Komorovsky and Desideri Intima-media thickness For the far (posterior) wall of the carotid artery, this index can be easily measured by ultrasound as the distance between the leading edge of the luminal echo (first bright line) and the leading edge of the media-adventitia echo (second bright line). For the near (anterior) wall, IMT is measured as the distance between the trailing edge of the first bright line and the trailing edge of the second bright line (Pignoli et al 1986; Iglesias del Sol 2001). In clinical trials, IMT has been used as a surrogate end point for evaluating the progression of atherosclerosis (de Groot et al 1998; Pitt et al 2000). The use of IMT for assessment of cardiovascular event risk has, however, a number of limitations. Although IMT has been shown to be a strong predictor of incident myocardial infarction in overall population aged ≥ 55 years (van der Meer et al 2004), and there is a good correlation between increased IMT and the presence of CAD, IMT is not a good predictor of its extent and severity and cannot predict the absence of significant CAD. Furthermore, IMT does not appear to have predictive value in populations with high prevalence of CAD, or in younger age groups where the prevalence is low (Adams et al 1995; Held et al 2001). Therefore, the American Heart Association Prevention V Conference (Greenland et al 2000) did not recommend routine IMT measurements in patients with low or high risk of cardiovascular disease, but stated that this may be appropriate in patients at intermediate risk of CAD (based on Framingham risk assessment). This means that if in a patient at intermediate risk of coronary event (6%–20% risk in 10 years) the carotid IMT of ≥ 1 mm is detected, he/she may be stratified as a high-risk patient and receive high- risk treatment accordingly. The assessment of IMT in various laboratories is not standardized. In some studies only the common carotid artery IMT has been considered (Held et al 2001; Cuomo et al 2002), in others, along with the common carotid artery IMT, the IMT in carotid bifurcation (bulb), and internal carotid artery has been measured (Iglesias del Sol et al 2001). Thereafter the results have been either averaged (Haluska et al 2004; Yildiz et al 2004) or the greatest IMT values have been used for analysis (Iglesias del Sol A et al 2001; Crouse et al 2002). These methodological differences limit the interpretation of results. Moreover, a relatively large proportion of variation in repeated measurements over time is likely to be due to measurement error. Most studies suggest, however, that the common carotid artery is the preferable site for the measurement of IMT because it is tubular and can be aligned perpendicular to the transducer beam. Reproducibility and yield of the common carotid artery IMT is therefore superior to that of IMT of the carotid bifurcation or internal carotid artery (Howard et al 1993; Crouse et al 1995). Recent consensus (Touboul et al 2004) concluded that there is no need “to treat” IMT values or to monitor IMT values in individual patients. IMT measurements are not recommended to predict events on an individual level, but may be used in clinical trials as a surrogate end point on a group level. The recommended standardized methods for IMT measurements are supposed to improve the power of studies incorporating IMT values and to facilitate the merging of databases for meta-analyses. Carotid plaques Carotid plaques in various studies have been defined either as distinct areas “with an IMT exceeding twice that of neighboring sites” (Held et al 2001, p 64) or “focal widenings of the vessel wall of > 50% relative to adjacent segments” (Hollander et al 2002, p 2873), or a “lesion with a focal IMT of 1.1 mm or more, with a localized protrusion of the vessel wall into the lumen (Honda et al 2004, p 1178). In another study, a cut-off point of 1.3 mm was used for a focal thickening of the IMT complex to be considered as a plaque (Kablak-Ziembicka et al 2004). According to the consensus statement (Touboul et al 2004), a plaque is defined as a focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the surrounding IMT value or demonstrates a thickness of ≥ 1.5 mm as measured from the media-adventitia interface to the intima-lumen interface. Obstructive plaques (causing > 50% lumen diameter narrowing) cause blood flow acceleration at the stenosis site and a peak systolic velocity > 125 cm/sec in the internal carotid artery is an indicator of its hemodynamically significant narrowing (Grant et al 2003). The presence of obstructive carotid plaques is associated with increasing risk of cerebrovascular events by atheroembolism, as the severity of the stenosis increases (NASCET 1991), and increased risk of cardiac death and myocardial infarction (Held et al 2001). The risk associated with the presence of non-obstructive carotid plaques remains a controversial problem. Like IMT, these plaques reflect the overall atherosclerotic burden, and, as compared with IMT, better predict cardiovascular death and nonfatal myocardial infarction (Held et al 2001). 132 Vascular Health and Risk Management 2005:1(2)