Commentary
Late spontaneous recanalization of symptomatic atheromatous internal carotid artery occlusion
Vascular 2015, Vol. 23(2) 211–216 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114535392 vas.sagepub.com
Montserrat G Delgado1, Pedro P Vega2, Carlos H Lahoz1 and Sergio Calleja1
Abstract Introduction: Definitive treatment of symptomatic atheromatous internal carotid artery occlusion remains controversial, as far as in rare cases, late spontaneous recanalization has been seen. Methods: We consecutively studied 182 patients (January 2003 to August 2012) with an ischemic stroke in the internal carotid artery territory and diagnosis of atheromatous internal carotid artery occlusion during hospitalization. Findings: Seven patients presented a late spontaneous recanalization (>3 months) of the internal carotid artery. We described therapeutic attitude according to usual care in these patients. Conclusions: The authors attempt to highlight the unusual condition of recanalization after a symptomatic atheromatous chronic internal carotid artery occlusion. If these patients can be treated similar to patients with asymptomatic carotid pathology, then this needs to be clarified. However, due to the risk of ipsi- and contralateral ischemic strokes, revascularization techniques should be considered in certain cases. More studies are needed to establish the most appropriate therapeutical approach in order to avoid arbitrary treatment of these patients.
Keywords Carotid occlusion, carotid recanalization, spontaneous recanalization
Introduction Definitive treatment of symptomatic chronic atheromatous internal carotid artery (ICA) occlusion remains controversial, as far as in rare cases, late spontaneous recanalization has been described. We describe therapeutic attitude according to usual care in seven patients with late recanalization (>3 months), and we review similar cases described in the literature.
Methods We studied consecutive patients with ischemic stroke admitted to the University Hospital of Oviedo (Spain) from January 2003 to August 2012. Inclusion criteria were ischemic stroke in the ICA territory, diagnosis of ICA occlusion during hospitalization using angiographic sequences of magnetic resonance angiography (MRA) or computed tomography angiography (CTA), and atheromatous etiology. Exclusion criteria were interventional treatment at the time of admittance or
during hospitalization, patients with previously known ICA occlusion, and ICA occlusion of etiology other than atheromatous. Patients with a diagnosis of ICA occlusion made using duplex echography without confirmation by other angiographic study were also excluded. After discharge, patients were followed up by carotid duplex. We defined late recanalization as more than three months from the initial diagnosis. If recanalization was suspected, a complementary angiographic study (MRA or CTA) was performed in order to avoid the possibility of mistaking a near occlusion of the ICA by echography. Because of its cost, 1 Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Spain 2 Department of Radiology Service, Hospital Universitario Central de Asturias, Oviedo, Spain
Corresponding author: Montserrat G Delgado, Servicio de Neurologı´a, Hospital Universitario Central de, C/ Celestino Villamil s/n, 33006 Oviedo, Spain. Email: [email protected]
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
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Vascular 23(2)
Figure 1. Patient 2—coronal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
Figure 2. Patient 3—coronal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
Figure 3. Patient 5—longitudinal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
availability, and efficacy, CTA was more frequently used than MRA. The CTA was obtained with a 64 multidetector-array technology in helicoidal with slice thickness 1.25 mm. Acquisition delay depended on the bolus test of 20 mL (15–20 s). Helical acquisition that
started from the aortic arch to the circle of Willis was initiated 20 s after the start of injecting 120-mL nonionic contrast medium. Projections were reconstructed in axial, sagittal, and coronal planes. All images were analyzed by a neuroradiologist.
