title: Changes of circadian blood pressure patterns after hemodynamic and thromboembolic brain infarction.
abstract: OBJECTIVE
  We investigated the changes of circadian blood pressure patterns after thromboembolic and hemodynamic brain infarction and evaluated the relation between circadian blood pressure variation, infarct location, and activation of the autonomic nervous system after thromboembolic stroke.
  
  
  METHODS
  Repeated 24-hour blood pressure measurements were performed in 45 patients with proven first-ever brain infarctions of different origins. Evaluation of serum norepinephrine concentration, prolongation of the QT interval, and degree of cardiac arrhythmias were used to determine the extent of sympathetic activation after thromboembolic stroke.
  
  
  RESULTS
  Whereas circadian blood pressure variation was significantly increased after hemodynamic infarction compared with a control group (diastolic, -25.2 +/- 4.5% versus -13.8 +/- 6.5%; p < .005), a clearly reduced variation was observed after thromboembolic infarction (diastolic, -5.2 +/- 6.9%). Blood pressure variation was positively related to serum norepinephrine concentration (r = .79; P < .01) after thromboembolic infarction. Patients with involvement of the insular cortex showed a nocturnal rise of blood pressure significantly more frequently (66.7% versus 11.8%; P < .005) and had higher norepinephrine levels (66.7 +/- 110 pg/mL versus 290 +/- 178 pg/mL; P < .01) than patients without insular cortex infarction, indicating increased sympathetic activity. This was associated with a significantly more frequent occurrence of QT prolongation and cardiac arrhythmias.
  
  
  CONCLUSIONS
  The observed differences in circadian blood pressure patterns may (1) help to distinguish the pathophysiological basis of the stroke, (2) help to explain worsening in some cases of hemodynamic stroke, (3) confirm the importance of the insular cortex for sympathetic activation, and (4) identify subgroups of patients with increased risk of myocardial infarction and arrhythmia.
authors.affiliation: Department of Neurology, Technical University of Munich, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Sander
authors.forename: J
authors.initials: J
authors.lastname: Klingelhöfer
mesh_terms: D000368:Aged; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001794:Blood Pressure; D002544:Cerebral Infarction / Q000503:physiopathology*; D002940:Circadian Rhythm; D003971:Diastole; D004569:Electroencephalography; D005260:Female; D007839:Functional Laterality; D006439:Hemodynamics; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012016:Reference Values; D012737:Sex Factors; D013599:Systole
chemical_list: D009638:Norepinephrine