Magnetic Resonance Imaging of Carotid Atherosclerosis

__Abstract__ Worldwide, about 17 million people die from cardiovascular disease (CVD) each year, chiefly from ischemic heart disease and stroke.(1) Amongst those, stroke, the most common manifestation of cerebrovascular disease, has been the leading cause of serious, long-term disability in adults worldwide (1990-2010) (2) There are two main types of stroke — ischemic and hemorrhagic. Ischemic stroke is more common and caused by an obstruction in the cerebral vasculature. The causes of ischemic strokes are heterogeneous, including atherosclerosis in the large arteries such as the carotid arteries (see fig 1.), lacunar infarctions and cardiogenic embolism. In this thesis, I will focus on carotid atherosclerosis as it is the most prominent to identify patients with a high risk of ischemic stroke. Atherosclerotic plaques can rupture which will lead to thrombo-embolization into the intracranial circulation or to acute occlusion of the carotid artery. Despite major advances in treatment strategies, ischemic stroke due to carotid atherosclerotic remains a serious public health problem. Current screening and diagnostic methods are insufficient to identify the plaques that have a high rupture risk and thus to select the individual before he is confronted with an ischemic stroke. One of the strategies to better face the challenges of cerebrovascular disease and improve well being of the population and of the individual includes early recognition of the vulnerable high-risk atherosclerotic plaque

High shear stress relates to intraplaque haemorrhage in asymptomatic carotid plaques

Background and aims Carotid artery plaques with vulnerable plaque components are related to a higher risk of cerebrovascular accidents. It is unknown which factors drive vulnerable plaque development. Shear stress, the frictional force of blood at the vessel wall, is known to influence plaque formation. We evaluated the association between shear stress and plaque components (intraplaque haemorrhage (IPH), lipid rich necrotic core (LRNC) and/or calcifications) in relatively small carotid artery plaques in asymptomatic persons. Methods Participants (n = 74) from the population-based

High shear stress relates to intraplaque haemorrhage in asymptomatic carotid plaques

AbstractBackground and aimsCarotid artery plaques with vulnerable plaque components are related to a higher risk of cerebrovascular accidents. It is unknown which factors drive vulnerable plaque development. Shear stress, the frictional force of blood at the vessel wall, is known to influence plaque formation. We evaluated the association between shear stress and plaque components (intraplaque haemorrhage (IPH), lipid rich necrotic core (LRNC) and/or calcifications) in relatively small carotid artery plaques in asymptomatic persons.MethodsParticipants (n = 74) from the population-based Rotterdam Study, all with carotid atherosclerosis assessed on ultrasound, underwent carotid MRI. Multiple MRI sequences were used to evaluate the presence of IPH, LRNC and/or calcifications in plaques in the carotid arteries. Images were automatically segmented for lumen and outer wall to obtain a 3D reconstruction of the carotid bifurcation. These reconstructions were used to calculate minimum, mean and maximum shear stresses by applying computational fluid dynamics with subject-specific inflow conditions. Associations between shear stress measures and plaque composition were studied using generalized estimating equations analysis, adjusting for age, sex and carotid wall thickness.ResultsThe study group consisted of 93 atherosclerotic carotid arteries of 74 participants. In plaques with higher maximum shear stresses, IPH was more often present (OR per unit increase in maximum shear stress (log transformed) = 12.14; p = 0.001). Higher maximum shear stress was also significantly associated with the presence of calcifications (OR = 4.28; p = 0.015).ConclusionsHigher maximum shear stress is associated with intraplaque haemorrhage and calcifications

Carotid wall volume quantification from magnetic resonance images using deformable model fitting and learning-based correction of systematic errors

Cardiovascular Aspects of Radiolog

Atherosclerotic Carotid Plaque Composition and Incident Stroke and Coronary Events

Background: Increasing evidence suggests that atherosclerotic plaque composition rather than plaque size is linked to ischemic cardiovascular events, yet largescale population-based data in asymptomatic individuals remain scarce. Objectives: This study sought to investigate carotid plaque composition in relation to incident stroke and coronary heart disease (CHD) in a population-based setting. Methods: Between 2007 and 2012, 1,349 persons (mean age 72 years, 49.5% women) from the population-based Rotterdam Study who were free from a history of stroke or CHD, in whom carotid ultrasonography showed subclinical atherosclerosis, and who underwent high-resolution magnetic resonance imaging of the carotid arteries to assess plaque characteristics. These included the presence of specific plaque components (intraplaque hemorrhage [IPH], lipid-rich necrotic core, and calcification), and measures of plaque size (maximum plaque thickness and presence of stenosis of more than 30%). Individuals were continuously followed for the occurrence of stroke or CHD until January 1, 2015. The authors used Cox regression models to assess the association of the plaque characteristics with the incidence of stroke and CHD, with adjustments for age, sex, and cardiovascular risk factors. Results: During a median of 5.1 years’ follow-up for stroke and 4.8 years for CHD, 51 individuals had a stroke and 83 developed CHD. Independent of maximum plaque thickness and cardiovascular risk factors, the presence of IPH was associated with incident stroke and CHD (fully adjusted hazard ratio: 2.42 [95% confidence interval: 1.30 to 4.50], and 1.95 [95% confidence interval: 1.20 to 3.14]). Presence of a lipid-rich necrotic core and calcification were not associated with stroke or CHD. Conclusions: The presence of IPH in the carotid atherosclerotic plaque is an independent risk factor for stroke and CHD. These findings indicate the promise of IPH as a marker of plaque vulnerability in healthy persons with subclinical atherosclerosis