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Male
Male
Female
5
6
7
86 y
64 y
86 y
66 y
79 y
67 y
78 y
Age
Dysarthria and left hemiparesis
Aphasia and right arm paresis
Left hemiparesis
Left hemiparesis
Language disturbances
Aphasia and right hemiparesis
Transient aphasia and right hand paresis
Symptomatology
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
Clopidogrel þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 100 þ LMWH 0.4
Initial treatment
10 May 2009
15 December 2009
22 December 2008
19 May 2008
19 February 2008
17 June 2008
15 June 2003
Date of occlusion
Subacute right watershed stroke (posterior and deep)
Subacute left watershed stroke (anterior, posterior and deep)
Leukoaraiosis and atrophy
Subacute subcortical right MCA stroke
Leukoaraiosis and atrophy
Chronic left anterior watershed and subacute MCA stroke
Chronic bilateral lacunar stroke
Brain CT at admission
Ophthalmic artery, no ComAA
Ophthalmic artery, left ComPA
Ophthalmic artery, bilateral ComPA, ComAA
Ophthalmic artery, right ComPA
Ophthalmic artery, ComAA
Ophthalmic artery, ComAA, left ComPA
ComAA, bilateral ComPA
Collateralization
Clopidogrel
03 January 2011
28 March 2011
Right hemispheric atrophy
Chronic left watershed stroke (anterior, posterior and deep)
Leukoaraiosis and atrophy
26 January 2012
Clopidogrel
ASA 300, atorvastatin 40
Chronic subcortical right MCA stroke
Leukoaraiosis and atrophy
Chronic cortical and subcortical lesions in left MCA territory
Bilateral lacunar infarction
Control brain CT
11 February 2009
06 August 2010
17 February 2009
17 December 2009
Date of recanalization
ASA 300, LMWH 0.6, atorvastatin 40
ASA 300 þ atorvastatin 20
ASA 300 þ LMWH 0.8/24 þ atorvastatin 80
Clopidogrel þ ASA 100 þ simvastatin
Treatment
Medical treatment
Medical treatment
Medical treatment
Medical treatment
Stenting on the left side
Left carotid endarterectomy after new left stroke
Medical treatment
Definitive treatment
Ovarian cystadenocarcinoma (died months later)
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Outcome
y: years; ComPA: communicating posterior artery; ComAA: communicating anterior artery; ASA: acetyl salicylic acid; LMWH: low-molecular-weight heparin; CT: computed tomography; MCA: middle cerebral artery.
Female
4
Male
2
Male
Male
1
3
Sex
Patient
Table 1. Patients with late spontaneous recanalization in our center.
Delgado et al. 213
73 y
85 y
67 y
75 y
66 y
67 y
70 y
55 y
65 y
Male
Male
Male
Male
Male
Female
Male
Female
Female
Male
Matic et al.4
Klonaris et al.5
Buslovich and Schanzer6
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Ipsilateral stroke
Ipsilateral TIA
Ipsilateral TIA
Amaurosis fugax
Ipsilateral TIA
Multiple cardiovascular risk factors
Left hemispheric transient attacks
Right-hand side weakness and numbness
Right arm paresis and right facial paresis
Left hemiparesis
Right hemiparesis, aphasia
Right hemiparesis
Symptomatology
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex
Carotid duplex and angiography
Carotid duplex
MRA
Digital subtraction angiogram
Carotid duplex confirmed by angiography
CTA
Carotid duplex confirmed by MRA
Carotid duplex confirmed by CTA
Diagnostic method
Right ICA occlusion
Right ICA occlusion
Right ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Right ICA occlusion, severe stenosis left ICA
Left ICA occlusion, 40–60% stenosis right ICA
Left ICA occlusion
Arterial pathology
ASA
ASA
ASA
Clopidogrel
ASA
Medical treatment
Coumadin
Medical treatment
Clopidogrel
Left carotid endarterectomy, ASA, statins
ASA, Clopidogrel, statins
Medical treatment
Treatment
7 years and 10 months
7 years and 4 months
6 months
11 months
1 year and 5 months
5 years
2 years and 9 months
1 year and 2 months
1 year
2 years
4 months
8 months
Time of recanalization
Carotid duplex and angiography
Carotid duplex
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and MRA
Carotid duplex and MRA
MRA
Carotid duplex and angiography
Carotid duplex and CTA
Carotid duplex and MRA
Carotid duplex
Diagnostic method
Asymptomatic
Asymptomatic
Asymptomatic
Asymptomatic
Contralateral TIA
Asymptomatic
Asymptomatic
Ipsilateral TIAs
Asymptomatic
Asymptomatic
Asymptomatic
Syncope
Symptoms at recanalization
y: years; TIA: transient ischemic attack; CTA: computed tomography angiography; MRA: magnetic resonance angiography; ASA: acetyl salicylic acid.
