title: Impact of acute mental stress on sympathetic nerve activity and regional blood flow in advanced heart failure: implications for 'triggering' adverse cardiac events.
abstract: BACKGROUND
  Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure.
  
  
  RESULTS
  Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
  
  
  CONCLUSIONS
  Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.
authors.affiliation: Department of Medicine, University of California, Los Angeles School of Medicine, 90095, USA.
authors.forename: H R
authors.initials: HR
authors.lastname: Middlekauff
authors.forename: A H
authors.initials: AH
authors.lastname: Nguyen
authors.forename: C E
authors.initials: CE
authors.lastname: Negrao
authors.forename: E U
authors.initials: EU
authors.lastname: Nitzsche
authors.forename: C K
authors.initials: CK
authors.lastname: Hoh
authors.forename: B A
authors.initials: BA
authors.lastname: Natterson
authors.forename: M A
authors.initials: MA
authors.lastname: Hamilton
authors.forename: G C
authors.initials: GC
authors.lastname: Fonarow
authors.forename: A
authors.initials: A
authors.lastname: Hage
authors.forename: J D
authors.initials: JD
authors.lastname: Moriguchi
mesh_terms: D000328:Adult; D001794:Blood Pressure; D003645:Death, Sudden / Q000209:etiology; D005542:Forearm / Q000098:blood supply / Q000294:innervation; D006333:Heart Failure / Q000150:complications / Q000401:mortality / Q000523:psychology*; D006339:Heart Rate; D006801:Humans; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000294:innervation; D012039:Regional Blood Flow; D012079:Renal Circulation; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014661:Vasoconstriction; D014664:Vasodilation