ABSTRACT
Pioneering work by pathologists, including Erling Falk and the late Michael Davies, established that structural disruption of atherosclerotic plaques is the main mechanism underlying myocardial infarctions and strokes.1 Key histologic features of disrupted plaques include thinning of the fibrous cap and depletion of structural collagens that provide most of the tensile strength.1 These observations suggest that dysregulated protease activity is responsible for weakening the plaque cap. In this chapter, we consider the evidence that matrix metalloproteinases (MMPs) promote plaque vulnerability and are therefore an appropriate target for plaque-stabilizing therapy.
