Importance of assessment of carotid plaques in the managementof acute ischemic stroke: floating intracarotid plaque

Published: 6 September 2023
Abstract Views: 281
PDF: 57
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.


Mobile atheromatous plaques affecting large arteries are a major risk factor for embolic strokes. We report a case of extensive embolic cerebral infarction secondary to a vulnerable internal carotid artery plaque. A 67-year-old female was admitted with sudden left-sided weakness. A computed tomography brain scan revealed early ischemic changes in the right middle cerebral territory. The ultrasound Doppler showed soft mobile plaque with thrombus in the right internal carotid artery causing 90% stenosis. Magnetic resonance imaging brain scan performed later showed extensive right cerebral infarction. A computed tomography angiogram revealed ulcerated non-occlusive soft tissue plaque in the right internal carotid artery. She was also diagnosed with bladder cancer during this admission and was managed medically due to her performance status. Unstable vulnerable plaques can be symptomatic even in the absence of significant carotid stenosis. Hence, early identification of the plaque vulnerability, using new imaging modalities, and its medical stabilization can help to reduce the risk of cerebrovascular insults. The etiopathogenesis of inflammation within unstable vulnerable plaques and its concordance with inflammatory markers is still unclear. It is feasible in our case the malignantprocess could also be contributing to the inflammation within the blood vessels promoting vulnerability of the plaques.

Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST - Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993;24:35-41. DOI:

The World Health Organization MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. WHO MONICA Project Principal Investigators. J Clin Epidemiol 1988;41:105-14. DOI:

North American Symptomatic Carotid Endarterectomy Trial Collaborators; Barnett HJM, Taylor DW, Haynes RB, et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. New Engl J Med 1991;325:445-53. DOI:

Casscells W, Naghavi M, Willerson JT. Vulnerable atherosclerotic plaque: a multifocal disease. Circulation 2003;107:2072-5. DOI:

Tofler GH, Stone PH, Maclure M, et al. Analysis of possible triggers of acute myocardial infarction (the MILIS study). Am J Cardiol 1990;66:22-7. DOI:

Yonetsu T, Jang IK. Advances in intravascular imaging: new insights into the vulnerable plaque from imaging studies. Korean Circ J 2018;48:1-15. DOI:

MacIsaac AI, Thomas JD, Topol EJ. Toward the quiescent coronary plaque. J Am Coll Cardiol 1993;22:1228-41. DOI:

Adla T, Adlova R. Multimodality imaging of carotid stenosis. Int J Angiol 2015;24:179-84. DOI:

Huang H, Virmani R, Younis H, et al. The impact of calcification on the biomechanical stability of atherosclerotic plaques. Circulation 2001;103:1051-6. DOI:

Nandalur KR, Baskurt E, Hagspiel KD, et al. Carotid artery calcification on CT may independently predict stroke risk. AJR Am J Roentgenol 2006;186:547-52. DOI:

Thrysøe SA, Oikawa M, Yuan C, et al. Longitudinal distribution of mechanical stresses in carotid plaques of symptomatic patients. Stroke 2010;41:1041-3. DOI:

Moulton KS, Vakili K, Zurakowski D, et al. Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis. P Natl Acad Sci USA 2003;100:4736-41. DOI:

Lovett JK, Rothwell PM. Site of carotid plaque ulceration in relation to direction of blood flow: an angiographic and pathological study. Cerebrovasc Dis 2003;16:369-75.

Buja LM, Willerson JT. Role of inflammation in coronary plaque disruption. Circulation 1994;89:503-5. DOI:

Ridker PM, Rifai N, Pfeffer MA, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation 1998;98:839-44. DOI:

Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. New Engl J Med 2000;342:836-43. DOI:

Haverkate F, Thompson SG, Pyke SD, et al. Production of C-reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997;349:462-6. DOI:

Ridker PM, Rifai N, Clearfield M, et al. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. New Engl J Med 2001;344:1959-65. DOI:

Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. New Engl J Med 1997;336:973-9. DOI:

Lovett JK, Rothwell PM. Site of carotid plaque ulceration in relation to direction of blood flow: an angiographic and pathological study. Cerebrovasc Dis 2003;16:369-75 DOI:

Eltemamy, M., Namushi, R., & Saravanan, N. (2023). Importance of assessment of carotid plaques in the managementof acute ischemic stroke: floating intracarotid plaque. Bleeding, Thrombosis, and Vascular Biology, 2(3).


Download data is not yet available.