(Stroke. 2000;31:2026.)
© 2000 American Heart Association, Inc.
Letters to the Editor |
Department of Radiology
Department of Neurosurgery
Department of Radiology,
Bia
ystok Medical Academy,
Bia
ystok, Poland
To the Editor:
The estimates of global cerebral blood flow volume with duplex Doppler sonography, published recently by Scheel and colleagues,1 are of great potential value in clinical practice. Therefore, a substantial dispersion of individual values of flow, as seen in Figure 2 of their article, deserves some comment, all the more so because the range of variability of direct cerebral blood flow measurements was reported to be not so wide.2 3 In this letter we try to contribute to an explanation of both the biological and methodological components of such excessive variability and offer a hypothesis for sex-related differences in flow volume through the external carotid artery, on which the authors were unable to comment. This, however, requires a concise presentation of our research on the effects of the menstrual cycle on cerebral circulation, a study which is still underway.
It has been shown4 5 that the range of blood flow velocities in major cerebral arteries is wider in premenopausal women than in age-matched men. To explore this phenomenon, we attempted to correlate the hormonal status of young women throughout the menstrual cycle with serial Doppler sonographic examinations of carotid arteries. We used a 7.5-MHz linear array transducer (Toshiba 140 SH) and our examination technique was similar to that of Scheel et al.1 To date, we have examined 7 healthy nulliparous women (age range 23 to 25 years) who met the strict entry criteria to the study. Subjects had their cycles standardized to a 28-day period, so the day of ovulation (confirmed also by direct sonographic follow-up of the follicle) was taken as being between days 14 and 15. Every participant was evaluated 11 times: during menses (cycle day 3), during the follicular phase (cycle days 6, 10, 12, 13, and 14), and during the luteal phase (cycle days 15, 16, 17, 20, and 24). All examinations were performed between 6 and 8 AM to minimize the effect of circadian rhythms on cerebral blood flow and metabolism.6 At the same time, cardiac output was investigated with Doppler sonography, and blood was sampled to determine the concentrations of 17ß-estradiol and progesterone and the hematocrit level. To compare changes of velocities in the internal and external carotid arteries, the values of all Doppler parameters were standardized by relating them to the base value of average velocities from 2 initial examinations (days 3 and 6) and were given as percentages.
We found that increased concentration of 17ß-estradiol corresponded
to an increase in the mean and end-diastolic blood flow
velocities within the internal carotid artery, with a higher rate of
these increments between days 10 and 15 of the cycle and an established
elevation in the luteal phase (Figure
).
The mean velocity increment amounted to 111±9% of the base value,
whereas the increment of the systolic velocity was much less
pronounced, at only 102±12% of the base value. As far as the external
carotid artery is concerned, the end-diastolic and mean
velocities were actually found to decrease with increased
concentrations of 17ß-estradiol (Figure
). Cardiac output increased
only slightly in the luteal phase of the cycle. The cross-sectional
area of the examined vessels remained unchanged during the entire
cycle, as did the hematocrit level.
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Our results illustrate the existence of significant changes in the level of flow volume within the carotid arteries throughout the menstrual cycle. The increased velocities, prevailing over the most of the cycle, undoubtedly contribute to variability in the cerebral blood flow, as observed by Scheel et al,1 and may also be responsible for the relatively higher average cerebral blood flow observed in women.
It is accepted that systolic velocity is mainly influenced by cardiac output, and the end-diastolic velocity is thought to increase with decreased peripheral vascular resistance.7 Thus, our results support the argument that the increased flow volume through the internal carotid artery, associated with high concentrations of plasma estrogen, is caused mainly by a decrease in vascular resistance in the brain, presumably due to the direct effect of estrogen on cerebralvessels.8 9 The contribution of increased cardiac output to the greater facilitation of cerebral blood flow was only minimal in our subjects. Furthermore, the flow increase was not correlated with the hematocrit level. Therefore, a relatively stable cardiac output with stable vascular capacity and decreased peripheral resistance in the territory supplied by the internal carotid artery should produce a decrease in flow volume through the external carotid arteryan effect that was actually found in our subjects. Because the reduced flow volume through the external carotid artery in women occurs throughout most of the menstrual cycle, it may appear, in an indiscriminate study, that the flow volume through the external carotid artery is lower in women than in men, an effect that Scheel et al were not able to explain.
