Komorovsky and Desideri compared with patients with stable angina. As in a general population, the ratio between complex and simple carotid plaques in patients with CAD is approximately 1:2 (Lombardo et al 2004); however, this ratio seems to grow with the increasing instability of patients due to the increased prevalence of complex carotid plaques (Lombardo et al 2004). These results are complementary to the recent findings, which showed that acute coronary syndrome patients with multiple complex coronary plaques had more either echolucent or echogenic carotid plaques and carotid calcifications compared with patients who only had a single complex coronary plaque (Kato et al 2003). The prognostic relevance of ultrasound characteristics of carotid plaques for cardiovascular events is somewhat controversial. In one of the studies it was demonstrated that in patients undergoing endarterectomy because of > 50% or > 70% stenosis, the echolucency of the removed carotid plaques was associated with the risk of myocardial infarction and stroke combined (Liapis et al 2002). Another study showed that a combined end point of death, myocardial infarction, or stroke was significantly more frequent in hypertensive patients with echolucent carotid plaques compared with comparable patients with echo-rich carotid plaques. Moreover, the multiple risk intervention program was beneficial in patients with echolucent carotid plaques, but not in those with echogenic carotid plaques (Schmidt et al 2003). Finally, Honda et al (2004) showed that echolucent carotid plaques predict coronary plaque complexity and the development of future coronary complications in patients with stable coronary artery disease. These studies, however, have some potential limitations. In the studies of Liapis et al (2002) and Schmidt et al (2003), the combined end points were used, and therefore, conclusions with regard to cardiovascular events only could not be made. Honda et al (2004) compared patients with echolucent carotid plaques with patients without carotid disease and patients with echogenic carotid plaques taken together. Such combination masked the risk associated with echogenic carotid plaques. Moreover, the overall prevalence of carotid disease in stable CAD patients was very high (79%), as was the prevalence of echolucent carotid plaques (52%). Conversely, it has been shown that in patients with acute coronary syndromes, either echogenic or echolucent carotid plaques are associated with lower event-free survival regardless of the treatment strategy (conservative treatment or myocardial revascularization) (Komorovsky et al 2005). However, the presence of echogenic carotid plaques appeared to be an independent predictor of cardiac death 134 and nonfatal myocardial infarction in these patients. Echogenic carotid plaques, when associated with complex coronary lesions, were associated with a particularly poor long-term event-free survival (Komorovsky et al 2005). One of the links that explain the associations between echogenic carotid plaques and cardiac events might be increased arterial stiffness, which is observed in patients with echogenic carotid plaques (Zureik et al 2003) and which, by itself, is associated with adverse cardiovascular outcomes (Boutouyrie et al 2002). Echogenic carotid plaques might also reflect the total burden of calcium and of athero- sclerosis, including that of the coronary arteries (Nossen et al 2001). The amount of coronary calcium and the fast progression of coronary calcifications, revealed by electron beam tomographic and multidetector scanning, has been previously associated with a greater risk of cardiovascular events (O’Rourke et al 2000; Keelan et al 2001). Finally, carotid calcifications may also reflect a diffuse coronary disease. The extent of non-obstructive atherosclerotic lesions has been found to be a strong predictor of coronary events, independent of severity and the number of flow-limiting coronary lesions (Bigi et al 2003). These data, however, do not completely resolve the existing controversy. Recent observations have suggested that inflammation may be a possible link between coronary and carotid plaque instability (Lombardo et al 2004). Complex carotid plaques were detected more frequently in patients with CAD and elevated serum C-reactive protein (> 3 mg/L) compared with patients with normal C-reactive protein levels. It may be that the degree of generalized inflammation, as reflected by C-reactive protein level, determines the echolucent plaque instability and the associated adverse outcomes. Moreover, higher interleukin- 6 and high-sensitivity C-reactive protein levels have been recently shown to be associated with lower echogenicity of carotid plaques (Yamagami et al 2004). These data are in contradiction with the previous studies, which failed to demonstrate significant associations between echolucency of carotid plaques and acute phase reactants such as fibrinogen (Kofoed et al 2003), C-reactive protein, orsomucoid (Grønholdt, Silesen, et al 2001), and intra- cellular adhesion molecule-1 (Okulla et al 2002). Although the acute phase reactants reflect the general inflammation and may not be significantly modulated by changes in the carotid arteries (Grønholdt, Silesen, et al 2001), we suggest that echolucent plaques in patients with inflammation might have a different risk than echolucent plaques without evident signs of inflammation. In support of this, there is increasing Vascular Health and Risk Management 2005:1(2)