Intra-arterial therapy for acute ischemic stroke

Abstract

Intra-arterial therapy (IAT) for acute ischemic stroke refers to endovascular catheter-based approaches to achieve recanalization using mechanical clot disruption, locally injected thrombolytic agents or both. IAT may be used in addition to intravenous tissue plasminogen activator (tPA) or in patients who do not qualify for tPA, usually because they are outside the approved 3-h timeframe window or have contraindications, such as elevated international normalized ratio or partial thromboplastin time. Recanalization rates correlate with clinical improvement, and with the newest catheters it is possible to achieve recanalization in roughly 80% of patients treated. However, while the catheters are approved by the Food and Drug Administration, there are still no randomized trial data demonstrating the role of current IAT therapy vs either tPA or standard management. IAT is reserved for patients with large artery occlusions in the basilar, distal carotid, or proximal middle cerebral arteries. Imaging the penumbra using magnetic resonance imaging or computed tomographic perfusion is currently the most frequently used way to identify patients who might benefit. However, the imaging and clinical criteria for identifying which patients benefit, and perhaps more importantly those who will do poorly despite IAT, remain unclear.

Fig. 1

A 49-year-old man presented within the 3-h window of time for intravenous (IV) tissue plasminogen activator (tPA) with a right middle cerebral artery syndrome and National Institutes of Health Stroke Score (NIHSS) score of 14 with dense hemianopsia, hemiplegia, and sensory loss, but minor neglect and no eye deviation. After IV tPA, the patient had no clinical improvement, and therefore he was taken for endovascular intervention. (a) Pre-tPA computed tomographic perfusion cerebral blood flow, (b) cerebral blood volume, and (c) time to peak images indicating that there was no necrotic core, but a marked delay in perfusion of the entire right middle cerebral artery (MCA) and PCA territories. (d) Right internal carotid artery angiogram reveals RICA occlusion (arrow). (e) A left intracerebral hemorrhage (ICH) injection shows a flow across the anterior communicating artery supplying collateral flow to the right ACA and MCA. Two large branch occlusions were noted at the M2-M3 level on the right, and these were believed to be the culprit lesions causing the symptoms. The CTP showed reasonably good CBF and CBV values in the RMCA cortex; therefore, the culprit lesion was unlikely to be the internal carotid artery (ICA) occlusion. (f, g) A microcatheter was advanced into the RMCA across the anterior communicating from the left ICA and microcatheter injection confirmed the presence of the branch occlusions (f, arrow; g, black arrow). (g) The microcatheter was advanced into the occluded segment of the superior division (white arrow) and tPA was infused. (h) The patient then became sleepy and with right gaze deviation. Left ICA injection demonstrated new RMCA occlusion (arrow). (i) RICA injection confirmed distal migration of the thrombus (arrow). (j) RICA injection after the first pass with the Penumbra device (Penumbra Inc., Alameda, CA) noting complete ICA recanalization (arrow) and partial recanalization of the RMCA. (k) RICA angiography after the second pass with the Penumbra device (Penumbra Inc.) demonstrating complete recanalization of the RMCA. (l) Final RICA lateral angiogram demonstrates recanalization of the majority of the RMCA territory, but persistent occlusion of a posterior division branch (arrow) and the fetal posterior cerebral artery (white arrow). (m) Final cervical RICA angiogram confirming normal ICA flow. (n, o) 24-h RMCA DWI images showing patchy but small RMCA and PCA strokes. The patient had significant clinical improvement with only mild residual left hand weakness and left homonymous hemianopsia with a mRS = 2 at discharge

Fig. 2

An 82-year-old man who presented within 3 h with basilar artery occlusion and received IV tPA with significant improvement. Then 48 h after the tPA, the patient developed coma and quadriparesis. (a) The angiogram demonstrated recurrent basilar artery occlusion (arrow). (b) After angioplasty with a 2.5 × 9 mm balloon, the Basilar Artery (BA) is recanalized, but there was a severe residual proximal BA stenosis (arrow) with poor distal flow. (c) After 3 × 15 mm self-expanding stent placement and postdilation, the BA and its branches are fully recanalized (arrow). Immediately after the stenting, the patient began to have progressive neurological improvement and is currently residing at home with his family with modified Rankin Scale (mRS) = 3