24.1.1 Clinical Presentation

A 60-year-old male patient presented to an outside center with severe right hemiparesis, neglect, and speech disturbance. Initial National Institutes of Health Stroke Scale (NIHSS) score was 17. He was transferred as a code stroke to a regional stroke center for further evaluation and treatment. At the time of assessment, he was three hours from symptom onset, with resolution of some symptoms. The NIHSS score improved to 2 and then 0. Past medical history was significant for prior ischemic heart disease with coronary artery bypass graft, hypertension, and dyslipidemia. Medications included aspirin 81 mg daily.

24.1.2 Imaging Workup and Investigations

Noncontrast computed tomography (NCCT) of the brain (Fig. 24.1a, b) demonstrated subtle loss of gray-white matter differentiation in the region of the insular ribbon on left (ASPECTS score of 9). No other early or established ischemic change was seen. There was no evidence of hemorrhage. CT angiography (CTA) performed from the level of the aortic arch demonstrated occlusion of the M1 segment of left middle cerebral artery (MCA) immediately beyond the anterior temporal branch origin with excellent collateralization to the distal MCA territory (Fig. 24.1c, d). There was evidence of atherosclerotic disease in the region of the left carotid bulb, with mixed calcific and soft plaque present, and resultant severe, greater than 90%, luminal stenosis (Fig. 24.1e).

CT perfusion demonstrated significant mismatch with prolonged time to peak (TTP) within the left MCA territory (Fig. 24.2a), and preservation of relative cerebral blood volume (rCBV; Fig. 24.2b).

In light of the presence of tandem disease and the possibility that carotid stenting and antiplatelet medication might be required, an urgent MRI was performed to assess established infarction, as this would help with assessing hemorrhagic risk. Diffusion weighted imaging showed a small area of diffusion restriction involving the left insular ribbon, and in the left frontal deep white matter (Fig. 24.3a, b). T2 gradient echo imaging showed relatively long length of thrombus in the M1 to M2 segment of left MCA (Fig. 24.3c, d).

24.1.3 Diagnosis

Tandem disease: left M1 segment of MCA occlusion, and tandem left internal carotid artery (ICA) severe stenosis.

24.1.4 Treatment

Although the patient had demonstrated significant clinical improvement, there was a concern that, given the CTA findings, he would later deteriorate, and limited available literature for this group of patients suggests they perform poorly in the long-term without treatment. Following discussion with the stroke physician, patient decision was made to proceed with treatment and intervention.

Endovascular Treatment

Materials

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  8-Fr short angiographic sheath.

  
  
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  8-Fr balloon guide catheter.

  
  
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  5-Fr VTK slip catheter.

  
  
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  0.035-angled hydrophilic wire.

  
  
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  Aviator Plus PTA balloon catheter 4 mm × 20 mm.

  
  
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  Synchro 14 microguidewire.

  
  
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  5-Fr H1 slip catheter.

  
  
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  Trevo 18 microcatheter.

  
  
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  Trevo XP Provue 4 × 20 mm stent retriever.

  
  
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  8-Fr Angioseal closure device

Technique

Intervention was performed with conscious sedation and local anesthetic. A single-wall right common femoral artery (CFA) puncture was performed, and the 8-Fr short vascular access sheath inserted. 2,500 IU heparin was administered intravenously following puncture. The 8-Fr balloon guide catheter was advanced to the left common carotid artery (CCA) over a 5-Fr VTK slip catheter, with the aid of an angled Terumo guidewire using roadmap guidance. Left common carotid angiography confirmed the presence of severe, more than 90% stenosis of the left ICA in the region of the carotid bulb (Fig. 24.4a, b). The caliber of the ICA beyond the occlusion was reduced, suggesting near occlusion. Angiography also confirmed persistent left M1 occlusion (Fig. 24.4c), which was distal to the origin of lenticulostriate perforators and the anterior temporal branch origin. The left anterior cerebral artery (ACA) territory filled normally, and collateralization to the left MCA territory from ACA was seen in the later phases of angiography.