Camporese et al.7
58 y
Female
Som and Schanzer3
64 y
74 y
Male
Shah et al.1
Age
Sex
Author
Table 2. Patients described in the literature with late recanalization of previous internal carotid artery (ICA) occlusion.
ASA
ASA
ASA
Clopidogrel
Warfarin
Carotid endarterectomy
Medical treatment
Left carotid endarterectomy
Left carotid endarterectomy
Right carotid endarterectomy
Left carotid endarterectomy
Left carotid endarterectomy
Definitive treatment
No
No
No
No
No
Calcified atherosclerotic plaque
No
Atherosclerotic plaque
Hard plaque (no intraplaque hemorrhage)
Fibrous plaque (no intraplaque hemorrhage)
No
Atherosclerotic plaque
Pathological study
214 Vascular 23(2)
Delgado et al.
215
Results An ICA occlusion was diagnosed in 182 patients; of these, symptomatic ICA occlusion was diagnosed in 162 patients. Eighteen (18/162) patients needed mechanical (17/18) or surgical (1/18) recanalization. Three (3/162) patients died due to an extensive hemispheric stroke (one of them after surgical treatment). Eight of 162 patients presented with dissection of the ICA, and 136/162 patients presented atheromatous ICA occlusion. Of the latter, seven patients presented a late spontaneous recanalization of the ICA (Figures 1 to 3). The cases are summarized in Table 1.
Discussion Spontaneous late recanalization of atheromatous chronic ICA occlusion may be due to the natural fibrinolysis of superimposed occlusion in the setting of preexisting severely stenotic ICA1 or due to the presence of the vasa vasorum providing collateral circulation.2 Apart from that, other factors take part in the recanalization: mechanism of occlusion, site of the occlusion, clot-size, composition, and age of the thromboembolic material. For all of these aspects, a late recanalization of atheromatous ICA occlusion is not a frequent event. The best management of this unusual condition remains unclear, as little data have been reported in the literature (Table 2).1,3–7 Whether these patients should receive the same treatment as patients with asymptomatic ICA stenosis remains unknown, as far as patients who suffered from an ipsilateral ischemic event longer than six months are currently classified as asymptomatic.8 In patients with asymptomatic ICA stenosis, medical treatment alone seems to be the best treatment for stroke prevention.9,10 However, recent studies which focused on the asymptomatic ICA stenosis support the idea that the combination of several factors may identify patients who will benefit from other therapeutic approaches apart from medical treatment. A complex atherosclerotic carotid plaque,11–13 positive cerebral CT findings such as silent infarcts,11–14 the degree of the carotid stenosis,11–13,15 disturbances in cerebral vasoreactivity,13 or history of contralateral transient ischemic attacks15 may identify those patients who will need interventional treatment.11–13 Moreover, patients with previous symptomatic carotid artery pathology would have a relatively unstable carotid plaque composition, with higher prevalence of intraplaque hemorrhage, compared with patients who have never experienced ipsilateral events.8 It would suggest that patients with past events might have different long-term ipsilateral stroke risks.8 For this reason, and due to the possibility of recanalization, patients with symptomatic
