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(Stroke. 1996;27:1970-1973.)
© 1996 American Heart Association, Inc.

Articles

Transcranial Doppler Assessment of Cerebrovascular Reactivity in Symptomatic and Asymptomatic Severe Carotid Stenosis

Mauro Silvestrini, MD; Elio Troisi, MD; Maria Matteis, MD; Letizia M. Cupini, MD Carlo Caltagirone, MD

the Clinic of Neurology, "Tor Vergata" University of Rome, and IRCCS "S Lucia," Rome, Italy.

Correspondence to M. Silvestrini, MD, Clinica Neurologica, Universita' di Roma "Tor Vergata," Ospedale "S Eugenio," P.le dell'Umanesimo 10, 00144 Rome, Italy.

	Abstract

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Background and Purpose Some studies have suggested a link between impaired cerebral hemodynamics and stroke in patients with carotid stenosis. The aim of this study was to assess the effects of severe carotid stenosis on cerebrovascular reactivity and the possible changes after endarterectomy.

Methods Using bilateral transcranial Doppler ultrasound, we studied the changes of flow velocity after hypercapnia in the middle cerebral arteries of 10 control subjects and 24 patients (13 symptomatic and 11 asymptomatic) with unilateral severe carotid stenosis before and after endarterectomy. Cerebrovascular reactivity was evaluated with the breath-holding index (BHI).

Results Before endarterectomy, BHI (mean value±SD) was significantly lower (P<.001) in the stenotic side of symptomatic patients (0.40±0.2) than in control subjects (1.12±0.3), the stenotic side of asymptomatic patients (0.80±0.4), and the normal side of both symptomatic (0.93±0.3) and asymptomatic (1.03±0.2) patients. On the other hand, no significant difference in BHI was detected in control subjects, on the normal side of symptomatic and asymptomatic patients, and the stenotic side of asymptomatic patients. After endarterectomy, BHI significantly increased (P<.0001) on the stenotic side of symptomatic patients (1.06±0.2) while remaining substantially stable on the normal side of both symptomatic and asymptomatic patients and on the stenotic side of asymptomatic patients.

Conclusions These findings suggest that the study of cerebrovascular reactivity to hypercapnia may be relevant in evaluating the functional effects of carotid stenosis. Further investigations are needed to confirm the reliability of the breath-holding method in the selection of patients who might benefit most from carotid endarterectomy.

Key Words: carotid stenosis • vasomotor reactivity • ultrasonics

	Introduction

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Abnormal cerebral hemodynamics appear to be an important determinant in the risk of stroke.^{1 2} This is especially true in patients with carotid occlusive disease. In fact, recent studies have documented a significant increased risk in stroke or transient ischemic attacks ipsilateral to a stenosis or occluded internal carotid artery in patients with impaired cerebrovascular reactivity.^{3 4} While the beneficial effects of carotid endarterectomy in the prevention of ischemic problems in patients with symptomatic severe carotid stenosis are now widely acknowledged,^{5 6} the value of surgery for managing asymptomatic carotid stenosis still remains in question.⁷ On the basis of these preliminary considerations, the study of the hemodynamic effects of asymptomatic carotid stenosis could provide an indication of the opportuneness of performing endarterectomy on a subgroup of patients. Transcranial Doppler (TCD) assessment of flow velocity changes after a vasodilatory stimulus has been used widely to assess cerebral vasoreactivity.^{8 9} This method has the advantage of being noninvasive and relatively inexpensive. Moreover, recent studies have shown a good correlation between the hemodynamic information supplied by TCD and regional cerebral blood flow methods.^{10 11 12}

Cerebrovascular reactivity with TCD usually has been assessed by measuring the change in cerebral blood flow velocity occurring in response to a vasodilatory stimulus such as CO₂ inhalation or acetazolamide administration. The breath-holding maneuver has been introduced recently as an alternative, simple method for studying cerebral hemodynamics. Preliminary experience suggests that it can be useful for obtaining functional information in patients with carotid occlusive disease.^{11 13}

The aim of the present study was to further investigate the efficacy of the breath-holding method for assessing cerebral hemodynamic changes associated with severe carotid stenosis. For this purpose, cerebrovascular reactivity to hypercapnia was compared in control subjects and in patients with symptomatic and asymptomatic carotid stenosis. Moreover, we sought to verify whether cerebrovascular reactivity changes occur after carotid endarterectomy. For this reason, the evaluation of the hemodynamic effects of breath-holding was repeated in patients after surgical management of carotid stenosis.