Left CCA angioplasty was performed with the intention of dilating the stenosis to a degree which would allow the guide catheter to pass and mechanical thrombectomy to be performed. A Synchro 14 guidewire was used to cross the left ICA stenosis, and navigated into the ICA beyond the narrowing. Over this, using a rapid exchange maneuver, a 4 mm × 20 mm Aviator Plus PTA balloon catheter was advanced and placed across the stenosis. Gentle balloon angioplasty was performed; the stenosis was purposefully underdilated, and the balloon was underinflated to less than 4 mm diameter. Initial waisting of the balloon, observed at the start of inflation, was no longer evident by the end of the inflation, and control angiogram showed improved caliber at the level of the stenosis to approximately 50% luminal narrowing (Fig. 24.4d, e). This appeared sufficient to allow passage of the guide catheter. An angled 0.038 Terumo guidewire was used to cross the residual stenosis, a 5-Fr H1 slip catheter was advanced over the Terumo, and the 8-Fr balloon guide catheter was then advanced to the level of midcervical ICA over the slip-cath/wire combination. Control angiography showed good antegrade flow in the ICA, with some contrast stasis below the distal end of the guide, presumably as the guide was partially occlusive at the level of the stenosis.

A Trevo microcatheter was rapidly navigated into the left M1 segment of MCA with the aid of a Synchro 14 guidewire. The wire was advanced through the left M1 thrombus and placed distally in the inferior division M2 branch. A 4 mm × 20 mm Trevo XP Provue stent retriever was then deployed from the inferior division back into the distal M1 segment across the thrombus. Control angiography with the stent retriever in situ showed some filling of the occluded vessel, with filling defects consistent with the thrombus in the stent (Fig. 24.4f). The stent retriever was left in position for 5 minutes to allow interaction with thrombus before retrieval. Retrieval was performed with flow arrest and continuous manual aspiration through the 8-Fr balloon guide catheter. A long length of clot was retrieved in the Trevo stent. Following this single pass, the control angiogram showed complete recanalization of the M1 segment and M2 branches, and complete reperfusion of the distal MCA territory (Fig. 24.4g, h).

The synchro wire was advanced through the 8-Fr guide catheter into the left ICA to maintain access across the ICA stenosis and the guide catheter was pulled back into the distal CCA. Control angiography showed that the left ICA remained patent, with approximately 50% residual narrowing at the level of the previously severe stenosis (Fig. 24.5a, b). As the patient had received full-dose IV-tPA and was on aspirin, a decision was made not to place a stent, as this would require additional antiplatelet therapy in the form of either a Reopro bolus or a loading dose of 300 mg po clopidogrel. Definitive treatment of the ICA (presumably unstable) plaque and residual stenosis was therefore deferred to the non-hyperacute setting. All devices were retrieved. An 8-Fr Angioseal closure device was placed in the right CFA.

24.2.1 Clinical Presentation

A 66-year-old male presented with a 6-hour history of right hemispheric stroke symptoms; his NIHSS score was 9. NCCT of the brain showed hyperdensity of the M1 segment of right MCA (Fig. 24.6a), with occlusion of the right M1 segment on CTA (Fig. 24.6b). The cervical right ICA appeared occluded. There existed evidence of developing ischemic change in the right parietooccipital watershed territory (Fig. 24.7), without early change elsewhere in the right MCA territory. The patient was outside the time window for intravenous thrombolysis and was brought for endovascular treatment (Fig. 24.6c) Left carotid angiography showed filling of the right ACA across the A Comm, with filling of the right carotid termination, and cut off in the proximal right M1 segment. The right A1 segment was hypoplastic. Late arterial phase of angiography showed leptomeningeal collateralization to the right MCA territory. Right common carotid injection at the level of the carotid bifurcation showed near occlusion of the right ICA. An 8-Fr guide catheter was placed in the right CCA. The stenosis was crossed and a PRECISE stent was deployed in the right carotid. A Rebar 18 microcatheter was then navigated through the ICA and across the right M1occlusion, and a Solitaire 4 × 20 mm stent was deployed from the right M1 segment of MCA to the supraclinoid ICA. The stent was left in situ for 5 minutes and then retrieved. The guide catheter remained in the right CCA. During retrieval, the Solitaire became entangled in the carotid stent and spontaneously detached. A second PRECISE stent was placed to jail the Solitaire against the carotid wall. Control angiography showed antegrade flow through the right ICA, and demonstrated successful recanalization of the right MCA. There was, however, reduced flow through the stents, with filling defects within the stents suggestive of developing thrombus. Intravenous aspirin had been administered during the procedure, and the patient was loaded with 300 mg Plavix via nasogastric tube. Follow-up CTA 5 days later showed the right CCA was occluded with no contrast opacification of the lumen within the stent. MRI of the brain showed completion of infarction in the right posterior parietal and temporal region, right head of caudate nucleus, and small volume infarcts in the centrum semiovale with preservation otherwise of right MCA territory (Fig. 24.7). The patient had demonstrated some on-table improvement at the end of the procedure with improved power in the left upper and lower limb; on day 7, modified Rankin scale (mRS) score was 1, and it was 0 on the 30-day clinical follow-up.