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Thrombotic Occlusion of the Common
Carotid Artery in Acute Ischemic Stroke
Vijay K Sharma
Consultant Neurologist
National University HospitalSingapore
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Introduction
The commonest cause of CCA occlusion is
attributed to atherosclerosis.
Less frequent causes include1,2,3
Takayasu arteritis
post-radiation arteriopathy cardiac embolism
Syphilis
trauma
homocystinuria etc.
1. Cull DL et al.Ann Vasc Surg1999;13:73-76.
2. Zardi EM et al. Eur J Neurol2006;13:423-424.
3. Tsai CF et al.J Neuroimaging2005;15:50-56.
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Introduction
Acute internal carotid artery (ICA)occlusions have been widely described in
acute ischemic stroke.
Acute CCA thrombosis has rarely, if ever,been reported in detail in patients with
acute cerebral ischemia.
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CCA thrombi in acute ischemic stroke
From September 2005 through May 2006, 47 ischemic stroke
patients received IV-TPA therapy.
Rapid sequence transcranial Doppler (TCD) and cervical
duplex ultrasound were performed in all cases before TPA
bolus.
Most of these patients underwent CT angiography of head
and neck immediately following the brain CT scan.
CCA patency was assessed in all patients during the cervical
duplex examination.
3 out of the 47 patients (6%) were found to have CCA
occlusions before TPA bolus.
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CCA thrombi in acute ischemic stroke
Times elapsed between symptom onset and TPA bolus were Case 1- 145 minutes
Case 2- 115 minutes
Case 3- 160 minutes
Mobile and acute CCA thrombi extending into the internalcarotid (ICA) and external carotid (ECA) arteries were seen inall 3 patients.
CCA occlusions were also seen on CT angiography of neck(n=3)
Conventional digital subtraction angiography, performed inone case confirmed the presence of CCA thromus in onecase.
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Clinical, imaging, sonographic characteristics with recanalization patterns,
neurological recovery and disposition data of the three cases with
acute CCA occlusions
Sharma VK et al. Eur J Neurol 2007;14:237-240
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Case 1- Sonographic and imaging findings
Acute mobile thrombi on transverse (a) and longitudinal (b) views
on B-mode cervical duplex sonography. Computerized tomographic
(c) of neck showing non-opacification (arrows) of right CCA. Final
cerebral infarctions seen on diffusion weighted MRI (d) Note the
thrombus in ICA also (b).
Schematic representation of
CCA occlusion & intracranial
flow patterns..Note anterior
cross-filling of ipsilateral MCA
via ACOM and flow reversal in
ipsilateral ACA.
1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1
segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery.
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Case 2- Sonographic and imaging findings
Acute mobile thrombi on transverse (a) and longitudinal
(b) views on B-mode cervical duplex sonography. s CT
angiogram of neck (c) showing non-opacification of left
CCA. Final cerebral infarctions seen on brain CT scan (d).
1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1
segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery.
Schematic representation of CCA
occlusion and intracranial flow
patterns. It shows thrombotic
occlusion of left CCA, ICA,
ECA,intracranial ICA, ipsilateral MCA
and ACA. No intracranial collateral
flow is seen.
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Case 3- Sonographic and imaging findings
Acute mobile thrombi on transverse (a) and longitudinal(b) views on B-mode cervical duplex sonography. Digital
subtraction angiograms (c) of neck showing non-
opacification of right CCA. Final cerebral infarctions seen
on diffusion weighted MRI (d)
Schematic representation of CCA
occlusion and intracranial flow
patterns. Thrombotic occlusion of
right CCA, ECA, ECA and intracranial
ICA with anterior cross-filling of
ipsilateral MCA via ACOM and flow
reversal in ipsilateral ACA.
1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1
segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery.
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Some salient features
All 3 patients had a history of atrial fibrillation andhypertension
Blood pressure was lowered with nicardipine andmaintained in the systolic range of 160 180 mm
Hg range during the IV-TPA infusion andimmediately thereafter.