atheromatous chronic ICA occlusion should deserve further attention. After reviewing previously published clinical cases, medical treatment seems to be as effective as interventional treatment in these patients. Although these studies were performed in the chronic phase when thrombus could have disappeared, pathological studies described in the literature show atheromatous fibrous plaques or calcified carotid plaques without any sign of unstable carotid pathology.1,4–6 In addition to patients with asymptomatic carotid pathology, ischemic cerebrovascular events have been described in these patients with late recanalization: an ipsilateral ischemic event, such as the case described by Buslovich and Hines6 or our second patient, or contralateral ischemic stroke, such as the case described by Camporese et al.7 or our first patient, supports that in some cases, the prognosis would not be as benign as expected. Revascularization techniques should be considered in these cases to improve not only the ipsilateral hemispheric circulation but also the collateral circulation to the contralateral hemisphere. The authors attempt to highlight the unusual condition of recanalization after a symptomatic atheromatous chronic ICA occlusion. If these patients can be treated similar to patients with asymptomatic carotid pathology, then this needs to be clarified. More studies are needed to establish the most appropriate therapeutical approach in order to avoid arbitrary treatment in these patients. Conflict of interest None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Shah PS, Hingorani A, Ascher E, et al. Spontaneous recanalization of an occluded internal carotid artery. Ann Vasc Surg 2010; 24: 954. 2. Colon GP, Deveikis JP and Dickinson LD. Revascularization of occluded internal carotid arteries by hypertrophied vasa vasorum: report of four cases. Neurosurgery 1999; 45: 634–637. 3. Som S and Schanzer B. Spontaneous recanalization of complete internal carotid artery: a clinical reminder. J Surg Tech Case Rep 2010; 2: 73–74. 4. Matic P, Ilijevski N, Radak S, et al. Recanalization of chronic carotid occlusion: a case report and review of the literature. Vascular 2009; 17: 281–283. 5. Klonaris C, Alexandrou A, Katsargyris A, et al. Late spontaneous recanalization of acute internal carotid artery occlusion. J Vasc Surg 2006; 43: 844–847.
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
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6. Buslovich S and Hines GL. Spontaneous recanalization of chronic internal carotid artery occlusions: report of 3 cases. Vasc and Endovasc Surg 2011; 45: 93–97. 7. Camporese G, Labropoulos N, Verlato F, et al. Benign outcome of objectively proven spontaneous recanalization of internal carotid artery occlusion. J Vasc Surg 2011; 53: 323–329. 8. van Lammeren GW, den Hartog AG, Pasterkamp G, et al. Asymptomatic carotid artery stenosis: identification of subgroups with different underlying plaque characteristics. Eur J Vasc Endovasc Surg 2012; 43: 632–636. 9. Kakisis JD, Avgerinos ED, Antonopoulos CN, et al. The European Society for Vascular Surgery guidelines for carotid intervention: an updated independent assessment and literature review. Eur J Vasc Endovasc Surg 2012; 44: 238–243. 10. King A, Shipley M, Markus H and for the ACES Investigators. The effect of medical treatments on stroke risk in asymptomatic carotid stenosis. Stroke 2013; 44: 542–546.
11. Paraskevas KI, Liapis CD and Veith FJ. Identifying asymptomatic carotid stenosis patients at high risk of cerebrovascular events: the missing piece of the puzzle? Angiology 2012; 63: 489–491. 12. Pecoraro F, Dinoto E, Mirabella D, et al. Basal cerebral computed tomography as diagnostic tool to improve patient selection in asymptomatic carotid artery stenosis. Angiology 2012; 63: 504–508. 13. De la Cruz-Cosme C and Segura T. Estenosis carotı´ dea asintoma´tica grave: una perspectiva neurolo´gica. Rev Neurol 2012; 55: 283–296. 14. Kakkos SK, Sabetai M, Tegos T, et al. Silent embolic infarcts on computed tomography brain scans and risk of ipsilateral hemispheric events in patients with asymptomatic internal carotid artery stenosis. J Vasc Surg 2009; 49: 902–909. 15. Nicolaides AN, Kakkos SK, Griffin M, et al. Severity of asymptomatic carotid stenosis and risk of ipsilateral hemispheric ischaemic events: results from the ACSRS study. Eur J Vasc Endovasc Surg 2005; 30: 275–284.
