title: Silent ischemia as a central problem: regional brain activation compared in silent and painful myocardial ischemia.
abstract: OBJECTIVE
  To test whether the silence of painless myocardial ischemia is caused by abnormal handling by the central nervous system of afferent messages from the heart.
  
  
  METHODS
  Nonrandomized study.
  
  
  METHODS
  A tertiary referral center (postgraduate medical school).
  
  
  METHODS
  2 matched groups of nondiabetic patients with coronary artery disease. Group A consisted of nine patients with reproducible stress-induced angina; group B consisted of nine patients with reproducible stress-induced myocardial ischemia but no angina.
  
  
  METHODS
  Intravenous placebo infusion and low-dose (5 and 10 micrograms/ kg per minute) and high-dose (20 to 35 micrograms/kg per minute) dobutamine infusions.
  
  
  METHODS
  Positron emission tomography was used to measure regional cerebral blood flow changes as an index of neuronal activation during painful and silent myocardial ischemia induced by intravenous dobutamine.
  
  
  RESULTS
  Regional cerebral blood flow changes during myocardial ischemia were compared with those during baseline conditions and during placebo infusion. During myocardial ischemia, regional cerebral blood flow increased bilaterally in the thalami and prefrontal, basal frontal, and ventral cingulate corticles in patients in group A. Both thalami were activated in group B, but cortical activation was limited to the right frontal region. A formal comparison of groups A and B showed significant differences (P < 0.01) in activation of the basal frontal cortex, ventral cingulate cortex, and left temporal pole. In both groups, thalamic regional cerebral blood flow remained increased after the symptoms and signs of ischemia had ceased.
  
  
  CONCLUSIONS
  Bilateral activation of the thalamus can be shown in both angina and silent ischemia; thus, peripheral nerve dysfunction cannot completely explain silent ischemia. Frontal cortical activation appears to be necessary for the sensation of pain. Abnormal central processing of afferent pain messages from the heart may play a determining role in silent myocardial ischemia.
authors.affiliation: Cyclotron Unit, Hammersmith Hospital, London, United Kingdom.
authors.forename: S D
authors.initials: SD
authors.lastname: Rosen
authors.forename: E
authors.initials: E
authors.lastname: Paulesu
authors.forename: P
authors.initials: P
authors.lastname: Nihoyannopoulos
authors.forename: D
authors.initials: D
authors.lastname: Tousoulis
authors.forename: R S
authors.initials: RS
authors.lastname: Frackowiak
authors.forename: C D
authors.initials: CD
authors.lastname: Frith
authors.forename: T
authors.initials: T
authors.lastname: Jones
authors.forename: P G
authors.initials: PG
authors.lastname: Camici
mesh_terms: D000344:Afferent Pathways / Q000502:physiology; D000368:Aged; D000787:Angina Pectoris / Q000503:physiopathology; D001921:Brain / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D004280:Dobutamine / Q000008:administration & dosage; D005260:Female; D006321:Heart / Q000294:innervation; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D010146:Pain / Q000503:physiopathology*; D013566:Sympathomimetics / Q000008:administration & dosage; D014055:Tomography, Emission-Computed
chemical_list: D013566:Sympathomimetics; D004280:Dobutamine