	Subjects and Methods

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The participants in the study were recruited from consecutive patients undergoing ultrasonic examination after a recent (range, 10 to 32 days before examination) transient ischemic attack or as a routine examination in vascular high-risk patients. Inclusion criteria were unilateral severe carotid stenosis and no evidence of permanent neurological deficit. In symptomatic patients, the transient neurological deficit had to be related to vascular failure in the territory of the middle cerebral artery ipsilateral to the carotid stenosis. All the selected patients underwent cerebral angiography, a cardiological examination including electrocardiography, and transthoracic echocardiography and brain computed tomography. Patients with evidence of bilateral carotid stenosis, brain infarction, or any kind of cerebral lesion and embolizing cardiopathy were excluded. The degree of carotid stenosis was measured according to the NASCET criteria.⁶

Twenty-three patients were included: 13 (8 men, 5 women; mean age±SD, 64±9.6) with symptomatic carotid stenosis and 11 (6 men, 5 women; mean age±SD, 63±11.8) with asymptomatic carotid stenosis. Degree of carotid stenosis (mean±SD) was 83.5±6% in symptomatic and 83.09±5.4% in asymptomatic patients. Ten healthy control subjects (6 men, 4 women; mean age±SD, 63±11) were also evaluated. They were recruited from consecutive patients undergoing ultrasonic examination, which excluded any carotid stenosis. Percentage of subjects with risk factors for vascular disease in the group of control subjects and symptomatic and asymptomatic patients, respectively, was 60%, 69.2%, and 63.6% for hypertension; 30%, 30.7%, and 36.3% for diabetes mellitus; and 40%, 23%, and 36.3% for hypercholesterolemia. The study was performed in the early morning. All subjects had abstained from caffeine- and alcohol-containing beverages and smoking for at least 12 hours before the study. Bilateral simultaneous flow velocity recording of the middle cerebral arteries (MCAs) was obtained with a Multi-Dop X/TCD transcranial Doppler instrument (DWL Elektronische Systeme GmbH). Two dual 2-MHZ transducers fitted on a headband and placed on the temporal bone window were used to obtain a bilateral continuous measurement. Vascular reactivity to hypercapnia was studied by calculating the breath-holding index (BHI). This index is obtained by dividing the percentage increase in mean flow velocity (MFV) occurring during breath-holding by the time (seconds) subjects hold their breath after a normal inspiration. The MFV at rest was obtained by the continuous recording of a 2-minute period of breathing normal room air. The MFV over 4 seconds was then recorded after a breath-holding period. A fixed period of 30 seconds was arbitrarily chosen for breath-holding. The efficacy of the breath-holding was checked by means of a respiratory activity monitor (Normocap-oxy, Datex). With this kind of procedure, this method of induction of hypercapnia proved to be effective and reproducible in the study of cerebral hemodynamics.^{14 15} Mean blood pressure and heart rate were continuously monitored by means of a blood pressure monitor (2300 Finapress, Ohmeda). All recordings were performed by the same operator, who was unaware of the patients' clinical status and of the results of the extracranial carotid studies. In patients, the examination was repeated 1 month after carotid endarterectomy. Control subjects performed the evaluation twice, at a 20- to 30-day time interval.

The study was approved by the local ethics committee, and each subject gave informed consent.

Data from control subjects were analyzed by use of a two-way ANOVA (BHI as dependent factor) with status (first examination, second examination) and side (right, left) as within-subject factors. Since the four values (right/left sidexfirst/second examination) were not statistically different, one of them was randomly selected for each subject; this data set was separately compared with the BHI in the MCAs ipsilateral and contralateral to carotid stenosis of symptomatic and asymptomatic patients before endarterectomy by application of a two-way ANOVA (BHI as dependent factor) with the group (control subjects, symptomatic patients and asymptomatic patients) as the between-subject factor and side (control subjects' random side, patients' normal side, and patients' stenotic side) as the within-subject factor. In patients, the effect of endarterectomy on cerebral vasoreactivity was analyzed by use of a three-way ANOVA (BHI as dependent) with the group (symptomatic and asymptomatic patients), status (before and after endarterectomy), and side (stenosis and normal) as within-subject factors.

	Results

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Table 1 shows mean values of MFV and BHI in control subjects and patients. Mean values of resting MFV were not statistically different in control subjects and patients, and they did not change significantly after carotid endarterectomy. Table 2 shows the individual values of BHI in control subjects and in patients before and after endarterectomy.

