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Inflammation in Carotid Atherosclerotic Plaque: A Dynamic Contrast-enhanced MR Imaging Study¹

¹ From the Department of Radiology (W.S.K., M.S.F., C.Y.), Division of Cardiology (K.D.O.), and Department of Surgery (T.S.H.), University of Washington, 815 Mercer St, Seattle, WA 98109; Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.P.); and VA Puget Sound Health Care System, Seattle, Wash (T.S.H.). Received August 10, 2005; revision requested October 18; revision received December 5; accepted December 14; final version accepted January 27, 2006. Supported by NIH grants R01-HL56874 and P01-072262 and AstraZeneca Pharmaceuticals. Assistance with mathematic modeling provided through the Resource Facility for Population Kinetics under the service clause of NIH grant EB-01975. Address correspondence to W.S.K. (e-mail: bkerwin{at}u.washington.edu).

Purpose: To prospectively evaluate if there is an association between plaque enhancement at magnetic resonance (MR) imaging and proinflammatory cardiovascular risk factors and plaque content.

Materials and Methods: This study was performed with informed consent, HIPAA compliance, and institutional review board approval. Contrast agent dynamics within carotid plaques were measured in 30 patients (29 men, one woman; mean age, 67.7 years ± 10.7 [standard deviation]) who were scheduled to undergo carotid endarterectomy. Measurements were based on kinetic modeling of images obtained at 15-second intervals during which a gadolinium-based contrast agent was injected. The time-varying signal intensities within the plaques were used to estimate the fractional plasma volume (v_p) and transfer constant (K^trans) of contrast material into the extracellular space. Pearson correlation coefficients were computed between blinded MR measurements and histologic measurements of plaque composition, including macrophages, neovasculature, necrotic core, calcification, loose matrix, and dense fibrous tissue. Correlation coefficients or mean differences were computed regarding clinical markers of cardiovascular risk.

Results: Analyzable MR images and histologic results were obtained in 27 patients. Measurements of K^trans correlated with macrophage (r = 0.75, P < .001), neovasculature (r = 0.71, P < .001), and loose matrix (r = 0.50, P = .01) content. Measurements of v_p correlated with macrophage (r = 0.54, P = .004), neovasculature (r = 0.68, P < .001), and loose matrix (r = 0.42, P = .03) content. For clinical parameters, significant associations were correlated with K^trans only, with decreased high-density lipoprotein levels (r = –0.66, P < .001) and elevated K^trans measurements in smokers compared with nonsmokers (mean, 0.134 min^–1 vs 0.074 min^–1, respectively; P = .01).

Conclusion: The correlations between K^trans and histologic markers of inflammation suggest that K^trans is a quantitative and noninvasive marker of plaque inflammation, which is further supported by the correlation of K^trans with proinflammatory cardiovascular risk factors, decreased high-density lipoprotein levels, and smoking.

© RSNA, 2006

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