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(Stroke. 1998;29:2447.)
© 1998 American Heart Association, Inc.

Letters to the Editor

Circadian Rhythm of Heart Rate Variability Is Reversibly Abolished in Ischemic Stroke

A. Bar-Ilan, PhD

Phanos Ltd

Kiryat Weizmann

Rehovot, Israel

To the Editor:

I read with great interest the article by Korpelainen et al,¹ and was very impressed with the finding that the circadian fluctuation in heart rate variability was abolished in the stroke patients. However, I have some difficulty with their attributing this effect to the infarction. I completely agree with the statement that, "The most powerful environmental rhythmic regulator is presumably daylight." It has been reported previously that (1) Light can suppress endogenous circadian amplitude² ; (2) photoperiod-responsive changes in human circadian rhythms may be suppressed by regular exposure to artificial light³ ; and (3) exposure to light of a critical strength at a critical phase can even drive the human circadian pacemaker to its region of singularity, akin to temporarily "stopping" the human circadian clock.⁴

In the article there is no detailed description of the environmental conditions, especially those that affect the circadian rhythms of the patients. Based on personal experience as a patient and as a subject in clinical trials, hospitalized for 3 to 7 days, as well as a parent staying for many weeks with a hospitalized child, I know how disruptive such an environment can be to the normal sleep/awake cycle, and it definitely feels like "jet lag syndrome." Currently, I am not familiar with a well-controled study documenting circadian rhythms under such "real-life hospital" conditions.

The "control" group in this paper is not an appropriate control for these effects, because they were studied in their homes and not exposed to the disruptive hospital environment. As for the "6-month reversibility," was this observed after the same period of hospitalization as the initial one, which was reported to range between 1 and 7 (median, 3) days? If this is not the case, then once again this may not be appropriate for comparison of circadian variations.

I am fully aware of the practical difficulties in establishing the proper control groups, but without such data it is possible to assume that the environmental conditions of the hospitals themselves could have made a significant contribution to the disappearance of the circadian fluctuations in heart rate variability; the contribution of the infarction per se cannot be determined.

References

1. Korpelainen JT, Sotaniemi KA, Huikuri HV, Myllylä VV. Circadian rhythm of heart rate variability is reversibly abolished in ischemic stroke. Stroke.. 1997;28:2150–2154.[Abstract/Free Full Text]

2. Jewett ME, Kronauer RE, Czeisler CA. Light-induced suppression of endogenous circadian amplitude in humans. Nature.. 1991;350:59–62.[Medline] [Order article via Infotrieve]

3. Wehr TA, Giesen HA, Moul DE, Turner EH, Schwartz PJ. Suppression of men's responses to seasonal changes in day length by modern artificial lighting. Am J Physiol.. 1995;269:R173–R178.[Abstract/Free Full Text]

4. Czeisler CA. Circadian clocks and their adjustments. In: CIBA Foundation Symposium 183. Chichester, UK: John Wiley & Sons Inc; 1995:254–302.

Response

Juha T. Korpelainen, MD, PhD; Kyösti A. Sotaniemi, MD, PhD; Vilho V. Myllylä, MD, PhD

Department of Neurology, University of Oulu, Oulu, Finland

We are delighted with Dr Bar-Ilan's interest in our study¹ concerning the effects of stroke on the circadian fluctuation of heart rate variability. We agree that a hospital environment may influence the normal sleep/awake cycle.

In our study, all the ECG recordings for the patients, ie, in the acute phase, at 1 month (data not presented) and at 6 months, were performed in the hospital. At the follow-up visits, the patients spent a few days in the same hospital department and under the same environmental conditions as in the acute phase.

However, we could show that the sleep/awake cycle of heart rate variability had normalized by 6 months after the brain infarction in the stroke patients. Thus, these patients could maintain their normal circadian rhythm of heart rate variability in the hospital despite the various potentially disruptive factors. Therefore, our conclusion is that stroke itself is the major determinant of the observed disappearance of the circadian fluctuation of heart rate variability.

References

1. Korpelainen JT, Sotaniemi KA, Huikuri HV, Myllylä W. Circadian rhythm of heart rate variability is reversibly abolished in ischenic stroke. Stroke.. 1997;28:2150–2154.

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