| BackgroundStroke is one of the leading causes of death worldwide. Each year, approximately 780000 people experience a new or recurrent stroke. Every 3 to 4 minutes, someone dies of a stroke on average. Patients who survived a transient ischemic attack is still at a risk of another ischemic cerebral event. Also, It is well accepted that atheromatous plaque is one of the major causes of stroke, and some researches find that up to 15% of cerebral infarctions are in association with embolic debris and thrombi at carotid bifurcation This is the reason why plaque vulnerability is drawing public attention in scientific field.The morphology and deformation is critical to the vulnerabilty of carotid plaques, characteristics on plaque morphology has been widely investigated. IMT (intima-media thickness) and plaque stenosis were both reported to be independent indicators associated with ischemic stroke. Besides, plaque characterization, low echogenic plaque, plaque area, plaque volume, remolding index, eccentric index have also been reported to predict a subsequent stroke. Evidence support that carotid endarterectomy for severe symptomatic (70 to 99%) stenosis reduces the stroke risk compared to medical therapy alone for patients with 70 to 99% symptomatic stenosis.Additional indicators other than morphological characteristics are needed to identify carotid artery lesions associated with a higher risk of stroke. Local mechanical environment is of great importance to plaque vulnerability. Stresses and strains mainly represent the local mechanical environment over endothelial and smooth muscle cells. Wall shear stress (WSS) is the frictional force exerted by circulating blood on endothelium and also an independent risk factor that involved with vulnerability. Low systolic WSS is identified as an atherosclerotic risk factor and may be responsible for a subsequent stroke. A higher level of tensile stress was proved to be related to plaque vulnerability and plaque rupture. The changes in the local mechanical factors further affect cellular processes such as cell proliferation, apoptosis, hypertrophy, migration, matrix synthesis and degradation, and therefore ultimately lead to observed structural and functional responses of remodeling.Vector velocity imaging (VVl) is an angle-independent imaging method that uses a complicated tissue tracking algorithm and applied to conventional grayscale images to give information on myocardial velocity vectors and derive myocardial mechanic parameters. This technique is now widely used in the diagnosis of cardiac diseases, such as heart failure, cardiomyopathy, hypertension and the benefit of cardiac resynchronization therapy for its potential to quantitatively assess regional and global myocardial functions.Limited researches have been focused on plaque deformation information derived from velocity vector imaging, by now, to our knowledge. Yue et al. investigated rotation of carotid plaques with this technique on short-axis view of carotid arteries. Wang et al. reported significantly lower radial velocities and higher circumferential strain rates of carotid artery in cerebral infarction subjects compared to those in the normals. However, research work on the longitudinal view of cartid arteries is rarely covered. Bending strain on the longitudinal view of an atherosclerotic plaque provide useful information of repetitive bending deformation of an atherosclerotic plaque and maybe responsible for plaque fatigue and rupture.Objective1. To investigate the local mechanical properties of carotid plaques with different types of ischemic ischemic cerebral vascular diseases using velocity vector imaging (VVl) technique. 2. To evaluate the segmental mechanical properties of atheromatous plaques.3. To investigate the difference of local mechanical properties among different locations on atheromatous plaques.4. To explore the diagnostic value of mechanical parameters derived from velocity vector imaging.Methods1. Study population and groupingStudy population:109 participants were enrolled in this study, of which 41 were diagnosed with acute ischemic infarction,17 were diagnosed with transient ischemic attack and 51 were without cerebrovascular history. All participants were with ischemic cerebrovascular diseases and carotid atherosclerosis and had gone through MRI or CT for diagnosis. Patients with hemorrhagic infarction, subarachnoid hmmorrhage, cardiac emboli, moyamoya disease were excluded in our study.Grouping:(1)according to clinical diagnosis:0 group is representative of subjects without cerebralvascular history, TIA group and 2 are representative of patients with transient ischemic attack and ischemic infarction, separately. (2)according to plaque location on segments of carotid artery:AM group includes plaques on initial segment and middle segment of carotid artery, Bl group includes those on carotid bifurcation and initiation of interal carotid artery. (3)according to where the region of intrerest (ROI) was placed:P1 is termed as proximal base group, P2 is termed as proximal shoulder group, P3 means top of plaque group, P4 is distal shoulder group, P5 is distal base group.2. Methods2.1 two-dimensional echocardiographyTwo-dimensional echocardiography was performed in all patients with image clips obtained after automated tissue tracking across three cardiac cycles. Visual information was acquired using a linear-array 10-14 MHz transducer (15L8W), with the frame rate controlled within 60～70 frame/sec.2.2 Post processing of image clipsVelocity vector imaging software (syngo VVl, Siemens) was used to derive tissue velocity, strain, and strain rate, with curves obtained after automated tissue tracking. Out of the consideration that the behaviors of deformation may differ in locations, under the influence of blood flow, plaque structure, and vessel movement, we selectively tracked atheromatous plaque at five locations that include distal base (P5), distal shoulder (P4), top (P3), proximal shoulder (P2) and proximal base (P1) in each satisfactory image clip. The