Plaque morphology in acute symptomatic intracranial atherosclerotic disease

Abstract

Background: Intracranial atherosclerotic disease (ICAD) is globally a major ischaemic stroke subtype with high recurrence. Understanding the morphology of symptomatic ICAD plaques, largely unknown by far, may help identify vulnerable lesions prone to relapse.

Methods: We prospectively recruited patients with acute ischaemic stroke or transient ischaemic attack attributed to high-grade ICAD (60%-99% stenosis). Plaque morphological parameters were assessed in three-dimensional rotational angiography, including surface contour, luminal stenosis, plaque length/thickness, upstream shoulder angulation, axial/longitudinal plaque distribution and presence of adjoining branch atheromatous disease (BAD). We compared morphological features of smooth, irregular and ulcerative plaques and correlated them with cerebral ischaemic lesion load downstream in MRI.

Results: Among 180 recruited patients (median age=60 years; 63.3% male; median stenosis=75%), plaque contour was smooth (51 (28.3%)), irregular (101 (56.1%)) or ulcerative (28 (15.6%)). Surface ulcers were mostly at proximal (46.4%) and middle one-third (35.7%) of the lesions. Most (84.4%) plaques were eccentric, and half had their maximum thickness over the distal end. Ulcerative lesions were thicker (medians 1.6 vs 1.3 mm; p=0.003), had steeper upstream shoulder angulation (56.2° vs 31.0°; p<0.001) and more adjoining BAD (83.3% vs 57.0%; p=0.033) than non-ulcerative plaques. Ulcerative plaques were significantly associated with coexisting acute and chronic infarcts downstream (35.7% vs 12.5%; adjusted OR 4.29, 95% CI 1.65 to 11.14, p=0.003). Sensitivity analyses in patients with anterior-circulation ICAD lesions showed similar results in the associations between the plaque types and infarct load.

Conclusions: Ulcerative intracranial atherosclerotic plaques were associated with vulnerable morphological features and had a higher cumulative infarct load downstream.

Figure 1

Plaque morphology evaluation in three-dimensional rotational angiography. (A–C) Smooth, irregular or ulcerative plaques (thin white arrows). (D) Length and maximum plaque thickness of an MCA plaque. (E and F) Two upstream plaque shoulder angulations of 17° and 61°. (G–I) Maximum plaque burden (thick white arrows) at proximal, middle and distal 1/3 of the MCA lesions. High-grade adjoining branch atheromatous disease was noted in figure parts G and I (arrow heads). (J) A concentric plaque of eccentricity index 0.08. (K) An eccentric plaque of eccentricity index 0.81. MCA, middle cerebral artery.

Figure 2

Maximal stenosis distribution in 132 MCA-M1 plaques and 14 BA plaques by axial and longitudinal views. A darker colour indicates a higher frequency. Upper panel: frequencies of cases with the maximum plaque thickness located over the superior, inferior, ventral and dorsal walls of MCA-M1 (left); or over the ventral, dorsal and lateral walls of BA (right). Lower panel: frequencies of cases with the maximum plaque thickness located at the proximal, middle or distal one-third along the longitudinal axis of MCA-M1 (left) and BA (right) plaques. BA, basilar artery; MCA-M1, M1 middle cerebral artery.

Figure 3

MRI and 3DRA images of a patient with an ulcerative MCA-M1 plaque and coexisting acute and chronic infarcts in cortical and subcortical regions. A patient with a history of hypertension presented with sudden onset of expressive dysphasia. The MRI exam conducted 1 day after symptom onset showed a cluster of early infarcts (high signal in DWI and low signal in apparent diffusion coefficient maps) at left posterior corona radiata (internal borderzone) and left temporal–parietal cortical and subcortical regions (including the posterior borderzone). There were also older small infarcts (high signal in T2 fluid-attenuated inversion recovery imaging and iso-intensity signal in apparent diffusion coefficient maps) in the same regions. The 3DRA exam conducted 4 weeks after the index stroke showed 80% stenosis of the left MCA-M1 with an ulcer in the plaque surface, that is, contrast appearing beneath the surface outline of the plaque (arrow). The patient received aspirin and clopidogrel treatment for 4 weeks since admission followed by lifelong aspirin treatment, in conjunction with stringent vascular risk factor control. The patient had no recurrent ischaemic stroke within 1 year after the index stroke. A repeated 3DRA exam at 1 year showed healing of the previously ulcerated MCA-M1 plaque. 3DRA, 3-dimensional rotational angiography; DWI, diffusion-weighted imaging; MCA-M1, M1 middle cerebral artery.