View this table: [in this window] [in a new window]   Table 1. Values of Resting Middle Cerebral Artery MFV and BHI in Control Subjects and Patients Before and After Endarterectomy

View this table: [in this window] [in a new window]   Table 2. Values of BHI Before and After Carotid Endarterectomy in Symptomatic and Asymptomatic Patients

Comparison of BHI in control subjects and in the two groups of patients before endarterectomy showed that the group effect was significant (F=5.6; P<.01; df, 2,31). In fact, the mean value of BHI was 1.12 in control subjects, 0.9 in asymptomatic patients, and 0.66 in symptomatic patients, considering both normal and stenotic sides. The side effect was significant (F=41.1; P<.001; df, 1,31). This was due to the fact that the mean value of BHI, considering both symptomatic and asymptomatic patients, was 0.6 on the stenotic side and 0.98 on the normal side. Finally, the groupxside interaction was significant (F=15.5; P<.001; df, 2,31). Post hoc comparison (Scheffe's test) showed that this was due to the fact that while no significant difference was found between control subjects and normal side in either group of patients and between control subjects and stenotic side in asymptomatic patients, BHI values were significantly lower on the stenotic side of symptomatic patients compared with control subjects (P<.001), the stenotic side of asymptomatic patients (P<.001), and the normal side of both symptomatic (P<.001) and asymptomatic (P<.001) patients.

With regard to the BHI values before and after endarterectomy, the groupxstatusxside interaction was significant (F=4.73; P<.05; df, 1,22). Post hoc comparison (Scheffe's test) revealed that this was due to the fact that mean value of BHI on the stenotic side was significantly lower before than after endarterectomy in symptomatic patients (P<.0001). On the contrary, no difference was found in asymptomatic patients. On the normal side, values of BHI were not significantly different before and after surgery in both groups of patients.

Heart rate and mean blood pressure showed a slight and comparable increase in the three groups of subjects at the end of the breath-holding period.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Due to the evidence of the beneficial effect of surgical management of symptomatic severe carotid stenosis on the risk of stroke,^{5 6} attention has been focused on the question of the efficacy of surgery in patients with asymptomatic stenosis.¹⁶ Clinical trials suggest that in these patients, carotid endarterectomy can significantly lower the risk of cerebrovascular events and death if surgery is performed in medical centers with documented low perioperative morbidity and mortality and if patients are carefully selected.¹⁷ This general indication will be best applied when selection criteria become evident. The degree and morphology of carotid stenosis may have relevance in this respect. In fact, the risk of stroke increases with the degree of carotid stenosis,^{18 19} and ulceration and lumen thrombus of the carotid plaque have been reported to play a role in symptom development.^{20 21} On the other hand, evidence exists about the relevance of abnormal intracerebral hemodynamics in the risk of stroke and transient ischemic attacks. Several studies suggest that measurement of cerebrovascular reactivity is a reliable assessment of the hemodynamic effects of a carotid stenosis.^{4 22} In fact, this approach takes into account the collateral supply. In this study, we found a significant difference in cerebral hemodynamic consequences between symptomatic and asymptomatic carotid stenosis. In fact, while no difference was present in control subjects, stenotic and normal side of asymptomatic patients and normal side of symptomatic patients, cerebrovascular reactivity was significantly lower ipsilateral to symptomatic carotid stenosis than in control subjects, on the stenotic side of asymptomatic patients, and on the normal side of both symptomatic and asymptomatic patients. Moreover, in symptomatic patients, we found a significant improvement of cerebrovascular reactivity after endarterectomy. In fact, the values of BHI significantly increased after surgery on the stenotic side. These findings suggest that reduced reactivity to hypercapnia can be considered a marker of increased risk of ischemia. This does not necessarily imply that cerebrovascular disorders in symptomatic patients should be considered exclusively on a hemodynamic basis. Other mechanisms, in particular microembolism, have been repeatedly reported and suggested as pathogenetic mechanisms of cerebral ischemia in patients with symptomatic carotid stenosis.^{23 24} These two mechanisms do not contradict each other. In fact, there is evidence suggesting that in areas of the brain where there is limited capacity for further capillary vasodilatation, microemboli are more likely to become symptomatic.²⁵

To investigate cerebrovascular reactivity, we used a simple, noninvasive method that appears to be particularly useful, especially after demonstration of the possible induction of intracerebral steal and transient ischemic attacks after acetazolamide administration.²⁶ A relevant aspect of our study is that in some patients with asymptomatic stenosis, the values of the BHI before endarterectomy were very low and similar to those of most symptomatic patients, and they significantly increased after surgery (Table 2; asymptomatic patients Nos. 3, 4, 7, and 8). This kind of hemodynamic behavior could suggest the need for a more aggressive approach toward this subgroup that could be predisposed to become symptomatic. This is obviously a hypothesis to evaluate further. In fact, the presence of a threshold of critically reduced cerebrovascular reactivity and its possible link with an increased risk of cerebral ischemic events in patients with asymptomatic carotid stenosis can only be demonstrated with prospective studies.

Received May 13, 1996; revision received July 19, 1996; accepted July 25, 1996.

	References

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Silvestrini, M. Articles by Caltagirone, C. Search for Related Content PubMed PubMed Citation Articles by Silvestrini, M. Articles by Caltagirone, C.