Medical research is oriented to vascular events’ prevention, either by the
inhibition of growth or by the early detection and stabilization of the
vulnerable atherosclerotic plaques. Numerous studies have been published in
literature, aiming to determine vulnerability,by means of associating
traditional risk factors, epidemiological data or morphological characteristics
of atheromatous plaque ,as these are provided by routine or highly specialized
imaging techniques. All of these studies though, focus to only a few factors
implicated in plaque instability.
The largest part of the current atherosclerosis research is targeted to the
attempt of modelling the systemic and the local events, leading in plaque
vulnerability. Of particular interest is the role of molecular signaling
pathways and of gene interactions. The experimental reproducing of atheromatous
plaque formation, growth and destabilization remains challenging, because of
the limitations that animal models present.
An holistic approach of atherosclerotic plaque vulnerability , considering
mechanical and flow parameters of the prone to disease arterial segments, the
circulating molecules, the enzymatic systems and the cells contributing to
plaque evolution, the dynamic transformation , function and degeneration of
arterial wall components are reviewed in this study