removable reference mark on B-mode image clips was put in the tissue across the lumen, during data analysis. Motion-related parameters such as tissue velocity, strain and strain rate were exported and later processed for the maximum, the minimum and the extreme variation values. According where the reference mark was placed, a positive value of velocity means the tracked site is moving towards the lumen center, while a negative one has the opposite meaning. Strain and strain is positive during plaque extension and negative during contraction.3. Statistical ananlysisSPSS 16.0 (SPSS Inc., Illinois, USA) was used for statistical analysis. Measures of grouped data are reported as mean±standard deviation. Discrete variables were analyzed by chi-square test. One-way ANOVA is used for multiple comparisons. Comparision between mechanic parameters of different locations is done with paired t test. LSD test is performed if equal variance is assumed. Dunnett's T3 is performed is if equal variance is not assumed. Binary logistic regression and ROC curve is done for diagnostic value of mechanic parameters for ischemic cerebral event. A P value of less than 0.05 is considered as significant.Results1. Comparisons of mechanical parameters among diagnostic groupsPeak velocity values:TIA group showed significantly higher P1-Vmax, P2-Vmax, P3-Vmax, P4-Vmin, P5-Vmin, T-Vmax, T-Vmin and T-Vcompared to NCD group. ACI group showed significantly higher T-Vmax, T-Vmin and T-V compared to NCD group. A significantly lower level of P1-Vmax, P2-Vmax, P3-Vmax, P4-Vmin, P5-Vmin, P1-V, P2-V, P4-V and P5-V were detected in ACI group in comparison to NCD group. Significance of peak strain and strain rate values was not detected among groups.2. Segmental comparisons of mechanical parameters among each diagnostic group2.1 Comparisons of mechanical parameters of low echogenic plaque between AM group and Bl groupAM-Vmin was significantly higher Bl-Vmin (P<0.05). No signifcance was detected in other parameters (P>0.05).2.2 Comparisons of mechanical parameters among diagnostic groups in AM segmentsTIA group showed significantly higher IM-Vmax and IM-Vmin compared to NCD group. ACI group showed significantly higher levels of IM-Vmin, M-S and IM-SRmin compared to NCD group. A significantly lower level of IM-Vmax, IM-V, IM-SRmin was detected in ACI group compared to TIA group.2.3 Comparisons of mechanical parameters among diagnostic groups in Bl segmentsTIA group showed significantly higher Bl-Vmax, Bl-Vmin and Bl-V (P<0.05)and a significantly lower BI-Smin(P<0.05)compared to NCD group. ACI group showed a significantly higher level of Bl-Vmin,and BI-SRmin and a significantly lower Bl-Smin (P<0.05) compared to NCD group. A significantly lower level of Bl-Vmax and Bl-Vwas detected in ACI group compared to TIA group.3. Comparisons of mechanical parameters among different locations3.1 Comparisons of mechanical parameters among different locations in symptomatic patientsPeak velocity values:Vmax, Vmin, V all showed a trend of first increase and then decrease. P1-Vmax is significantly higher than P2-Vmax, P3-Vmax and P4-Vmax (P<0.05). P5-Vmax is significantly higher than P3-Vmax and P4-Vmax (P<0.05). P1-V is significantly higher than P2-V and P3-V. P5-V is significantly higher than P2-V, P3-V and P4-V. P1-Vmin is significantly higher than P2-Vmin (P<0.05), P4-Vmin is significantly higher than P3-Vmin, P5-Vmin is significantly higher than P2-Vmin, P3-Vmin and P4-Vmin(P<0.05).Peak strain values:Smax, Smin, S all showed a trend of first increase and then decrease. P2-Smin is significantly higher than P4-Smin (P<0.05), P2-S is significantly higher than P1-Sand P5-S (P<0.05).Peak strain rate values:SRmax showed a increasing intendancy from P1 to P5, P5-SRmax is significantly higher than P1-SRmax (P<0.05).3.2 Comparisons of mechanical parameters among different locations on asymptomatic plaquesPeak velocity values:A decreasing trend was detected in Vmax, Vmin and V from P1 to P4. Both P1-V and P2-V are significantly higher than P4-V (P<0.05).Peak strain values:A trend of first increase and then decrease was detected in Smax, Smin and S. However no significance was detected among different locations.Peak strain rate values:No agreement on trend was detected in SRmax, SRmin and SR. Besides, no significance of strain rate was detected among different locations.4. Predictors of a subsequent ischemic cerebral eventIn order to test if mechanical parameters are indicative of a ischemic cerebralvascular event (both acute ischemic stroke and TIA), we used four binary logistic regression models in which peak velocity values, morphological parameters, extreme velocity parameters and total parameters were included.Model 1 (model of peak velocity values):includes P1-Vmax, P2-Vmax, P3-Vmax, P4-Vmin, P5-Vmin, P1-V, P2-V, P4-V and P5-V. An AUC of 0.713 was detected in this model. Model 2 (model of morphological parameters):include Ds, Dd, IMT, Lp. AUC was 0.634 in model 2.Model 3 (model of extreme velocity parameters):Vmax, Vmin and V were included in this model, an AUC of 0.659 was detected.Model 4(model of total parameters):Model 4 includes both morphological and mechanical parameters. AUC for this model is 0.812, which means the abiblity for predication is highly elevated. The sensitivity and specificity were 0.780 and 0.836 at the cut-off point.Conclusion1. Vector velocity imaging is an angle-independent visual and quantitative method for the quantitatively assessment of carotid atheromatious plaque vulnerability.2. Result of segmental analysis of velocity, strain and strain rate showed that radial velocity varies in segments. Therefore, this parameter might be more susceptible to hemodynamic states.3. A characteristic of asymmetry was detected among different locations on carotid plaques, the asymmetrical properties may be more detectabl in symptomatic plaques.4. A model that combines the morphological and mechanical parameters may better diagnosis patients with ischemic cerebralvascular diseases.
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