Table 2.

MRI Protocols and Study Definitions

Study Number	Study First Author and Year	MRI Field Strength	MRI Scanner Platform	Coil Type Used	T1‐Weighted Imaging Sequence Parameters	Field of View	Matrix	Acquired Resolution	Contrast Agent Administered	Number of MRI Readers	Definitions of Abnormal Vessel Wall Enhancement	Vessel Site Evaluated for Enhancement	Culprit and Non‐Culprit Plaque Definition
1	van der Kolk 201114	7.0‐T	Philips Healthcare	16‐channel receive coil	Magnetization preparation inversion recovery turbo spin‐echo sequence; TR/TE 6050/23, inversion time 1770 ms	220×180×13 mm3	N/A	0.8×0.8×0.8 mm3	0.1 mL/kg of gadobutrol	2 with consensus	After coregistering pre‐ and postcontrast scans, the images were subtracted and directly compared to determine enhancing areas and concomitant vessel wall anatomy. The infundibulum was used to assess whether normal contrast enhancement had taken place	Intracranial internal carotid artery	Culprit (defined during data extraction for meta‐analysis): Vessel immediately upstream of a stroke of undetermined etiology or stroke attributable to ipsilateral large vessel atherosclerosis; Non‐culprit plaque: vessels studied in the intracranial circulation but not meeting definition of culprit plaque
2	Kim 201215	3.0‐T	Conventional MRI: Signa, GE Medical Systems; High Resolution‐MRI: Veiro, Siemens Healthcare	8‐channel head coil	T1‐weighted: TR/TE 600/12	120×120 mm	384×269	N/A	Gadolinium	2 with a 3rd reader available to resolve disagreements	Atheromatous plaque: Eccentric or focal signal intensity within the vessel lumen on MRI. Abnormal enhancement: enhancement on T1‐enhanced images. Vulnerable symptomatic plaque: eccentric or focal signal intensity within vessel lumen on MRI accompanied by intraplaque heterogeneous signal intensity on T1 and T2 images and plaque	Middle cerebral artery	Vulnerable symptomatic plaque: eccentric or focal signal intensity within vessel lumen on MRI accompanied by intraplaque heterogeneous signal intensity on T1 and T2 images and plaque enhancement on T1‐enhanced images. Stable symptomatic plaque: eccentric or focal signal intensity within vessel lumen on MRI in the absence of the features described earlier in vulnerable symptomatic plaque. Culprit plaque defined as plaques upstream of ipsilateral ischemic infarctions
3	Skarpathiotakis 201316	3.0‐T	HDX platform, GE healthcare	8‐channel head coil	T1 FLAIR TR/TE 2108/12, inversion time 860 ms	16×22 cm	N/A	384×384	7.5‐mL gadobutrol	1	Enhancement similar to pituitary parenchyma=strong; less than pituitary parenchyma=mild; no change from precontrast images=absent	Middle cerebral artery	Number of atherosclerotic plaques were tabulated and divided into plaques in stroke territory (culprit) and nonstroke territory (non‐culprit) vasculature
4	Vakil 201317	1.5‐T	Avanto/Espree, Siemens	Receive‐only head coil	T1‐weighted spin‐echo: TR/TE 663/15	220 to 240 mm	256×256	N/A	0.1 mmol/kg of gadopentetate dimeglumine	2 with a 3rd reader available to resolve disagreements	Qualitative assessment: 1=definite non‐enhancement, 2=suspected non‐enhancement, 3=uncertain, 4=suspected enhancement, 5=definite enhancement. A plaque with an average >3=enhancing, while plaque with an average <3=nonenhancing. Plaque enhancement was quantified as the relative increase in lesion T1‐signal postcontrast: mean T1 signal intensity in the outer wall area on postcontrast divided by its precontrast signal	Supraclinoid internal carotid artery	A symptomatic intracranial atherosclerotic plaque (culprit) was defined as presenting with acute neurologic symptoms and/or restricted diffusion weighted abnormalities corresponding to the vascular distribution of the intracranial stenosis. Non‐culprit plaques were asymptomatic plaques
5	Qiao 201418	3.0‐T	Achieva and Vista, Philips Healthcare	Body coil for transmission and 8‐channel head coil for reception	3D black blood T1: TR/TE 2000/38	180×180×40 mm	450×450×100	0.4×0.4×0.4 mm	0.1 mmol/kg of gadopentetate dimeglumine	1 reader for plaque identification and 2 for assessment of enhancement	Qualitative 3‐point scale: grade 0 enhancement similar to or less than normal vessels in the same individual; grade 1: enhancement was greater than that of grade 0 but less than that of the pituitary infundibulum; grade 2: enhancement was similar to or greater than that of the infundibulum	Cavernous and supraclinoid internal carotid artery	1. Culprit: (a) the only lesion within the vascular territory of the stroke; (b) the most stenotic lesion when multiple plaques were present within the same vascular territory of the stroke. 2. Probably culprit: when the plaque was not the most stenotic lesion within the same vascular territory of the stroke. 3. Nonculprit: when the plaque was not within the vascular territory of the stroke
6	Teng 201519	3.0‐T	HDX, GE Healthcare	8‐channel phased array brain coil	T1‐weighted: TR/TE 567/16	10×10 cm2	320×256	N/A	0.2 mmol/kg gadopentetic acid	3 (2 residents, 1 neuroradiologist) with consensus	Average signal intensity enclosed between the lumen and outer wall normalized to adjacent gray matter. If normalized value >1.0=plaque enhancement	MCA	Culprit plaque: a lesion arising on the ipsilateral side to an ischemic stroke on neuro‐imaging with accompanying clinical symptoms; Non‐culprit plaque: either a plaque occurring in a contralateral artery of a symptomatic patient or one in asymptomatic controls
7	Xu 201520	3.0‐T	Discovery MR750, GE Healthcare	16‐channel phase array coil	T1‐weighted: TR/TE 600/12 ms	12×12 cm	256×256	N/A	0.1 mmol/kg of gadopentetate dimeglumine	2 with consensus	Enhancement between the outer wall boundary and vessel lumen on postcontrast images	Middle cerebral artery	Culprit: Atherosclerotic plaques upstream and ipsilateral to diffusion‐weighted imaging hyperintensity in the same vascular territory. All other plaques studied considered non‐culprit
8	Zou 201521	3.0‐T	Magnetom Verio, Siemens	32‐channel head coil	T1‐weighted SPACE: TR/TE 938/24 ms	N/A	N/A	0.5 to 0.7 mm3	0.1 mmol/kg of gadopentetate dimeglumine	2 with consensus	Mean signal intensities of the MCA vessel wall on registered pre‐ and post‐contrast T1w‐SPACE were measured and normalized to gray matter. Signal intensity change ≥20% was defined as plaque enhancement	Middle cerebral artery	Culprit plaque: a lesion arising on the ipsilateral side to an ischemic stroke confirmed on brain MRI; Non‐culprit plaque: plaque occurring in a contralateral artery of a symptomatic patient

MCA indicates middle cerebral artery; MRI, magnetic resonance imaging; N/A, data not available; SPACE, sampling perfection with application optimized contrasts using different flip‐angle evolution; T, Tesla; TE, time to echo; TR, time to repetition.