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Late spontaneous recanalization of symptomatic atheromatous internal carotid artery occlusion
Vascular 2015, Vol. 23(2) 211–216 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114535392 vas.sagepub.com
Montserrat G Delgado1, Pedro P Vega2, Carlos H Lahoz1 and Sergio Calleja1
Abstract Introduction: Definitive treatment of symptomatic atheromatous internal carotid artery occlusion remains controversial, as far as in rare cases, late spontaneous recanalization has been seen. Methods: We consecutively studied 182 patients (January 2003 to August 2012) with an ischemic stroke in the internal carotid artery territory and diagnosis of atheromatous internal carotid artery occlusion during hospitalization. Findings: Seven patients presented a late spontaneous recanalization (>3 months) of the internal carotid artery. We described therapeutic attitude according to usual care in these patients. Conclusions: The authors attempt to highlight the unusual condition of recanalization after a symptomatic atheromatous chronic internal carotid artery occlusion. If these patients can be treated similar to patients with asymptomatic carotid pathology, then this needs to be clarified. However, due to the risk of ipsi- and contralateral ischemic strokes, revascularization techniques should be considered in certain cases. More studies are needed to establish the most appropriate therapeutical approach in order to avoid arbitrary treatment of these patients.
Keywords Carotid occlusion, carotid recanalization, spontaneous recanalization
Introduction Definitive treatment of symptomatic chronic atheromatous internal carotid artery (ICA) occlusion remains controversial, as far as in rare cases, late spontaneous recanalization has been described. We describe therapeutic attitude according to usual care in seven patients with late recanalization (>3 months), and we review similar cases described in the literature.
Methods We studied consecutive patients with ischemic stroke admitted to the University Hospital of Oviedo (Spain) from January 2003 to August 2012. Inclusion criteria were ischemic stroke in the ICA territory, diagnosis of ICA occlusion during hospitalization using angiographic sequences of magnetic resonance angiography (MRA) or computed tomography angiography (CTA), and atheromatous etiology. Exclusion criteria were interventional treatment at the time of admittance or
during hospitalization, patients with previously known ICA occlusion, and ICA occlusion of etiology other than atheromatous. Patients with a diagnosis of ICA occlusion made using duplex echography without confirmation by other angiographic study were also excluded. After discharge, patients were followed up by carotid duplex. We defined late recanalization as more than three months from the initial diagnosis. If recanalization was suspected, a complementary angiographic study (MRA or CTA) was performed in order to avoid the possibility of mistaking a near occlusion of the ICA by echography. Because of its cost, 1 Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Spain 2 Department of Radiology Service, Hospital Universitario Central de Asturias, Oviedo, Spain
Corresponding author: Montserrat G Delgado, Servicio de Neurologı´a, Hospital Universitario Central de, C/ Celestino Villamil s/n, 33006 Oviedo, Spain. Email: [email protected]
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
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Vascular 23(2)
Figure 1. Patient 2—coronal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
Figure 2. Patient 3—coronal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
Figure 3. Patient 5—longitudinal sections of CT angiography showed a left ICA occlusion (a) and recanalization (b) (white arrows).
availability, and efficacy, CTA was more frequently used than MRA. The CTA was obtained with a 64 multidetector-array technology in helicoidal with slice thickness 1.25 mm. Acquisition delay depended on the bolus test of 20 mL (15–20 s). Helical acquisition that
started from the aortic arch to the circle of Willis was initiated 20 s after the start of injecting 120-mL nonionic contrast medium. Projections were reconstructed in axial, sagittal, and coronal planes. All images were analyzed by a neuroradiologist.
