(Stroke. 1999;30:2759-e.)
© 1999 American Heart Association, Inc.
Letters to the Editor |
Cerebrovascular Reactivity in Internal Carotid Artery Occlusion
Division of Neurology, Department of Medicine, Queen Mary Hospital, Hong Kong
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To the Editor:
Vernieri and colleagues1 concluded in their recent article that treatment options in internal carotid artery occlusion can be differentiated on the basis of cerebral hemodynamic status. Specifically, their results has demonstrated that the breath-holding index (BHI) in the middle cerebral artery detected by transcranial Doppler ultrasonography (TCD) is predictive of cerebrovascular ischemic symptoms ipsilateral to the internal carotid artery occlusion. Finally, the authors suggest the use of BHI in selecting patients for the classic or a new type of surgical extracranial/intracranial bypass study. I would like to raise the following comments.
First, "carotid stump syndrome" is a well-known phenomenon: continual episodes of transient ischemic attack (TIA) and/or stroke ipsilateral to an occluded internal carotid artery; embolism has been implicated in the pathogenesis, and border-zone infarction is less common.2 3 The source of emboli includes the ipsilateral internal carotid artery stump, the ipsilateral external carotid artery, the contralateral internal and external carotid arteries, the vertebrobasilar system, and the heart. In the study by Vernieri and colleagues,1 patients with significant stenosis of the contralateral carotid artery system, significant vertebral artery disease, or cardiac source of emboli were excluded. These exclusions might have resulted in a lower rate of ischemic stroke, especially on the side contralateral to the carotid artery occlusion, and augmented the importance of hemodynamic mechanisms in producing cerebrovascular ischemia. In addition, I am interested in knowing whether there was any significant stenosis in the external carotid artery ipsilateral to the internal carotid artery occlusion.
Second, CT or MRI of the brain was performed at baseline in all the patients with internal carotid artery occlusion, but the neuroimaging findings were not described in the article.1 This information may be important because some "asymptomatic" patients and some symptomatic patients with "TIA only" could have "silent" cerebral infarcts. Specifically, I wonder whether the neuroimaging findings at baseline can predict outcome events and whether there is an alternative way of categorizing the patients with internal carotid artery occlusion.
Third, TCD findings are affected by both intracranial and extracranial arterial diseases,4 and near-occlusion may be misdiagnosed as occlusion by carotid ultrasonography.5 Conventional angiography was performed in all 42 symptomatic patients and in 3 of 23 asymptomatic patients. I would like to know the reasons for performing conventional angiography in these patients, because carotid endarterectomy is not considered in patients with an occluded internal carotid artery.6 If the invasive angiography was performed to detect significant intracranial disease, this information was not available from 20 of 23 asymptomatic patients; I wonder whether MR angiography was used in some of the patients.
Fourth, apnea for 30 seconds after a "normal" inspiration was used to elicit changes in the mean flow velocity at the middle cerebral artery and generate the BHI, and some training was arranged for the patients.1 Thirty seconds of apnea is quite long, and I wonder whether hyperventilation (and thus hypocapnia) was present before the definitive recording. A difference between the initial end-tidal CO2 and the end-tidal CO2 prior to breath-holding would reveal any significant hyperventilation. I also wonder whether the BHI should be corrected for or adjusted according to the degree of change in the end-tidal CO2, since this is the chief driving force for changes in the mean flow velocity.
Fifth, I am interested in knowing how "stable" or reproducible the BHI is in an individual patient. This is an important factor in determining the usefulness of the BHI in selecting patients with internal carotid artery occlusion for any type of surgical extracranial/intracranial bypass study.1 It would be interesting to have repeated measurements of the BHI during follow-up to see whether a change in the BHI may occur before any cerebrovascular ischemic event.
Finally, the authors emphasized the importance of hemodynamic mechanism in producing ischemic cerebrovascular events, and hypertension was present in 39 of 65 patients.1 I am interested in knowing the aggressiveness of blood pressure control in these 39 patients, because treatment of hypertension may compromise the cerebral hemodynamics in the presence of internal carotid artery occlusion and inadequate collaterals.7 In addition, the authors did not elaborate on the use of medical treatment such as aspirin and the control of vascular risk factors, nor explain how the outcome events were documented.