All the patients were kept in the head-down (flat)position.1
1. Wojner-Alexander AW et al. Neurology2005;64:1354-1357.
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Some salient features
At 2 hours after IV-TPA bolus, TCD showed complete proximalMCA recanalization in 2 cases despite persistent occlusions ofthe proximal CCA/ICA.
None of our patients achieved CCA or ICA recanalization.
None of our cases showed intracerebral hemorrhage onsubsequent imaging studies.
No immediate neurological improvement was noted during IV-TPA infusion.
NIHSS scores dropped from 10 points at TPA bolus to 5 points
at discharge from the hospital (case 1). NIHSS scores dropped from 12 points at TPA bolus to 3 pointsat discharge from the hospital (case 3).
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Discussion Our patients had CCA occlusions with mobile
intraluminal thrombi. In presence of AF, these thrombi are presumed to
have originated from the heart.
No evidence for a significant underlying
atheromatous lesions were noted ultrasonography. This is in contrast to the existing literature on chronic
CCA occlusions that are mostly atherosclerotic innature.1,2,3
We excluded dissections in the carotid arteries oraortic arch by ultrasound and other imagingmodalities (CTA or DSA).
1. Cull DL et al.Ann Vasc Surg1999;13:73-76.
2. Zardi EM et al. Eur J Neurol2006;13:423-424.3. Tsai CF et al.J Neuroimaging2005;15:50-56.
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Discussion- types of CCA occlusions
Types of CCA occlusion- Type I- isolated CCA occlusion, ICA is patent
and perfused by a retrograde flow originating at
the circle of Willis or in the ECA.1
Type II- CCA occlusion accompanied by
occlusions of ipsilateral ECA and ICA
Type-I CCA occlusions are more frequent.
All our patients had type-II CCA occlusions.
1. Gerlock AJ et al. Applications of noninvasive vascular
techniques. Philadelphia: WB Saunders;1988:88-111.
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DiscussionImportance of intracranial collaterals in CCA occlusions
When acute CCA occlusions extend into the cervical ICA,intracranial collateral flow through communicating arteriesbecomes of utmost significance.
Similar to an isolated ICA occlusion, the competence andefficiency of the circle of Willis collaterals determine theextent and severity of ischemic damage.1,2
T-occlusion of the terminal ICA carries a relatively poorprognosis with failed recanalization by systemicthrombolysis.3
Two out of three of our patients had collateral flows throughthe anterior communicating artery, and milder strokeseverity compared to the patient with CCA occlusion andtandem T-type ICA occlusion.
1. Linfante I et al. Stroke 2002 ;33:2066-2071.
2. El-Mitwalli A et al. Stroke 2002;33:99-102.3. Georgiadis D et al. Neurology2004;63:22-
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Discussion- therapeutic options
Acute thrombus in a large artery like CCArepresents a high clot-burden.
Endovascular therapy1, clot removal by
Mechanical embolectomy 2, and combinedintravenous-intra-arterial thrombolysis3,
alone or in combination, may help in
achieving recanalization in acute largeartery occlusions in acute stroke.
1. Snugg RM et al.AJNR2005;26:2591-2594.
2. Smith WS et al. Stroke 2005;36:1432-1440.
3. The IMS study investigators. Stroke 2004;35:904-
912.
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Conclusions
We have described the sonographic and imaging featuresof CCA occlusions with tandem lesions treated withintravenous TPA.
Acute occlusions of the carotid arteries in acute ischemic
strokes are associated with poor outcomes. However, given the potential for an intracranial
recanalization, patients with acute CCA thromboticocclusions and accompanying tandem lesions may benefitfrom systemic thrombolysis.1,2,3
Acute CCA occlusions should not be considered to belargely associated with poor outcome and a contra-indication for IV-TPA.
1. Linfante I et al. Stroke 2002 ;33:2066-2071.
2. El-Mitwalli A et al. Stroke 2002;33:99-102.
3. Christou I et al. J Neuroimaging2002;12:119-
123.
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Contributors
Tsivgoulis Georgios, MD
Lao, Annabelle Y, MD
Flaster, Murray, MD, PhD Frey, James L MD
Malkoff, Marc D, MD
Alexandrov Andrei V, MD