Shoyo ikei o tomonatta nyubo nenekigan : shinkei naibunpitsu bunka no ketsuraku, saibo setchaku kyokusei inshi hatsugen teika o tomonau atarashii sabusetto no kanosei

Purpose: To investigate intraplaque hemorrhage (IPH) development and change over time. Materials and Methods: Institutional review board approval and written informed consent from all participants were obtained. From a population-based study on subclinical atherosclerosis, 40 participants with IPH at baseline magnetic resonance (MR) imaging (53 carotids with IPH) were randomly selected and were matched with 27 control subjects (53 carotids without IPH) to undergo a second MR examination (mean interval, 17 months 6 4 [standard deviation]) to assess IPH change. IPH volume change was evaluated by using both a visual rating scale and an automated volumetric segmentation tool. Cardiovascular risk factors for IPH volume change were investigated with linear regression analyses. Results: IPH remained present in 50 (94%) of the 53 carotids with IPH at baseline, and it developed in fve (7%) of the 40 carotids without IPH at baseline. Visual progression of IPH volume was present in 14 (26%) of the 53 carotids with IPH at baseline, and regression was present in 16 (30%). Mean quantitative change in IPH volume was 213.7 mm3 ± 62.6 per year of follow-up. Male sex (men vs women, 37.7 mm3; 95% confdence interval [CI]: 11.0, 64.4; P =.006), smoking (smokers vs nonsmokers, 45.2 mm3; 95% CI: 7.1, 83.4; P =.020), and hypertension (subjects with hypertension vs those without hypertension, 32.5 mm3; 95% CI: 7.7, 57.2; P =.010) were associated with IPH volume change. Conclusion: During 17 months of follow-up, both visual progression and regression of IPH volume occurs, whereas quantitatively IPH volume decreases. This suggests that IPH is a dynamic process with potential for either growth or resolution over time

Serial Noninvasive Assessment of Apoptosis During Right Ventricular Disease Progression in Rats

Right ventricular (RV) function is the major determinant of survival in patients with pulmonary hypertension. Yet, the pathophysiologic basis of RV disease is unresolved. We aimed to study the role of apoptosis in RV disease by monitoring it serially during disease progression using in vivo (99m)Tc-annexin-V ((99m)Tc-annexin) scintigraphy and study whether the reduction in apoptosis resulting from chronic treatment with valsartan can be detected by (99m)Tc-annexin scintigraphy. METHODS: RV disease after pulmonary hypertension was induced by monocrotaline injection in rats. The following 3 groups were studied: rats treated with monocrotaline (monocrotaline rats), rats treated with monocrotaline plus valsartan (valsartan rats), and age-matched controls (control rats). Serial echocardiography and in vivo (99m)Tc-annexin scintigraphy were performed. Apoptosis was confirmed by (99m)Tc-annexin autoradiography and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling. Fibrosis was assessed by picrosirius red staining. RESULTS: In monocrotaline rats, in vivo (99m)Tc-annexin uptake peaked early and declined thereafter but remained elevated, compared with baseline. These stage-dependent changes of in vivo (99m)Tc-annexin uptake were paralleled by changes in autoradiography and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling. Valsartan rats had longer RV failure-free survival than did monocrotaline rats and had reduced apoptosis. These changes were accompanied by commensurate delays in RV hypertrophy and RV dilation. Valsartan rats also had less fibrosis than monocrotaline rats at all disease stages. CONCLUSION: RV disease progression is associated with an early increase in RV apoptosis, as monitored using serial in vivo (99m)Tc-annexin scintigraphy. Delay in RV disease progression by valsartan is accompanied by reduction in RV apoptosis. Apoptosis plays a role in RV disease progression and may be assessed by serial in vivo (99m)Tc-annexin scintigraph

Joint intensity-and-point based registration of free-hand B-mode ultrasound and MRI of the carotid artery

Purpose: To introduce a semiautomatic algorithm to perform the registration of free-hand B-Mode ultrasound (US) and magnetic resonance imaging (MRI) of the carotid artery. Methods: The authors' approach combines geometrical features and intensity information. The only user interaction consists of placing three seed points in US and MRI. First, the lumen centerlines are used as landmarks for point based registration. Subsequently, in a joint optimization the distance between centerlines and the dissimilarity of the image intensities is minimized. Evaluation is performed in left and right carotids from six healthy volunteers and five patients with atherosclerosis. For the validation, the authors measure the Dice similarity coefficient (DSC) and the mean surface distance (MSD) between carotid lumen segmentations in US and MRI after registration. The effect of several design parameters on the registration accuracy is investigated by an exhaustive search on a training set of five volunteers and three patients. The optimum configuration is validated on the remaining images of one volunteer and two patients. Results: On the training set, the authors achieve an average DSC of 0.74 and a MSD of 0.66 mm on volunteer data. For the patient data, the authors obtain a DSC of 0.77 and a MSD of 0.69 mm. In the independent set composed of patient and volunteer data, the DSC is 0.69 and the MSD is 0.87 mm. The experiments with different design parameters show that nonrigid registration outperforms rigid registration, and that the combination of intensity and point information is superior to approaches that use intensity or points only. Conclusions: The proposed method achieves an accurate registration of US and MRI, and may thus enable multimodal analysis of the carotid plaque