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(Stroke. 1995;26:2071-2074.)
© 1995 American Heart Association, Inc.
Articles |
Transcranial Doppler Ultrasound in Hypertensive Versus Normotensive Patients After Aneurysmal Subarachnoid Hemorrhage
From the Department of Neurosurgery, University Hospital, Lund, Sweden.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose Arterial hypertension is a negative prognostic risk factor after aneurysmal subarachnoid hemorrhage (SAH). Transcranial Doppler ultrasound is commonly used for measuring blood flow velocities to predict cerebral ischemia due to vasospasm after SAH. Our purpose was to evaluate the influence of arterial hypertension on blood flow velocities in the cerebral circulation after aneurysmal SAH.
Methods With transcranial Doppler ultrasound we compared the blood flow velocities in matched groups of hypertensive and normotensive patients with aneurysmal SAH. Twenty-four patients with arterial hypertension were examined daily during a 2-week period. As controls, 24 normotensive patients, also with SAH, were matched by age, sex, neurological status, and clinical outcome.
Results Minimum, mean, and maximum flow velocities in the middle cerebral artery in the hypertensive patients were significantly lower than in the normotensive individuals, with P=.02 for minimum, P=.02 for mean, and P=.02 for maximum. There was no statistical significance for pulsatility index differences in these groups (P=.45). Diastolic notch was noted in two of the hypertensive and in six of the normotensive patients.
Conclusions The results indicate that even moderately increased flow velocities in hypertensive patients may represent significant vasospasm.
Key Words: blood flow velocity • hypertension • subarachnoid hemorrhage • ultrasonics
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The use of TCD and the value of measuring blood flow velocities to predict cerebral ischemia due to vasospasm after SAH are widely accepted.1 2 3 4 5 6 7 8 9 10 11 12 13 14 A velocity increase of more than 50 cm/s within 24 hours has been shown to be a reliable predictor for development of delayed cerebral ischemia.15 16
The physiological variables known to influence blood velocity in the intracranial arteries are age, hematocrit, sex, metabolic factors, and cardiac output.17 The influence of AH on blood flow velocities after SAH has to our knowledge not been evaluated.
Preexisting AH is a negative prognostic risk factor after aneurysmal SAH.18 19 20 21 22 23 AH also increases the risk for the formation of multiple aneurysms.18 24 Chronically elevated blood pressure causes structural changes in the cerebral arterioles and small arteries, predisposing them to thrombosis and hemorrhage.23 25 AH induces medial thickness in the cerebrovascular bed, resulting in an increased peripheral resistance.26 27
The aim of this study was to compare TCD parameters (velocity, waveform, PI, diastolic notch) after SAH in normotensive patients versus patients with verified AH.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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From 1992 to 1994, 24 patients with aneurysmal SAH and AH treated at our department were examined with TCD daily during a 2-week period. As matched controls, 24 normotensive patients with SAH were recruited from the same time span. Hypertensive and normotensive patients were matched by (1) age, (2) sex, (3) neurological status evaluated according to the Reaction Level Scale (RLS 85)28 at admission, and (4) clinical outcome. We matched the patients to avoid influences that might affect the TCD flow velocities (Table
).
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Arterial Hypertension
A patient was classified as having AH if he or she had undergone
antihypertensive treatment at the time of the SAH or if there was a
medical record of previous treatment confirmed by medical files
and/or relatives. A patient with elevated blood pressure on
admission only was not classified as having AH.
It was not considered relevant to compare the arterial blood pressure between the normotensive and the hypertensive groups during the stay at our unit because the blood pressure presumably was affected by such factors as headache, physiological conditions, and intravenous administration of the calcium antagonist nimodipine. Statistically, one or two of the normotensive patients might have an unidentified AH. However, at follow-up 3 to 6 months after discharge all 24 patients in the normotensive group showed a normal arterial blood pressure.
TCD
All transcranial measurements were conducted
transtemporally with the use of a 2-MHz transducer, and the
examinations on the neck were performed with a 4-MHz probe (EME TC-64
Eden Medical Electronics).
The transcranial recordings were routinely performed on the MCA. The normal range for mean flow velocity is 62±12 cm/s. Arterial narrowing or vasospasm is suspected when the mean flow velocity in the MCA exceeds 120 cm/s.
Permanent recordings were documented on a videographic printer (Sony VP 850) for later analysis.
TCD Parameters Studied
In addition to minimum, mean, and maximum flow velocities, the
waveform was studied for (1) the presence or absence of
diastolic notch, (2) the width of the complexes, and (3)
the PI. PI is the amplitude of the blood flow velocity waveform
(systolic minus end-diastolic values) divided by the
velocity mean value.29
Anti-Ischemic Treatment
The calcium antagonist nimodipine was administered
to all patients as a preventive treatment for cerebral vasospasm. In
patients with delayed ischemia, a combination of colloids and
crystalloids was given, aiming at a central venous pressure between 10
and 12 cm H2O. In some patients with arterial
blood pressure below 160 mm Hg, additional dopamine was given.
