(Stroke. 1995;26:1805-1810.)
© 1995 American Heart Association, Inc.
Articles |
Is Blood Pressure Really a Triggerfor the Circadian Rhythm of Subarachnoid Hemorrhage?
From Neurochirurgische Abteilung, Donauspital (G.K., R.S.) and Rudolfstiftung (F.B.), Vienna, Austria.
Correspondence to Dr Günther Kleinpeter, Neurochirurgische Abteilung, Donauspital, Langobardenstraße 122, A-1220 Vienna, Austria.
Background and Purpose 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 (
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
(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.
Key Words: blood pressure • circadian rhythm • subarachnoid hemorrhage
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