Background and Purpose-It has been hypothesized that high structural stress in atherosclerotic plaques at critical sites may contribute to plaque disruption. To test that hypothesis, 3D fluid-structure interaction models were constructed based on in vivo MRI data of human atherosclerotic carotid plaques to assess structural stress behaviors of plaques with and without rupture. Methods-In vivo MRI data of carotid plaques from 12 patients scheduled for endarterectomy were acquired for model reconstruction. Histology confirmed that 5 of the 12 plaques had rupture. Plaque wall stress (PWS) and flow maximum shear stress were extracted from all nodal points on the lumen surface of each plaque for analysis. A critical PWS (maximum of PWS values from all possible vulnerable sites) was determined for each plaque. Results-Mean PWS from all ulcer nodes in ruptured plaques was 86% higher than that from all nonulcer nodes (123.0 versus 66.3 kPa, PϽ0.0001). Mean flow maximum shear stress from all ulcer nodes in ruptured plaques was 170% higher than that from all nonulcer nodes (38.9 versus 14.4 dyn/cm2, PϽ0.0001). Mean critical PWS from the 5 ruptured plaques was 126% higher than that from the 7 nonruptured ones (247.3 versus 108 kPa, Pϭ0.0016 using log transformation). Conclusion-The results of this study show that plaques with prior ruptures are associated with higher critical stress conditions, both at ulcer sites and when compared with nonruptured plaques. With further validations, plaque stress analysis may provide additional stress indicators helpful for image-based plaque vulnerability assessment. (Stroke.

IgG4-RD is a systemic inflammatory and sclerosing disease. Parotid and lacrimal involvement (formerly called Mikulicz's disease), lymphadenopathy and pancreatitis are the most common manifestations. Patients with IgG4-RD showed favourable responses to treatment with glucocorticoids and immunosuppressive agents.

ResearchLocal critical stress correlates better than global maximum stress with plaque morphological features linked to atherosclerotic plaque vulnerability: an in vivo multi-patient study AbstractBackground: It is believed that mechanical stresses play an important role in atherosclerotic plaque rupture process and may be used for better plaque vulnerability assessment and rupture risk predictions. Image-based plaque models have been introduced in recent years to perform mechanical stress analysis and identify critical stress indicators which may be linked to rupture risk. However, large-scale studies based on in vivo patient data combining mechanical stress analysis, plaque morphology and composition for carotid plaque vulnerability assessment are lacking in the current literature.Methods: 206 slices of in vivo magnetic resonance image (MRI) of carotid atherosclerotic plaques from 20 patients (age: 49-71, mean: 67.4; all male) were acquired for model construction. Modified Mooney-Rivlin models were used for vessel wall and all plaque components with parameter values chosen to match available data. A morphological plaque severity index (MPSI) was introduced based on in vivo plaque morphological characteristics known to correlate with plaque vulnerability. Critical stress, defined as the maximum of maximum-principalstress (Stress-P 1 ) values from all possible vulnerable sites, was determined for each slice for analysis. A computational plaque stress index (CPSI, with 5 grades 0-4, 4 being most vulnerable) was defined for each slice using its critical stress value and stress interval for each CPSI grade was optimized to reach best agreement with MPSI. Correlations between CPSI and MPSI, plaque cap thickness, and lipid core size were analyzed. Results:Critical stress values correlated positively with lipid core size (r = 0.3879) and negatively with cap thickness (r = -0.3953). CPSI classifications had 71.4% agreement with MPSI classifications. The Pearson correlation coefficient between CPSI and MPSI was 0.849 (p < 0.0001). Using global maximum Stress-P 1 value for each slice to define a global maximum stress-based CPSI (G-CPSI), the agreement rate with MPSI was only 34.0%. The Pearson correlation coefficient between G-CPSI and MPSI was 0.209. Conclusion:Results from this in vivo study demonstrated that localized critical stress values had much better correlation with plaque morphological features known to be linked to plaque rupture risk, compared to global maximum stress conditions. Critical stress indicators have the potential to improve image-based screening and plaque vulnerability assessment schemes.

Atherosclerotic plaque rupture leading to stroke is the major cause of long-term disability as well as the third most common cause of mortality. Image-based computational models have been introduced seeking critical mechanical indicators, which may be used for plaque vulnerability assessment. This study extends the previous 2D critical stress concept to 3D by using in vivo magnetic resonance image (MRI) data of human atherosclerotic carotid plaques and 3D fluidstructure interaction (FSI) models to: identify 3D critical plaque wall stress (CPWS) and critical flow shear stress (CFSS) and to investigate their associations with plaque rupture. In vivo MRI data of carotid plaques from 18 patients scheduled for endarterectomy were acquired using histologically validated multicontrast protocols. Of the 18 plaques, histology-confirmed that six had prior rupture (group 1) as evidenced by presence of ulceration. The remaining 12 plaques (group 2) contained no rupture. The 3D multicomponent FSI models were constructed for each Copyright © 2010 by ASME plaque to obtain 3D plaque wall stress (PWS) and flow shear stress (FSS) distributions. Threedimensional CPWS and CFSS, defined as maxima of PWS and FSS from all vulnerable sites, were determined for each plaque to investigate their association with plaque rupture. Slice-based critical PWS and FSS were also calculated for all slices for more detailed analysis and comparison. The mean 3D CPWS of group 1 was 263.44 kPa, which was 100% higher than that from group 2 (132.77, p = 0.03984). Five of the six ruptured plaques had 3D CPWS sites, matching the histology-confirmed rupture sites with an 83% agreement. Although the mean 3D CFSS (92.94 dyn/cm 2 ) for group 1 was 76% higher than that for group 2 (52.70 dyn / cm 2 ), slice-based CFSS showed no significant difference between the two groups. Only two of the six ruptured plaques had 3D CFSS sites matching the histology-confirmed rupture sites with a 33% agreement. CFSS had a good correlation with plaque stenosis severity (R 2 = 0.40 with an exponential function fitting 3D CFSS data). This in vivo MRI pilot study using plaques with and without rupture demonstrates that 3D critical plaque wall stress values are more closely associated with atherosclerotic plaque rupture then critical flow shear stresses. Critical wall stress values may become indicators of high risk sites of rupture. Future work with a larger population will establish a possible CPWS-based plaque vulnerability classification.