ABSTRACT
Atherosclerosis is predominantly a clinically silent process, and a substantial percentage
of patients are first aware of its consequences through the acute and catastrophic
event of thrombosis. Extensive basic and clinical research in the 1990s revealed that
plaque disruption initiates the majority of thromboses. Furthermore, recent studies
indicate that inflammation plays a major role in the pathophysiology, from initiation
of the atheroma to the actual thrombosis itself. Attention has now focused on morphological,
mechanical, and biochemical characteristics that increase plaque vulnerability, as
determination of these features may allow identification of plaques that are most
likely to cause symptoms and acute events in the future. This article reviews basic
pathophysiologic aspects of atherosclerotic plaque development and rupture to provide
the necessary background for understanding the crucial role of inflammation in acute
coronary syndromes.
KEYWORDS
Atherosclerosis - inflammation - plaque rupture - unstable atheroma