![]() ![]() 4 The exact pathogenic mechanism of calcified nodules is not known, but activated macrophages can deposit large amounts of calcium, which can eventually fracture due to cyclic torsion of the artery to form a calcific protruding nodule. On histology, eruptive calcified nodules appear as microthrombi around a nodule that is protruding through the plaque surface, and calcified nodules are the least common atherothrombotic cause of ACS. 16 On histopathological examination, downstream embolization of thrombi to the microvasculature of the coronary arteries in IFC-ACS is a common finding, and IFCs are more likely to cause embolization than RFCs (71% versus 42% p=0.01). IFCs are mostly associated with negative remodeling and RFCs are associated with positive remodeling. Negative remodeling is defined as a decrease in the vessel diameter distal to the culprit lesion of ACS, whereas positive remodeling is an increase in the diameter of the vessel. In addition to collagen composition, IFCs and RFCs can be distinguished by the distinct patterns of vascular remodeling they are associated with. 14 Plaques with IFCs can cause ACS in healthy young females and smokers. 7,13 IFCs are non-ruptured fibroatheromas that are mostly composed of type III collagen in comparison, RFCs mostly contain type I collagen. In IFCs there is a communication between the luminal thrombus and intimal wall (with proteoglycans acting as the tissue–thrombus interface) that may lead to coronary obstruction. ![]() 7,11 This cascade of events leads to the formation of the red thrombus superimposed on RFCs, which is primarily composed of fibrin and red blood cells. The necrotic core is highly thrombogenic and its exposure leads to the release of tissue factor, which acts as an intermediary for thrombus formation. 6,9,10 Rupture of the fibrous cap leads to exposure of the necrotic core formed within the plaque to the intravascular milieu. Microcalcification is thought to make plaques vulnerable to rupture under high radial strain because it can act as a nidus for debonding of the fibrous cap. Microcalcification ( ~10 μm in size) is generated by necrotic macrophages or smooth muscle cells. 7 Ruptures usually occur in the shoulder region at rest and either in the shoulder region or the mid-fibrous cap during exercise. 7 The most vulnerable region in the fibrous cap is the shoulder region, which is where the normal tissue meets the atherosclerotic plaque. ![]() 5,6 In addition to the biomechanical stress, inflammatory processes, driven primarily by activated macrophages, that release proteases can degrade the thin cap and contribute to the rupture of the thin fibrous cap. Thin cap fibroatheromas (TCFAs) can rupture as a result of biomechanical forces that are generated by shear stress and turbulent blood flow. They are made up of foam cells that are deposited beneath the endothelium, and eventually progress to fibroatheromas. 4 The pathophysiology of these three substrates of ACS is briefly reviewed below.įatty streaks are the initial atherosclerotic substrate. 4 Three culprit phenotypes accounted for most cases: ruptured fibrous caps (RFCs 35%), intact fibrous caps (IFCs 35%), and calcified nodules (5%). In a large post-mortem study of 442 individuals with sudden cardiac death, acute thrombotic events were responsible for 234 (53%) of the deaths. Plaque Rupture, Plaque Erosion, and Calcified Nodules: Histopathological InsightsĪtherosclerotic plaques with a disrupted fibrous cap (ruptured or eroded) and eruptive calcified nodules can lead to ACS. We discuss how intravascular imaging may be used to optimize the outcomes of percutaneous coronary intervention (PCI) in ACS. This review summarizes the data on the common atherothrombotic and non-atherothrombotic causes of ACS. IVUS and OCT generate high-resolution images of the coronary artery that help delineate the pathogenesis of atherosclerosis, specifically the major contributors for atherothrombotic events leading to unstable angina, MI, and sudden cardiac death. 1–3 Intravascular ultrasound (IVUS) and optical coherence tomography (OCT) enable in vivo visualization of culprit lesions for ACS. Historically, the first descriptions of atherosclerotic lesions underlying acute coronary syndromes (ACS) were provided by post-mortem studies. ![]()
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