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 (vp) and transfer constant (Ktrans) 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 Ktrans 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 Ktrans only, with decreased high-density lipoprotein levels (r = -0.66, P < .001) and elevated Ktrans measurements in smokers compared with nonsmokers (mean, 0.134 min(-1) vs 0.074 min(-1), respectively; P = .01). CONCLUSION: The correlations between Ktrans and histologic markers of inflammation suggest that Ktrans is a quantitative and noninvasive marker of plaque inflammation, which is further supported by the correlation of Ktrans with proinflammatory cardiovascular risk factors, decreased high-density lipoprotein levels, and smoking.
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 (vp) and transfer constant (Ktrans) 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 Ktrans 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 Ktrans only, with decreased high-density lipoprotein levels (r = -0.66, P < .001) and elevated Ktrans measurements in smokers compared with nonsmokers (mean, 0.134 min(-1) vs 0.074 min(-1), respectively; P = .01). CONCLUSION: The correlations between Ktrans and histologic markers of inflammation suggest that Ktrans is a quantitative and noninvasive marker of plaque inflammation, which is further supported by the correlation of Ktrans with proinflammatory cardiovascular risk factors, decreased high-density lipoprotein levels, and smoking.
Authors: Jianming Cai; Thomas S Hatsukami; Marina S Ferguson; William S Kerwin; Tobias Saam; Baocheng Chu; Norihide Takaya; Nayak L Polissar; Chun Yuan Journal: Circulation Date: 2005-11-21 Impact factor: 29.690
Authors: C R Weiss; A E Arai; M N Bui; K O Agyeman; M A Waclawiw; R S Balaban; R O Cannon Journal: J Magn Reson Imaging Date: 2001-12 Impact factor: 4.813
Authors: Chun Yuan; William S Kerwin; Marina S Ferguson; Nayak Polissar; Shaoxiong Zhang; Jianming Cai; Thomas S Hatsukami Journal: J Magn Reson Imaging Date: 2002-01 Impact factor: 4.813
Authors: Bruce A Wasserman; William I Smith; Hugh H Trout; Richard O Cannon; Robert S Balaban; Andrew E Arai Journal: Radiology Date: 2002-05 Impact factor: 11.105
Authors: Mohammad Madjid; Morteza Naghavi; Basit A Malik; Silvio Litovsky; James T Willerson; Ward Casscells Journal: Am J Cardiol Date: 2002-11-21 Impact factor: 2.778
Authors: Kevin D O'Brien; David M Shavelle; Michael T Caulfield; Thomas O McDonald; Katherine Olin-Lewis; Catherine M Otto; Jeffrey L Probstfield Journal: Circulation Date: 2002-10-22 Impact factor: 29.690
Authors: Li Dong; Williams S Kerwin; Huijun Chen; Baocheng Chu; Hunter R Underhill; Moni Blazej Neradilek; Thomas S Hatsukami; Chun Yuan; Xue-Qiao Zhao Journal: Radiology Date: 2011-04-14 Impact factor: 11.105
Authors: Stephan Metz; Ambros J Beer; Marcus Settles; Jaroslav Pelisek; René M Botnar; Ernst J Rummeny; Peter Heider Journal: Int J Cardiovasc Imaging Date: 2010-10-24 Impact factor: 2.357
Authors: Baocheng Chu; Marina S Ferguson; Huijun Chen; Daniel S Hippe; William S Kerwin; Gador Canton; Chun Yuan; Thomas S Hatsukami Journal: JACC Cardiovasc Imaging Date: 2009-07