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Male
Male
Female
5
6
7
86 y
64 y
86 y
66 y
79 y
67 y
78 y
Age
Dysarthria and left hemiparesis
Aphasia and right arm paresis
Left hemiparesis
Left hemiparesis
Language disturbances
Aphasia and right hemiparesis
Transient aphasia and right hand paresis
Symptomatology
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
Clopidogrel þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 300 þ LMWH 0.6
ASA 100 þ LMWH 0.4
Initial treatment
10 May 2009
15 December 2009
22 December 2008
19 May 2008
19 February 2008
17 June 2008
15 June 2003
Date of occlusion
Subacute right watershed stroke (posterior and deep)
Subacute left watershed stroke (anterior, posterior and deep)
Leukoaraiosis and atrophy
Subacute subcortical right MCA stroke
Leukoaraiosis and atrophy
Chronic left anterior watershed and subacute MCA stroke
Chronic bilateral lacunar stroke
Brain CT at admission
Ophthalmic artery, no ComAA
Ophthalmic artery, left ComPA
Ophthalmic artery, bilateral ComPA, ComAA
Ophthalmic artery, right ComPA
Ophthalmic artery, ComAA
Ophthalmic artery, ComAA, left ComPA
ComAA, bilateral ComPA
Collateralization
Clopidogrel
03 January 2011
28 March 2011
Right hemispheric atrophy
Chronic left watershed stroke (anterior, posterior and deep)
Leukoaraiosis and atrophy
26 January 2012
Clopidogrel
ASA 300, atorvastatin 40
Chronic subcortical right MCA stroke
Leukoaraiosis and atrophy
Chronic cortical and subcortical lesions in left MCA territory
Bilateral lacunar infarction
Control brain CT
11 February 2009
06 August 2010
17 February 2009
17 December 2009
Date of recanalization
ASA 300, LMWH 0.6, atorvastatin 40
ASA 300 þ atorvastatin 20
ASA 300 þ LMWH 0.8/24 þ atorvastatin 80
Clopidogrel þ ASA 100 þ simvastatin
Treatment
Medical treatment
Medical treatment
Medical treatment
Medical treatment
Stenting on the left side
Left carotid endarterectomy after new left stroke
Medical treatment
Definitive treatment
Ovarian cystadenocarcinoma (died months later)
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Clinically stable since then
Outcome
y: years; ComPA: communicating posterior artery; ComAA: communicating anterior artery; ASA: acetyl salicylic acid; LMWH: low-molecular-weight heparin; CT: computed tomography; MCA: middle cerebral artery.
Female
4
Male
2
Male
Male
1
3
Sex
Patient
Table 1. Patients with late spontaneous recanalization in our center.
Delgado et al. 213
73 y
85 y
67 y
75 y
66 y
67 y
70 y
55 y
65 y
Male
Male
Male
Male
Male
Female
Male
Female
Female
Male
Matic et al.4
Klonaris et al.5
Buslovich and Schanzer6
Downloaded from vas.sagepub.com at Elsevier Scirus on May 23, 2015
Ipsilateral stroke
Ipsilateral TIA
Ipsilateral TIA
Amaurosis fugax
Ipsilateral TIA
Multiple cardiovascular risk factors
Left hemispheric transient attacks
Right-hand side weakness and numbness
Right arm paresis and right facial paresis
Left hemiparesis
Right hemiparesis, aphasia
Right hemiparesis
Symptomatology
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex
Carotid duplex and angiography
Carotid duplex
MRA
Digital subtraction angiogram
Carotid duplex confirmed by angiography
CTA
Carotid duplex confirmed by MRA
Carotid duplex confirmed by CTA
Diagnostic method
Right ICA occlusion
Right ICA occlusion
Right ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Left ICA occlusion
Right ICA occlusion, severe stenosis left ICA
Left ICA occlusion, 40–60% stenosis right ICA
Left ICA occlusion
Arterial pathology
ASA
ASA
ASA
Clopidogrel
ASA
Medical treatment
Coumadin
Medical treatment
Clopidogrel
Left carotid endarterectomy, ASA, statins
ASA, Clopidogrel, statins
Medical treatment
Treatment
7 years and 10 months
7 years and 4 months
6 months
11 months
1 year and 5 months
5 years
2 years and 9 months
1 year and 2 months
1 year
2 years
4 months
8 months
Time of recanalization
Carotid duplex and angiography
Carotid duplex
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and angiography
Carotid duplex and MRA
Carotid duplex and MRA
MRA
Carotid duplex and angiography
Carotid duplex and CTA
Carotid duplex and MRA
Carotid duplex
Diagnostic method
Asymptomatic
Asymptomatic
Asymptomatic
Asymptomatic
Contralateral TIA
Asymptomatic
Asymptomatic
Ipsilateral TIAs
Asymptomatic
Asymptomatic
Asymptomatic
Syncope
Symptoms at recanalization
y: years; TIA: transient ischemic attack; CTA: computed tomography angiography; MRA: magnetic resonance angiography; ASA: acetyl salicylic acid.
Camporese et al.7
58 y
Female
Som and Schanzer3
64 y
74 y
Male
Shah et al.1
Age
Sex
Author
Table 2. Patients described in the literature with late recanalization of previous internal carotid artery (ICA) occlusion.
