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Subclinical microembolization identified on diffusion-weighted magnetic resonance imaging is recognized as an important outcome measure for carotid revascularization procedures. It is generally believed that arch manipulation is the primary reason for developing microemboli in the contralateral hemisphere during carotid artery stenting. However, we identified three patients who developed postprocedure microemboli of the contralateral hemisphere despite a known chronic contralateral internal carotid artery occlusion. Our cases highlight that ipsilateral microemboli may be an underappreciated but an important source of contralateral lesions through patent intracranial collateral pathways.
Subclinical microembolization identified on diffusion-weighted magnetic resonance imaging (DWI) is increasingly recognized as an important outcome measure following carotid artery stenting (CAS). Embolic events are not isolated to the ipsilateral cerebrum; rather, they have also been detected with a high frequency in the contralateral hemisphere.1,2 The common hypothesis is that small debris originating from the aortic arch and cardiac sources travels via a patent contralateral internal carotid artery (ICA) to the contralateral cerebrum. We herein describe three patients with chronic contralateral ICA occlusions who nonetheless sustained microemboli to the contralateral cerebral hemisphere following CAS.
Over a period of 7 years, a total of 262 CAS procedures were performed and all patients received pre- and postprocedure magnetic resonance imaging (MRI) when appropriate. Among 14 patients with a known chronic contralateral ICA occlusion who underwent CAS, three patients demonstrated new contralateral microemboli on postoperative MRI (Table). Two patients were considered high cardiac risk and the third had a high lesion that deemed him a better candidate for an endovascular approach. All three contralateral ICA occlusions were identified on preoperative duplex ultrasound and magnetic resonance angiogram evaluations. Time-of-flight MRIs also demonstrated patent anterior communicating arteries (ACOMs) in two patients and prominent posterior communicating arteries (PCOMs) in the other patient (Fig 1, A and B).
The procedures were performed by an experienced vascular surgeon and a vascular surgery fellow as described previously.3 Briefly, following access and early systemic anticoagulation (100 u/kg intravenous heparin), an arch aortogram was performed when necessary. The carotid artery was cannulated with a telescopic technique4 followed by routine placement of an embolic protection device (EPD). One patient required prestent angioplasty using 2- and 3-mm angioplasty balloons to enable stent traversal. Stents were deployed and poststent balloon angioplasty was standard. One patient required intravenous administration of atropine and neosynephrine for persistent hypotension. All three patients remained neurologically intact. DWI evaluations were performed prior to discharge the following day. Each patient was discharged on 6 weeks of clopidogrel, daily aspirin, and a statin. All three patients did well without neurologic deficit at 1- and 6-month follow-up evaluations.
New ipsilateral lesions were identified in the occipital and parietal lobes of one patient, parietal lobe of another, and middle cerebral artery distribution of the third. Contralateral microemboli were identified in the frontal lobes of two patients and in the distribution of the middle cerebral artery of the third despite contralateral carotid occlusions (Figs 2 and and3).3). These lesions were determined to be acute based on DWI images and apparent diffusion coefficient maps.
Three patients demonstrated evidence of new contralateral microemboli following CAS despite the presence of chronically occluded contralateral ICA and the absence of neurologic symptoms. Unlike previous studies and common belief, this unique series provides structural evidence of another major underappreciated source of contralateral hemispheric microemboli.
Periprocedural subclinical embolic events during CAS have been the focus of considerable debate since its inception. The reported incidence of microemboli is not insignificant.1,2,5,6 Embolic protection device, flow reversal systems, and dextran administration have all been implemented with varying degrees of success in an attempt to decrease the incidence of microemboli.7 A substantial percentage of these poststent emboli have been demonstrated in the contralateral hemisphere.1,2 Although the long-term neurologic consequence of these events remains uncertain, there is a commitment to preventing their occurrence secondary to concern of an increased risk of vascular dementia.8
There remain multiple hypotheses for the formation of contralateral microemboli. The main culprit appears to be wire manipulation in and around the diseased aortic arch. Another theory suggests that a cardiac source may be the nidus for contralateral embolic events. Direct embolization from these two sources was unlikely in our patients given that these patients had contralateral chronic ICA occlusion. The ICA stump syndrome, in which the external carotid artery serves as a conduit for emboli from the proximal ICA occlusion, is a known entity with an annual ipsilateral stroke risk of up to 5%.9–12 Some authors have demonstrated continued distal embolization from an occluded ICA.13 However, preoperative DWI evaluations did not demonstrate embolic sequelae before the CAS procedures. These new lesions in both hemispheres were identified within 48 hours of the procedure and were consistent with the radiologic appearance of acute lesions, suggesting procedure-related emboli. Another potential source is a patent contralateral vertebral artery. Although this is plausible, the patient with ipsilateral occipital lesions had a contralateral lesion in the frontal lobe, a well-developed ACOM, but absence of PCOM, which make the vertebral source unlikely. Two of our patients also demonstrated new ipsilateral microemboli in the frontal lobes, and all contralateral lesions were in the distribution of anterior circulation, thereby raising the suspicion that the ipsilateral ICA and anterior pathway collaterals remain the source.
Our cases highlight a major source of subclinical embolization to the contralateral hemisphere, particularly when the embolic debris is small. We believe this occurred through intercerebral collateralization whereby particles traveled via interhemisphere communicating arteries. An intact Circle of Willis occurs in 21% to 50% of patients.14–16 There are multiple posterior-anterior and interhemispheric collateral pathways. The anterior pathway, intact in 99% of patients,17 allows blood flow across the ACOM from the anterior cerebral artery. Although absent or hypoplastic in up to 30% of the population,14 the PCOM is another recognized important source of primary collateral circulation for the contralateral middle and anterior cerebral territories. A small (<1 mm in diameter) ipsilateral PCOM is shown to be an independent risk factor for ischemic cerebral infarction in patients with ICA occlusions.18 Our patients had asymptomatic contralateral internal carotid occlusions, which likely contributed to their well-developed PCOM. Unfortunately, the ACOM or PCOM may potentially serve as a major highway for embolic particles as well.19
Contralateral cerebral embolization during CAS is not rare. This series demonstrates that the role of the Circle of Willis in interhemispheric embolization may be underestimated during CAS. We herein provide structural evidence of intracranial primary collateral pathways, particularly via the ACOM and PCOM, as important sources of interhemispheric microembolization. Furthermore, it underscores the need for continued meticulous procedural technique and improved embolic protection during CAS.
Author conflict of interest: none.
The views expressed in this manuscript are those of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.
Presented at the Fortieth Annual Symposium of the Society for Clinical Vascular Surgery, Las Vegas, Nev, March 14–17, 2012.
The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest.