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(Circulation. 2006;113:e660-e661.)
© 2006 American Heart Association, Inc.

Images in Cardiovascular Medicine

Serial High-Spatial-Resolution, Multisequence Magnetic Resonance Imaging Studies Identify Fibrous Cap Rupture and Penetrating Ulcer Into Carotid Atherosclerotic Plaque

Baocheng Chu, MD, PhD; Chun Yuan, PhD; Norihide Takaya, MD, PhD; Jason R. Shewchuk, MD; Alexander W. Clowes, MD; Thomas S. Hatsukami, MD

From the Departments of Radiology (B.C., C.Y., N.T., J.S.) and Surgery (A.C., T.S.H.), University of Washington; and Department of Surgery (T.S.H.), VA Puget Sound Heath Care System, Seattle, Wash.

Correspondence to Dr Baocheng Chu, Department of Radiology, Box 357115, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195. E-mail chubc{at}u.washington.edu

A 67-year-old woman with a history of bilateral carotid artery stenosis and 4 episodes of myocardial infarction had left arm claudication for 1 month. Diffusion-weighted magnetic resonance imaging (MRI) did not identify acute cerebral infarction. Transcranial Doppler imaging did not reveal any emboli. She had been followed by a clinical research study, PRIMARI (Plaque Rupture In MAgnetic Resonance Imaging). A baseline high-spatial-resolution, multisequence MRI performed 10 months previously showed an atherosclerotic plaque with intraplaque hemorrhage in the right internal carotid artery (Figure 1A through 1D) and a calcified plaque in the left carotid artery. Both arteries had intact fibrous cap.^1,2 A repeat MRI identified fibrous cap rupture and an ulcer penetrating into the plaque in the right internal carotid artery (Figure 1E through 1H). Contrast-enhanced 2-dimensional spoiled GRASS and carotid angiography confirmed the presence of the fibrous cap rupture and ulcer (Figure 2). There was no change in the left carotid artery between baseline and follow-up MR scans. Significant left subclavian artery stenosis identified on the carotid angiogram was considered to be the underlying cause of her left arm claudication. Although there was no cerebral embolization that originated from fibrous cap rupture and ulcer, serial-high-spatial resolution, multisequence carotid MRI identified the atherosclerotic plaque with intraplaque hemorrhage at baseline and fibrous cap rupture and ulcer during follow-up study. This case suggests that intraplaque hemorrhage may be a driving force for plaque progression and that silent plaque rupture can also occur in carotid atherosclerosis.^3,4

View larger version (97K): [in this window] [in a new window]   Figure 1. A through D, Matched baseline images (A, 3-dimensional time of flight; B, T2-weighted; C, pre–contrast-enhanced, T1-weighted; and D, post–contrast-enhanced, T1-weighted), obtained by high-spatial-resolution MRI (matrix, 256x256; field of view, 160x120 mm; slice thickness, 2 mm), demonstrate carotid atherosclerotic plaque and luminal stenosis in the right internal carotid artery. A dark band between the lumen and arterial wall (arrow, A) suggests intact fibrous cap.1 Hyperintense signal on images A, B, and C suggests presence of intraplaque hemorrhage.2 Follow-up MR images E through G (corresponding to images A through C, respectively, in sequence and location) demonstrate surface disruption (open arrows) and penetrating ulcer into the plaque. The signal within the ulcer demonstrates hyperintense signal on E, mixed hyperintense and hypointense signal on F, hypointense signal on G, and contrast enhancement on H. This signal pattern suggests turbulent flow within the ulcer. Note slight location mismatch between post–contrast-enhanced T1-weighted images at baseline (D) and follow-up (H). This mismatch resulted from the patient’s minimum motion during image H acquisition.

View larger version (99K): [in this window] [in a new window]   Figure 2. A, Contrast-enhanced, 2-dimensional spoiled GRASS image (matrix, 256x256; field-of-view, 160x120 mm; thickness, 3 mm; one multisequence of follow-up MRI) reveals contrast-enhanced blood flow protruding into the plaque, suggesting rupture and ulcer (open arrow). B, Carotid angiogram performed 1 day after A reveals approximately 5-mm ulcer (open arrow) projecting from the right internal carotid artery (20 mm distal to the bifurcation). This ulcer corresponds in location to the one seen on A and in Figure 1E through 1H.

	Acknowledgments

 
This study was supported by National Institutes of Health grants R01-HL-61851 and R01-HL-073401.

Disclosures

None.

	References

Top References

 

1. Hatsukami TS, Ross R, Polissar NL, Yuan C. Visualization of fibrous cap thickness and rupture in human atherosclerotic carotid plaque in vivo with high-resolution magnetic resonance imaging. Circulation. 2000; 102: 959–964.[Abstract/Free Full Text]
   
2. Chu B, Kampschulte A, Ferguson MS, Kerwin WS, Yarnykh VL, O’Brien KD, Polissar NL, Hatsukami TS, Yuan C. Hemorrhage in the atherosclerotic carotid plaque: a high-resolution MRI study. Stroke. 2004; 35: 1079–1084.[Abstract/Free Full Text]
   
3. Takaya N, Yuan C, Chu B, Saam T, Polissar NL, Jarvik GP, Issac C, McDonough J, Natiello C, Small R, Ferguson MS, Hatsukami TS. Presence of intraplaque hemorrhage stimulates progression of carotid atherosclerotic plaques. Circulation. 2005; 23: 2768–2775.
   
4. Burke AP, Kolodgie FD, Farb A, Weber DK, Malcom GT, Smialek J, Virmani R. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression. Circulation. 2001; 103: 934–940.[Abstract/Free Full Text]
   

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