title: Is blood pressure really a trigger for the circadian rhythm of subarachnoid hemorrhage?
abstract: OBJECTIVE
  Circadian blood pressure changes are not infrequently cited as a trigger for the onset of subarachnoid hemorrhage (SAH). Our purpose was to determine the reliability of this chronorisk and study the variability and consequences of it as it occurs in hypertensive and normotensive individuals.
  
  
  METHODS
  Of 273 consecutive patients with proven SAH of aneurysmal origin seen between January 1990 and December 1993, we studied 120 (44%) for whom the exact time of hemorrhage could be reliably determined. Beyond the recognition of a circadian rhythm for this collective, the patients were then sorted by blood pressure, yielding one group each of 80 normotensive (group N, 66.7%) and hypertensive (group H, 33.3%) individuals. The differential chronorisk of these two groups was studied.
  
  
  RESULTS
  A circadian rhythm with a definitive characteristic acrophase was observed for the entire group, occurring between 9 AM and 10 AM (chi 2 test, P < .0005) with a possible secondary peak in the afternoon hours. The separation into two blood pressure groups somewhat surprisingly revealed a different curve for each group (chi 2 test, P = .01). Statistical analysis of each group's separate chronorisk revealed that this acrophase only holds true for hypertensive individuals, whereas normotensive patients not only lack a morning peak, but an apparent elevation in the afternoon is statistically irrelevant, leading to the impression that SAH in normotensive persons seems to be subject to no circadian rhythm at all.
  
  
  CONCLUSIONS
  The incidence of SAH conforms to circadian blood pressure variation in hypertensive patients, similar to the diurnal rhythms observed with strokes and myocardial infarctions. This leads to the hypothesis that blood pressure elevation is a trigger for the onset of bleeding in this group. In clear contrast, normotensive individuals with cerebrovascular aneurysms seem to have a random 24-hour distribution of SAH onset times, thus leaving the nature of a possible trigger mechanism unresolved.
authors.affiliation: Neurochirurgische Abteilung, Donauspital, Vienna, Austria.
authors.forename: G
authors.initials: G
authors.lastname: Kleinpeter
authors.forename: R
authors.initials: R
authors.lastname: Schatzer
authors.forename: F
authors.initials: F
authors.lastname: Böck
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology; D002940:Circadian Rhythm; D015331:Cohort Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D015994:Incidence; D002532:Intracranial Aneurysm / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology; D015203:Reproducibility of Results; D012307:Risk Factors; D013345:Subarachnoid Hemorrhage / Q000209:etiology* / Q000503:physiopathology