Chapter 17: Pathogenesis of Coronary Thrombosis and Myocardial Infarction

Chapter Summary

This chapter discusses the most recent advances in the understanding of the pathophysiology of vulnerable plaque formation and provides new insights into the molecular mechanisms and sequence of events that drive thrombus formation at the culprit site (see Fuster and Hurst’s Central Illustration). High-risk atherosclerotic plaques are characterized by a high inflammatory burden tightly intertwined with the formation of leaky neovessels that penetrate from the adventitia, favoring intra-plaque hemorrhage. Atherosclerotic plaque disruption (either fibrous cap rupture or superficial erosion) exposes thrombogenic surfaces that trigger a complex and coordinated activation of platelets and the coagulation system, leading to thrombus formation and the perpetuation of the inflammatory response. Recent large-scale clinical trials have verified the benefits of anti-inflammatory therapies in the reduction of cardiovascular events. Other factors are also known to affect or modulate thrombus growth either locally (eg, degree of stenosis and lesion injury, and fluid dynamics) or systemically (traditional and newly identified cardiovascular risk factors and extracellular vesicles). Further progress toward better characterization of rupture-prone atherosclerotic plaques and the higher susceptibility to thrombosis (the so-called vulnerable patient) will reduce the risk of atherothrombotic events, the leading cause of morbidity and mortality worldwide.