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Vernieri F, Pasqualetti P, Passarelli F, Rossini
PM, Silvestrini M. Outcome of carotid artery occlusion is predicted by
cerebrovascular reactivity. Stroke.. 1999;30:593–598.
[Abstract/Free Full Text] -
Cote R, Barnett HJ, Taylor DW. Internal carotid
occlusion: a prospective study. Stroke.. 1983;14:898–902.
[Abstract/Free Full Text] - Quill DS, Colgan MP, Sumner DS. Carotid stump syndrome: a colour-coded Doppler flow study. Eur J Vasc Surg.. 1989;3:79–83.[Medline] [Order article via Infotrieve]
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Wilterdink JL, Feldmann E, Furie KL, Bragoni M,
Benavides JG. Transcranial Doppler ultrasound battery
reliably identifies severe internal carotid artery stenosis.
Stroke.. 1997;28:133–136.
[Abstract/Free Full Text] - Gortler M, Niethammer R, Widder B. Differentiating subtotal carotid artery stenosis from occlusion by color-coded duplex sonography. J Neurol.. 1994;241:301–305.[Medline] [Order article via Infotrieve]
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Moore WS, Barnett HJM, Beebe HG, Bernstein EF, Brener
BJ, Brott T, Caplan LR, Day A, Goldstone J, Hobson RW II, Kempczinski
RF, Matchar DB, Mayberg MR, Nicolaides AN, Norris JW, Ricotta JJ,
Robertson JT, Rutherfold RB, Thomas D, Toole JF, Trout HH III,
Wiebers DO. Guidelines for carotid endarterectomy:
a multidisciplinary consensus statement from the Ad Hoc Committee,
American Heart Association. Stroke.. 1995;26:188–201.
[Abstract/Free Full Text] -
Ruff RL, Talman WT, Petito F. Transient
ischemic attacks associated with hypotension in hypertension
associated with carotid stenosis. Stroke.. 1981;12:353–355.
[Abstract/Free Full Text]
Response
Clinica Neurologica, Università di Roma Tor Vergata, IRCCS S. Lucia
AFaR-CRCCS: Divisione di Neurologia, Ospedale Fatebenefratelli, Isola Tiberina, Rome, Italy
Key Words: carotid occlusion • cerebrovascular
circulation • stroke
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We thank Dr Cheung for his interest in our work. However, we are quite concerned about some of his comments regarding the general interpretation of our results.1
Dr Cheung suggests that our finding of an increased risk of cerebral ischemic events ipsilateral to a carotid occlusion in the presence of reduced cerebrovascular reactivity can be due to some problems with the selection of patients, which leads to an increased probability of hemodynamic with respect to embolic infarcts. We think that the study of the outcome of carotid occlusion should not be interpreted as a challenge for supporters of the embolic and hemodynamic mechanisms of ischemic cerebrovascular events. In the Discussion section, we have emphasized that the relationship between impaired cerebral hemodynamics and the risk of ischemic events does not automatically mean that all TIAs and strokes occurring in patients with carotid occlusion are exclusively on an hemodynamic basis. It is probable that the hemodynamic and embolic mechanism can act synergically.2 Moreover, in the final part of the Discussion section, we have acknowledged that the possible application of our results to some of the conditions mentioned by Dr Cheung (ie, significant stenosis of the carotid system contralateral to the occlusion) should be validated by additional studies. For these considerations, we do not share all the concerns expressed in the first comment of Dr Cheung’s letter. Regarding the second point, information about baseline brain CT or MR is required. The inclusion of patients and their classification as TIA, stroke, and asymptomatic patients was based on clinical criteria confirmed by neuroradiological findings. We agree that the study of any further way of categorizing the patients (including the neuroimaging finding) and predicting their outcome can be of interest. However, as clearly specified in the article, our aim was to study the possibility of obtaining prognostic indications on the basis of intracranial hemodynamic status and clinical characteristics of patients, with particular attention to vascular risk factors. Basal neuroimaging findings, as well as other variables, were not the object of our study. Conventional angiography was performed in hospitalized patients as part of a routine investigation aimed to optimize treatment and exclude significant contralateral carotid or ipsilateral external carotid stenosis as well as severe intracranial atherosclerotic disease. The problem of the possible presence of intracranial significant stenosis cannot be fully excluded in asymptomatic patients, in whom angiography was not performed. However, no sign of such a condition was detected on transcranial Doppler basal investigation. Moreover, we would like to add that in Caucasian subjects, the presence of severe intracranial steno-occlusive disease, as opposed to extracranial atherosclerosis, is not frequent.3 MR angiography was performed in about one-third of asymptomatic patients, as part of an ongoing study. The results of this evaluation were always in accordance with ultrasonographic findings.