ASA
ASA
ASA
Clopidogrel
Warfarin
Carotid endarterectomy
Medical treatment
Left carotid endarterectomy
Left carotid endarterectomy
Right carotid endarterectomy
Left carotid endarterectomy
Left carotid endarterectomy
Definitive treatment
No
No
No
No
No
Calcified atherosclerotic plaque
No
Atherosclerotic plaque
Hard plaque (no intraplaque hemorrhage)
Fibrous plaque (no intraplaque hemorrhage)
No
Atherosclerotic plaque
Pathological study
214 Vascular 23(2)
Delgado et al.
215
Results An ICA occlusion was diagnosed in 182 patients; of these, symptomatic ICA occlusion was diagnosed in 162 patients. Eighteen (18/162) patients needed mechanical (17/18) or surgical (1/18) recanalization. Three (3/162) patients died due to an extensive hemispheric stroke (one of them after surgical treatment). Eight of 162 patients presented with dissection of the ICA, and 136/162 patients presented atheromatous ICA occlusion. Of the latter, seven patients presented a late spontaneous recanalization of the ICA (Figures 1 to 3). The cases are summarized in Table 1.
Discussion Spontaneous late recanalization of atheromatous chronic ICA occlusion may be due to the natural fibrinolysis of superimposed occlusion in the setting of preexisting severely stenotic ICA1 or due to the presence of the vasa vasorum providing collateral circulation.2 Apart from that, other factors take part in the recanalization: mechanism of occlusion, site of the occlusion, clot-size, composition, and age of the thromboembolic material. For all of these aspects, a late recanalization of atheromatous ICA occlusion is not a frequent event. The best management of this unusual condition remains unclear, as little data have been reported in the literature (Table 2).1,3–7 Whether these patients should receive the same treatment as patients with asymptomatic ICA stenosis remains unknown, as far as patients who suffered from an ipsilateral ischemic event longer than six months are currently classified as asymptomatic.8 In patients with asymptomatic ICA stenosis, medical treatment alone seems to be the best treatment for stroke prevention.9,10 However, recent studies which focused on the asymptomatic ICA stenosis support the idea that the combination of several factors may identify patients who will benefit from other therapeutic approaches apart from medical treatment. A complex atherosclerotic carotid plaque,11–13 positive cerebral CT findings such as silent infarcts,11–14 the degree of the carotid stenosis,11–13,15 disturbances in cerebral vasoreactivity,13 or history of contralateral transient ischemic attacks15 may identify those patients who will need interventional treatment.11–13 Moreover, patients with previous symptomatic carotid artery pathology would have a relatively unstable carotid plaque composition, with higher prevalence of intraplaque hemorrhage, compared with patients who have never experienced ipsilateral events.8 It would suggest that patients with past events might have different long-term ipsilateral stroke risks.8 For this reason, and due to the possibility of recanalization, patients with symptomatic
atheromatous chronic ICA occlusion should deserve further attention. After reviewing previously published clinical cases, medical treatment seems to be as effective as interventional treatment in these patients. Although these studies were performed in the chronic phase when thrombus could have disappeared, pathological studies described in the literature show atheromatous fibrous plaques or calcified carotid plaques without any sign of unstable carotid pathology.1,4–6 In addition to patients with asymptomatic carotid pathology, ischemic cerebrovascular events have been described in these patients with late recanalization: an ipsilateral ischemic event, such as the case described by Buslovich and Hines6 or our second patient, or contralateral ischemic stroke, such as the case described by Camporese et al.7 or our first patient, supports that in some cases, the prognosis would not be as benign as expected. Revascularization techniques should be considered in these cases to improve not only the ipsilateral hemispheric circulation but also the collateral circulation to the contralateral hemisphere. The authors attempt to highlight the unusual condition of recanalization after a symptomatic atheromatous chronic ICA occlusion. If these patients can be treated similar to patients with asymptomatic carotid pathology, then this needs to be clarified. More studies are needed to establish the most appropriate therapeutical approach in order to avoid arbitrary treatment in these patients. Conflict of interest None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
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