngology and ‡Psychiatry and Psychotherapy, Jena University Hospital, Jena, Germany.
authors.forename: Steffen
authors.initials: S
authors.lastname: Schulz
authors.forename: Julia
authors.initials: J
authors.lastname: Ritter
authors.forename: Katrin
authors.initials: K
authors.lastname: Oertel
authors.forename: Katharina
authors.initials: K
authors.lastname: Witt
authors.forename: Karl-Jürgen
authors.initials: KJ
authors.lastname: Bär
authors.forename: Orlando
authors.initials: O
authors.lastname: Guntinas-Lichius
authors.forename: Andreas
authors.initials: A
authors.lastname: Voss
mesh_terms: D000328:Adult; D000368:Aged; D001158:Arteries / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology*; D005260:Female; D006319:Hearing Loss, Sensorineural / Q000175:diagnosis* / Q000503:physiopathology; D003639:Hearing Loss, Sudden / Q000175:diagnosis* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors; D055815:Young Adult