The breath-holding method has been widely employed in the study of cerebrovascular reactivity. A recent study4 on functional MRI confirmed the ability of voluntary apnea to provide information about cerebral hemodynamic status. We agree that a hyperventilation before apnea can alter the results. For this reason, as clearly described in the Subjects and Methods section, subjects hold their breath for 30 seconds after normal respiratory activity, which was checked by means of a respiratory monitor. At the end of the apnea period, the end-tidal CO2 does not reach a stable value, so that the recording of such a variable can only be used to confirm the efficacy of the apnea and the full cooperation of the study subjects. The problem of the reproducibility of the breath-holding index (BHI) values in individual patients, as underlined by Dr Cheung, is of fundamental importance for determining the usefulness of this method in selecting patients with carotid occlusion for any type of surgical extracranial/intracranial bypass study. We have experience that with all the methodological precautions used in our study, individual BHI values are highly reproducible.5 As a further confirmation of this, 15 patients with normal and 12 with pathological BHI were investigated on 2 (18 patients) or 3 occasions (9 patients) at 2- to 3-month intervals. In all cases, the results confirmed the inclusion of every single patient in the normal or pathological BHI group. The problem of pharmacological treatment in patients with carotid occlusion is debated. All patients included in our study were on antiplatelet therapy with aspirin 325 mg daily (88%) or ticlopidine 500 mg daily (12%). Furthermore, all patients had the best medical treatment for any treatable vascular risk factor. In particular, careful attention was paid in the treatment of hypertension, with the aim of obtaining values of systolic and diastolic pressure, respectively, in the range of 130 to 145 and 80 to 85 mm Hg. A more aggressive treatment was avoided, as suggested by the study of Widder et al.6
Finally, patients in our study were followed up by telephone every 3 months and reevaluated clinically every 6 months by 1 designated individual, who was unaware of the transcranial Doppler data investigator. In the case of events not directly observed in our hospital, clinical records were acquired for an exact description. In particular, special attention was paid to transient neurological deficits that were accepted as TIAs only if a rigorous evaluation had been performed during the first hours/days after the onset of symptoms, including the exclusion of other possible causes of transient neurological deficits.
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References |
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TopIntroductionReferencesIntroduction References |
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- Vernieri F, Pasqualetti P, Passarelli F, Rossini PM, Silvestrini M. Outcome of carotid artery occlusion is predicted by cerebrovascular reactivity. Stroke.. 1999;30:593–598.
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Caplan LR, Hennerici M. Impaired clearance of emboli
(washout) is an important link between hypoperfusio, embolism, and
ischemic stroke. Arch Neurol.. 1998;55:1475–1482.
[Abstract/Free Full Text] -
Kappelle LJ, Eliasziw M, Fox AJ, Sharpe BL, Barnett
HJM. Importance of intracranial atherosclerotic disease in patients
with symptomatic stenosis of the internal carotid
artery. Stroke.. 1999;30:282–286.
[Abstract/Free Full Text] -
Kastrup A, Li T-Q, Takahashi A, Glover GH, Moseley ME.
Functional magnetic resonance imaging of regional cerebral blood
oxygenation changes during breath holding.
Stroke.. 1998;29:2641–2645.
[Abstract/Free Full Text] - Silvestrini M, Troisi E, Matteis M, Cupini LM, Bernardi G. Effect of smoking on cerebrovascular reactivity. J Cereb Blood Flow Metab.. 1996;16:746–749.[Medline] [Order article via Infotrieve]
- Widder B, Kleiser B, Krapf H. Course of cerebrovascular reactivity in patients with carotid artery occlusion. Stroke.. 1994;25:1963–1967.[Abstract]
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