In this letter we do not provide absolute values of intravascular blood flow volume in our subjects. Nevertheless, our data may be related to the results of Scheel et al,1 since we have measured the cross-sectional area of the examined vessels with manual tracing and have found them stable during the whole menstrual cycle. It may be of interest to add that we have found a significant difference in the cross-sectional area of the examined vessels between the systole and diastole. On the basis of 184 measurements, we have estimated this difference to be an average of 27.1±9.4% (28.6±4.6 mm2 in systole and 22.5±4.1 mm2 in diastole, t=27, P<0.001) for the common carotid artery, and 14.6±13.5% (12.7±2.7 mm2 in systole and 11.2±2.6 mm2 in diastole, t=8, P<0.001) for the internal carotid artery.
Scheel et al do not specify in which phase of the cardiac cycle they measured the diameter of the vessels, although the differences in the vessel caliber during systole and diastole appear to be quite substantial. Consistency in measurements with respect to the cardiac cycles may improve the reproducibility and decrease the variability of flow volume measurements. Which phase of the cardiac cycle should be selected for appropriate calculation of the vessel diameter and how the flow should be calculated as a product of this cross-sectional area and the flow velocities measured is, of course, a major question that needs to be addressed separately.
References
1.
Scheel P, Ruge C, Petruch UR, Schöning M.
Color duplex measurement of cerebral blood flow volume in healthy
adults. Stroke. 2000;31:147150.
2. Shirahata N, Henriksen L, Vorstrup S, Holm S, Lauritzen M, Paulson OB, Lassen NA. Regional cerebral blood flow assessed by 133Xe inhalation and emission tomography: normal values. J Cereb Blood Flow Metab. 1985;9:861866.
3. Yonas H, Darby JM, Marks EC, Durham SR, Maxwell C. CBF measured by Xe-CT: approach to analysis and normal values. J Cereb Blood Flow Metab. 1991;11:716725.[Medline] [Order article via Infotrieve]
4.
Krejza J, Mariak Z, Walecki J, Szydlik P, Lewko J,
Ustymowicz A. Transcranial color Doppler sonography of
basal cerebral arteries in 182 healthy subjects: age and sex
variability and normal reference values for blood flow
parameters. AJR Am J Roentgenol. 1999;172:213218.
5. Ackerstaff RGA, Keunen RWM, van Pelt W, Montauban van Swijndregt AD, Stijnen T. Influence of biological factors on changes in mean cerebral blood flow velocity in normal ageing: a transcranial Doppler study. Neurol Res. 1990;12:187191.[Medline] [Order article via Infotrieve]
6. Barlett EJ, Brodie JD, Wolf AP, Christman DR, Laska E, Meissner M. Reproducibility of cerebral glucose metabolic measurements in resting human subjects. J Cereb Blood Flow Metab. 1988;8:502512.[Medline] [Order article via Infotrieve]
7. McDonald DA. The numerical analysis of circulatory wave-forms. In: McDonald DA, ed. Blood Flow in Arteries. Baltimore, Md: Williams & Wilkins; 1974:146173.
8.
Mendelsohn ME, Karas RH. The protective effects of
estrogen on the cardiovascular system. N
Engl J Med. 1999;340:18011811.
9. Gangar KF, Vyas S, Whitehead M, Crook D, Meire H, Cambell S. Pulsatility index in internal carotid artery in relation to transdermal estradiol and time since menopause. Lancet. 1991;338:839842.[Medline] [Order article via Infotrieve]
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