.. The pathological mechanisms leading from stable lesions to the formation of vulnerable Seliciclib CDK2 plaques remain in doubt, and the associated clinical events are unpredictable.12 Several attempts have been made to use imaging techniques such as magnetic resonance imaging (MRI) to monitor the formation and progression of selleck chem atherosclerotic plaques in rodents and rabbits.12-14 Skogsberg et al.15 reported that in atherosclerosis-prone

mice with human-like hypercholesterolemia, atherosclerotic lesions initially progressed slowly and then showed a rapid expansion. Subsequent to advanced lesions, a plateau trend existed Inhibitors,research,lifescience,medical in these atherosclerotic mice. Accumulation of lipid-poor macrophages was demonstrated to be associated with the rapid expansion Inhibitors,research,lifescience,medical phase. It is important to mention that the atherosclerotic lesion

is not pathologically homogeneous and atherosclerosis, far from being a linear model, is at times rapid and at others slow.16 The unpredictable and often episodic nature of atherosclerosis progression can be explained by the rapid increase of stenosis Inhibitors,research,lifescience,medical severity due to thrombosis.7 According to our proposed practical classification of atherosclerosis phases, atherosclerosis velocity includes the time-dependent development of the plaque from endothelial injury to acute arterial thrombosis. In terms of the phases of atherosclerosis, there is little information available on the evaluation of the factors that affect the duration of infrastructural and subsequent rupture-induced occlusion separately. If investigators

focus on the concept of “time” for atherosclerosis development, it may result in considerable prevention of cardiovascular events. As a consequence, atherosclerosis-related Inhibitors,research,lifescience,medical morbidity/mortality can be effectively prevented. Inhibitors,research,lifescience,medical Description of Atherosclerosis Velocity Our suggested description of atherosclerosis velocity (v) is described in this section. It is worthy of note that this formula/description is intended, for the time being, only to further clarify the concept of atherosclerosis velocity. Accordingly, it is completely hypothetical and its application should be tested in several animal and human studies. v=(V×I index)÷t V0 (%) is the true percentage of lumen stenosis/ or plaque volume at t0 time. V1 (%) is the true percentage of lumen stenosis/ or plaque volume at t1 time. V (%): V1-V0 t (months): t1-t0 v: atherosclerosis velocity (% or nm Dacomitinib / months) The I index represents the instability of a plaque and either can be valued 1 for a plaque that does not experience any clinical acute event during time t or can be valued 2 for a plaque that experiences acute occlusion/ thrombosis. “I” is a parameter that may change during further investigations and new items or new scoring might be added to this parameter. If new imaging methods in the future (e.g.