Stroke, a leading cause of death or disability worldwide, is frequently dependent on the rupture
of carotid atherosclerotic plaques. It is therefore extremely important to study the mechanisms of
formation, progression and eventually rupture of the plaques.
Vulnerability of the plaque, the intrinsic tendency to lose its integrity and consequently to induce a
dramatic atherothrombotic or embolic event, is still an elusive concept because many players are involved
and the clinical picture is frequently the sum of different contrasting (pro-inflammatory and
This review will discuss recent advancements in the comprehension of this topic. In particular inflammatory activation at
the level of the carotid plaque will be described in the attempt to underline the main factors for the formation, the chronic
persistence and the risk of rupture. Since these topics can be studied in humans only with plaque samples obtained following
endarterectomy, research has tried to evaluate the role of different biomarkers which could be useful for the definition
of the vulnerability of a carotid plaque, or, with more clinical relevance, of a patient; some recent results from our group
will be discussed. A significant help for clinical decisions may also come from imaging tools, both well established ultrasound
and more sophisticated options, such as magnetic resonance and positron emission tomography.
This large amount of scientific information should allow the development of new therapeutic approaches for the effective
prevention of cerebrovascular events.