Читать книгу Interventional Cardiology - Группа авторов - Страница 24

The different pathologic characterization of atherosclerotic lesions largely depends on the thickness of the fibrous cap and its grade of inflammatory infiltrate, which is in turn largely constituted by macrophages and activated T lymphocytes. Typically, the accumulating plaque burden is initially accommodated by an adaptive positive remodelling with expansion of the vessel external elastic lamina and minimal changes in lumen size [77,78]. The plaque contains monocyte‐derived macrophages, smooth muscle cells, and T cells. Interaction between these cells types and the connective tissue appears to determine the development and progression of the plaque itself, including important complications, such as thrombosis and rupture. Atherosclerotic lesions expand outward radially, in the direction away from the lumen to preserve the lumen calibre [7]. Plaque with limited lipid accumulation and thicker fibrous caps are referred as “stable plaques” [7]. On the other hand, thin‐cap fibroatheromas (TCFAs) or “vulnerable plaques” are likely the precursors of plaque ruptures, usually in the proximal segments of the major coronary arteries, where most plaque ruptures and thrombi are seen [79–81]. Burke et al. identified a cut‐off value for cap thickness of 65 microns to define a vulnerable coronary plaque [80]. Rupture occurs where the cap is thinnest and most infiltrated by foam cells.72 Despite the predominant hypothesis focusing on the responsibility of a specific vulnerable atherosclerotic plaque rupture [82,83] for acute coronary syndromes, some pathophysiologic, clinical and angiographic observations seem to suggest the possibility that the principal cause of coronary instability is not to be found in the vulnerability of a single atherosclerotic plaque, but in the presence of multiple vulnerable plaques in the entire coronary tree, correlated with the presence of a diffuse inflammatory process [84–87]. The gradual loss of SMCs from the fibrous cap and infiltrating macrophages degrade the collagen‐rich cap matrix lead to TCFAs formation, as ruptured caps contain less collagen and SMCs with numerous foam cells compared with intact caps [88–90]. Emotional or physical stress, such as anger, anxiety, work stress, earthquakes, war, sexual activity, hyperthermia, infections, and cocaine use, is known to cause plaque rupture [91]. Plaque rupture exposes the contents of the plaque to the blood compartment, where thrombogenic material in the plaque core produced by macrophages and smooth muscle cells can trigger thrombosis, the most dreaded complication of atherosclerosis, resulting in acute coronary syndrome or stroke [7].