Statistical Analysis
The TCD recordings in the different groups were compared
by Mann-Whitney U test; P<.05 was considered
significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Minimum, mean, and maximum flow velocities in the MCA in the hypertensive patients were significantly lower compared with flow velocities in the normotensive patients. The hypertensive mean values were similar to the minimum values for the normotensive patients. The differences were statistically significant, with P=.02 for minimum, P=.02 for mean, and P=.02 for maximum flow velocities in the MCA (Figure
). Thirteen patients
(54%) in the normotensive group and 8 patients (33%) in the
hypertensive group showed mean flow velocities in the MCA exceeding 120
cm/s.
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In the normotensive group, 8 patients (33%) developed delayed ischemic deficit compared with 5 hypertensive patients (21%). Clinical outcome after 3 months was equal: 1 patient in each group showed permanent symptoms attributable to delayed ischemia. There was no statistical significance for any PI differences in these groups (P=.45). Diastolic notch was noted in 2 of the hypertensive and in 6 of the normotensive patients. Four patients (17%) with hypertension had more than one aneurysm compared with none of the normotensive patients.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The results of this study indicate a significant difference in TCD minimum, mean, and maximum blood flow velocities between patients who previous to the SAH had either normotensive or hypertensive arterial blood pressure. We could not find any significant differences in the waveform30 or the PI between these groups. The reduced velocity in the MCA in hypertensive patients could from a theoretical point of view be explained by a relatively larger MCA diameter, ie, less vasospasm. A more attractive explanation, however, would be that the increased peripheral resistance in hypertensive patients accounts for the decreased MCA flow velocity. This phenomenon mimics what happens in healthy subjects with induced hypocapnia31 : the peripheral vasoconstriction significantly reduces the MCA blood flow velocity.
Another explanation is an altered (reduced) cardiac output in hypertensive individuals. A combination of these effects cannot be excluded. Furthermore, an increased medial thickness, with or without luminal changes, has been observed in the cerebral vascular bed in chronic hypertension.23 26 27 32 PI is an arithmetic measure describing waveform appearance. Theoretically, the pulsatile spectra would be influenced/changed in patients with chronic arterial hypertension. Deviations that increase pulsatility include systemic factors such as bradycardia, aortic valve incompetence, and/or increases in vascular resistance distal to the large conductance arteries.17 Similarly, damped appearance may represent the effects of a proximal stenosis or a lowered vascular resistance distal to the circle of Willis.
In SAH, however, PIs are known not to be useful in detecting vasospasm and give no supplementary information on local changes in vascular resistance.33 Consequently, increased peripheral resistance in chronic hypertension may not be expected to influence PI. Ferrara et al34 in 1995 examined patients with AH who were otherwise healthy and not on medication. In contrast to our results, they demonstrated no difference in MCA flow velocity between hypertensive and normotensive individuals. This difference is unclear. However, several differences are present between the two reports. First, the patients in the series of Ferrara et al had no intracranial pathology. Second, the mean age in our series is 10 years older. It is well known that the peripheral resistance increases with duration of the disease (AH). Third, a substantial percentage (23%) of the patients of Ferrara et al had never been on antihypertensive treatment, ie, their disease was recently discovered and most probably had been of shorter duration. In our hypertensive group all patients were on medication for AH. Letcher et al35 showed in 1983 that patients with marginal elevations of arterial pressure exhibit increased blood viscosity in direct proportion to the degree of blood pressure elevation.
An increased blood viscosity results in decreased cerebral blood flow, which might contribute to the lower TCD flow velocities demonstrated among the AH patients in our study. A crucial factor in this study is patient matching. The physiological variables that are known to influence blood velocity in the intracranial arteries are age, hematocrit, sex, metabolic factors, and cardiac output.17 Age and sex are the only two parameters that from a practical point of view are possible to correctly match. Thus, these two parameters, combined with neurological status on admission and clinical outcome, were matched. Several authors have reported that hypertensive blood pressure predisposes individuals to stroke and the formation of aneurysms in the cerebral arteries.18 24 There are strong indications for multiplicity of aneurysms in AH patients, which was also observed in this study, in which 17% of the hypertensive versus none of the normotensive patients had multiple aneurysms. AH is a negative prognostic risk factor after aneurysmal SAH. Brandt et al36 in 1991 demonstrated that the preventive use of the calcium antagonist nimodipine probably eliminates the difference in outcome between hypertensive and normotensive patients. Except for the vascular effects, nimodipine seems to have a direct neuronal protective effect. It has been demonstrated that nimodipine has a more pronounced effect on potential operated channels and therefore is expected to be more potent in hypertensive patients.36
In agreement with our previous nimodipine study,36 there was no difference in clinical outcome between the hypertensive and normotensive patients in this study. Based on the observed results, even moderately increased TCD flow velocities in hypertensive patients may represent significant vasospasm with compromised cerebral blood flow. Consequently, such patients should be subjected to additional anti-ischemic treatment, including hypervolemia, hemodilution, and induced hypertension.
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Selected Abbreviations and Acronyms |
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Footnotes |
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Reprint requests to H. Säveland, MD, Department of Neurosurgery, University Hospital, S-221 85 Lund, Sweden.
Received April 3, 1995; revision received July 10, 1995; accepted July 13, 1995.
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References |
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