Without thrombosis, coronary atherosclerosis is generally benign. It is plaque disruption, or fissuring, and subsequent thrombosis that make coronary atherosclerosis dangerous. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may cause the development of unstable angina, myocardial infarction, and sudden death. The risk of plaque disruption depends more on plaque type (composition) than on plaque size and stenosis severity. Both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The resultant thrombotic response, which affects the clinical presentation and outcome, is partly determined by the reactivity of the circulating platelets and the balance between the coagulation and fibrinolytic systems. To prevent and treat life-threatening coronary thrombosis, the medical community should seek new ways to identify and treat dangerous, vulnerable plaques and to optimize antithrombotic treatment.