In search of a marker of vulnerable carotid plaque: is the key in the heart?

0021-9150/$ e see front matter 2012 Elsevier Irela doi:10.1016/j.atherosclerosis.2012.01.032 Atherosclerosis is the main cause of cardiovascular disease [1]. The mortality of atherothrombotic cardiovascular disease has fallen dramatically in the past decades but the prevalence, burden, and costs of the disease is increasing due to the prolonged survival of patients with chronic sequelae [2]. It must be also considered that nearly 50% of major occlusive atherosclerotic cardiovascular events are unheralded, accounting for>700,000 hard events annually only in the US [2]. Noteworthy, nearly 70% of acute coronary events result from coronary lesions that are not hemodynamically significant or flow limiting before the event [3]. Atherosclerosis, considered being a progressive immune inflammatory disease of medium and large sized arteries, often begins in childhood and adolescence and frequently remains clinically dormant until plaque rupture or plaque erosion leads to abrupt thrombosis triggering acute clinical events [4]. Accurately identify individuals at risk of atherothrombotic events is highly desirable. The term “vulnerable plaque” (a.k.a. “high-risk plaque” and “thrombosis-prone plaque”) is used to designate a plaque at high risk of disruption leading to thrombosis. Themost common type of suspected vulnerable plaque is an inflamed thin-cap fibroatheroma in particular those with superficial erosion. Specificity of this kind of lesion for predicting plaque rupture is limited because not all of them will rupture, nor will all ruptures lead to a vascular event. To overcome these