Plaque Distribution of Stenotic Middle Cerebral Artery and Its Clinical Relevance
Background and Purpose—Microanatomy studies reveal that most penetrating branches of middle cerebral artery (MCA) arise from the dorsal–superior surface of the trunk. Using high-resolution MRI, we sought to explore the plaque distribution of MCA atherosclerosis and its clinical relevance in relation to the orifices of penetrating arteries.
Methods—We retrospectively analyzed the imaging and clinical data of 86 patients with atherosclerotic MCA stenosis. On high-resolution MRI, plaques were categorized based on the involvement of the superior, inferior, ventral, or dorsal MCA wall. The relationship of plaque distribution and clinical presentation was analyzed.
Results—A total of 92 stenotic MCAs (40 symptomatic and 52 asymptomatic) on 828 image slices were studied. Overall, of the 251 slices with identified plaques, plaques were more frequently located at the ventral (44.8%) and inferior (31.7%) wall as compared with the superior (14.3%) and dorsal wall (9.0%; P<0.001). Symptomatic MCA stenosis had more superior (P=0.016) and less inferior (P=0.023) wall plaques than asymptomatic stenosis. Within the group of symptomatic MCA stenosis, vessels with penetrating artery infarctions had more superior (P=0.001) but less ventral (P=0.038) and inferior (P=0.024) plaques than without penetrating artery infarctions.
Conclusions—MCA plaques tend to locate opposite to the orifices of penetrating arterial branches. Further studies are required to investigate whether MCA plaque distribution is an independent determinant of stroke occurrence and its subtypes.
The characterization of plaque distribution on atherosclerotic arterial walls has important clinical implications. Studies on coronary atherosclerosis suggest plaques tend to form at the segments opposite to flow dividers.1 The existence of a plaque close to a branch vessel ostia has been shown to increase the risk of branch occlusion after coronary stenting.2 Until now, in vivo studies describing the distribution of plaques in the intracranial arterial wall have been lacking. This study was designed to examine the plaque distribution of atherosclerotic middle cerebral arteries (MCAs) using high-resolution MRI.
Patients and Methods
We retrospectively reviewed our single-institutional high-resolution MRI database (2007 to 2009) for patients with MCA atherosclerotic stenosis (>50%) detected by MR angiography. All patients fulfilled the following criteria: (1) lack of coexistent ipsilateral internal carotid artery stenosis (>50%); (2) no evidence of cardioembolism; and (3) image quality good enough for plaque identification. Symptomatic and asymptomatic stenosis were defined based on clinical presentations as described previously.3 The hospital ethics committee approved this study and all patients signed a written consent.
Details of our high-resolution MRI protocol were described elsewhere.3 A plaque was identified if there was eccentric wall thickening, whereas the thinnest part was estimated to be <50% of the thickest point by visual inspection.3 All cross-sections with eccentric plaque were classified based on their plaque orientation being centered on the superior, inferior, dorsal, or ventral side of the vessel (Figure 1). Each cross-section was grouped into 1 of the 4 quadrants. In cases in which the plaque was distributed between 2 quadrants, the quadrant with the maximal plaque thickness was chosen.4 Penetrating artery infarctions were defined as ischemic lesions seen in the territory of lenticulostriate arteries on diffusion-weighted images. All images were reviewed by 2 experienced readers (W.-H.X. and M.-L.L.) who were blinded to clinical data. The differences between the 2 observers were solved by consensus.
Quantitative data are expressed as mean±SD and qualitative data are expressed as percentage. For each stenosis, the percentage of individual plaque distribution was calculated (Supplement; http://stroke.ahajournals.org). The mean superior, inferior, dorsal, and ventral plaque orientation of the total group was derived from the individual percentage distribution.4 The comparison of the plaque distribution among different walls was performed by a Kruskal-Wallis test of the mean percentage of the distribution for each individual stenosis followed by Bonferroni correction for multiple comparisons. Data comparisons between symptomatic and asymptomatic vessels and between the vessels with and without penetrating artery infarction were conducted with the Wilcoxon test. A probability value of <0.05 was considered statistically significant.
Eighty-six patients were included in the study. Patients' clinical characteristics are presented in the Supplement. Plaques were identified in 251 of a total of 828 image slices on high-resolution MRI. Nine image slices with noneccentric wall thickening in 8 asymptomatic vessels were not included in this analysis. Overall, plaques were more frequently located at the ventral (44.8%) and inferior (31.7%) wall as compared with the superior (14.3%) and dorsal wall (9.0%; P<0.001, Kruskal-Wallis test; Supplement). The plaque distribution in different groups is outlined in the Table. Symptomatic MCA stenosis had significantly more superior and less inferior plaques than asymptomatic vessels (Figure 2). Within the group of symptomatic MCA stenosis, vessels with penetrating artery infarction had significantly more superior but less ventral and inferior plaques than without penetrating artery infarction.
Microanatomy studies suggest most of penetrating arteries, which may be considered as flow dividers, arise dorsally from the upper part of MCA wall.5 In this study, plaques were observed predominantly in the ventral and inferior wall, the locations opposite to the orifices of penetrating arteries. Therefore, MCA plaque distribution appears following the same rule as coronary atherosclerosis.1 These findings are meaningful. A major concern of intracranial angioplasty has been the forceful displacement of neighboring atheromatous material into branch vessel ostia. The opposite location of most MCA plaques and penetrating artery orifices suggests that such “snow-plowing” effect in intracranial angioplasty might be uncommon. Previous studies have indicated that the incidence of side branch occlusion after MCA stenting is indeed very low.6
Our study also revealed that symptomatic MCA stenosis had more superior but less inferior plaque location than asymptomatic stenosis. The occurrence of penetrating artery infarction has a positive association with superior wall plaques but a negative correlation with ventral and inferior wall plaques. Superior wall plaques are more likely to be symptomatic, possibly because they are nearer to the orifices of penetrating arteries. The growing superior MCA wall plaques, with or without thrombosis formation in situ, may be easier to occlude a local branch directly causing an infarct. Alternatively, the shedding of emboli may occlude downstream vessels through the nearby orifices. Our results suggest that plaque distribution may play an important role in stroke related to MCA atherosclerosis. Further studies are required to investigate whether MCA plaque distribution is an independent determinant of stroke occurrence and its subtypes.
Sources of Funding
This study was supported by the National Key Technology R&D Program of China (2006BAI01A10).
The online-only Data Supplement is available at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.111.618132/-/DC1.
- Received February 16, 2011.
- Revision received April 10, 2011.
- Accepted April 14, 2011.
- © 2011 American Heart Association, Inc.