الفهرس 
الملخص العربى
Initiation of atherosclerosisOnly 14 pages are availabe for public view
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Abstract
Atherosclerosis without thrombosis is in general a benign disease. However, acute thrombosis frequently complicates the course of coronary atherosclerosis, causing unstable angina, myocardial infarction, and sudden death. The mechanism responsible for the sudden conversion of a stable disease to a life-threatening condition is usually plaque disruption with superimposed thrombosis. The risk of plaque disruption depends more on plaque composition and vulnerability (plaque type) than on degree of stenosis (plaque size). Major determinants of vulnerability of a plaque to rupture are size and consistency of the atheromatous core, thickness of the fibrous cap covering the core, and ongoing inflammation within the cap. Plaque disruption tends to occur at points at which the plaque surface is weakest and most vulnerable, which coincide with points at which stresses resulting from biomechanical and hemodynamic forces acting on plaques are concentrated. Therefore, the risk of plaque disruption is a function of both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces). The former predisposes the plaque to rupture, and the latter may precipitate it. (Falk et al, 1995)
Greater understanding of the biology of atherothrombotic disease drives interest in detection of vulnerable plaque. The ability to detect and monitor vulnerable plaque is keenly sought to define its natural history and support studies of progression and regression. A number of novel imaging modalities have recently been proposed to identify specific areas of plaque vulnerability. Defining the optimal imaging modality of vulnerable-plaque detection will depend on whether treatment continues to be pharmacologic plaque stabilization, in which case an overall risk of vulnerable plaque would suffice, or locally directed therapy, requiring precise anatomic definition.
Ultimately, population screening with traditional risk factors, newer serum markers, and possibly gene chips will define a group of high-risk patients in whom noninvasive imaging is appropriate. Features of plaque vulnerability detected noninvasively might justify invasive modalities. Currently, however, the optimum approach to vulnerable-plaque detection incorporates structural definition of a high-resolution modality, such as OCT or intravascular MRI, with biologic processes detected by spectroscopy or thermography. (MacNeill et al, 2003)
In vivo, high-resolution, multicontrast MRI holds the best promise of noninvasively imaging high-risk plaques. MR allows serial assessment of progression and regression of atherosclerosis. Application of MRI opens new areas for diagnosis, prevention, and treatment (eg, lipid-lowering drug regimens) of atherosclerosis in all arterial locations. (Fayad et Fuster, 2001)
Despite strong evidence for the ”vulnerable plaque” concept, some qualifications and unanswered questions exist. It is clear that when assessing the vulnerability of coronary plaque there is a continuum of risk. At one end is the highly vulnerable plaque, with a large lipid-rich pool, a thin fibrous cap, and significant inflammation, and at the other the highly fibrous or calcified plaque with little or no lipid pool. It is in the grey area between that assessment of vulnerability and risk of rupture becomes more difficult. Although many of the commonly used medications in cardiovascular medicine have positive effects on long term plaque stabilisation, the time course of these changes is unclear. Acute plaque stabilization and passivation may require targeted LDD via a catheter or stent platform with combined treatment of anti-thrombotic and anti-inflammatory/immunomodulating drugs. It seems reasonable to assume that a combined pharmacological approach with local and systemic administration will achieve both optimal early periprocedural efficacy and long term prophylactic efficiency for plaque passivation and stabilization. (Spratt et Camenzind, 2004)