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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.

eFig 17-01 Chapter 17: Pathogenesis of Coronary Thrombosis and Myocardial Infarction


Atherosclerosis is a systemic and nonresolving chronic inflammatory disease that occurs in the intima of large and medium-sized arteries (ie, aorta, carotids, coronaries, and peripheral arteries) and is characterized by intimal thickening caused by the accumulation of cells and lipids (Fig. 17–1).1 Atherothrombosis mainly represents the clinical manifestation of this pathology in which atherosclerotic plaque rupture or erosion triggers the formation of an acute thrombus, obstructing coronary blood flow and reducing the oxygen supply to the myocardium, leading to the onset of acute coronary syndromes (ACS).2,3 ACS represents a spectrum of ischemic myocardial events that share similar pathophysiology; these include unstable angina (UA)/non–ST-segment elevation myocardial infarction (UA/NSTEMI) and ST-segment elevation myocardial infarction (STEMI), which may lead to the occurrence of sudden cardiac death.

Figure 17–1.

Simplified diagram of the evolution of coronary atherosclerosis. Phases and morphology of lesion progression. Roman numbers designate the sequence of atherosclerotic lesion progression according to histological classification being type I the initial lesion that contains scattered foam cells and type VI those plaque that have undergone fissure, hematoma, and thrombus superimposition. Type V lesions have been subclassified into those plaques that contain a rich lipid core and connective tissue (type Va lesion), those largely calcified (type Vb), or those rich in fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).

The early atherosclerotic lesions might progress without ...

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