In vivo intima–media thickness (IMT) measured non-invasively by high resolution B-mode ultrasonography is considered as a valid and reliable indicator of the local and generalized expansion of

subclinical, later, clinical atherosclerosis [8]. IMT is defined as the distance between blood-intima and media-adventitia interfaces of arterial wall [14]. Most often it is measured at the common carotid artery (CCA), because high measurement precision can be obtained in this artery. These are made over a distance of 1 cm at levels 1–2 cm proximal to the bifurcation; a mean value for the selected area is obtained using automated wall-tracking software [5], [15] and [16]. Nevertheless, in vivo carotid IMT determination aims primarily the far arterial wall (the side further to the US transducer) since an accurate Trichostatin A clinical trial measurement of the near wall IMT is extremely difficult and requires a Bcl-2 apoptosis high level of technical expertise [17] and [18]. Moreover, meta-analysis revealed that circumferential scanning of the carotid artery and calculation of the mean maximum carotid IMT provides a more accurate measurement of carotid atherosclerosis

[19]. In addition, anatomy, motion artifacts or ultrasound equipment can also influence in vivo IMT determination [20], [21], [22] and [23]. A variety of non-invasive imaging techniques and softwares have been used to improve in vivo IMT determination and to increase the reliability of IMT as marker Aspartate of atherosclerosis [18], [20], [22], [23], [24] and [25]. However, these IMT measuring methods have not been validated yet and a quick and reliable method for initial in vitro testing of new techniques and softwares, apart from the widely used in vivo US, is also needed. The present study addresses these deficiencies. It has been suggested that

changes in intensity of shear stress influence the arterial wall responses from less to more proliferative phenotypes, which may underlie the differences in genetic effects on CCA IMT and bifurcation IMT [26]. Further research is required to clarify genetic effects and local gene expression patterns, which could influence pathological processes in arterial walls and hence the arterial IMT. Therefore, a better knowledge of gene-IMT associations, i.e. taking into consideration US IMT measurements in the context of gene expression profile data could improve the accuracy and reliability in prediction of the progression of atherosclerotic vascular disease. It is accepted that freezing of excised tissues could result in alteration of microanatomic structure especially because of ice crystal formation [27]. On the other hand, histological preparation of arterial sections affects vascular and plaque dimensions [28], [29], [30] and [31].