New Insights into Pathophysiology and New Risk Factors for ACS

Figures

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  Figure 1. Histomorphological Characteristics of plaque erosion, plaque rupture, and a stable plaque. The top three photos report the cross-sectional area of a culprit lesion displaying a plaque erosion in a patient with acute coronary syndrome (A), a culprit lesion displaying a plaque disruption in a patient with acute coronary syndrome (B), and a stable unrelated plaque from a non-culprit site in another patient dying from sudden cardiac death (C). The boxed areas in the top panels are magnified in the bottom panels for better histological characterization. (A) The eroded plaque shows subcritical stenosis, an unremarkable necrotic core, and overlying thrombus on an intact fibrous cap. The cap is rich in smooth muscle cells and proteoglycans, and there is minimal inflammation at the base of the thrombus. The plaque does not show any positive remodeling. (B) Conversely, a positively remodeled, critically occlusive atherosclerotic plaque with a cholesterol crystal-rich large necrotic core (NC) covered by a very thin and inflamed fibrous cap, which is disrupted (area between the arrowheads). Smooth muscle cells are visible in the medial layer and thin fibrous cap and are minimally present at…

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  Figure 2. Regulation of NLRP3 inflammasome activation. The main external and intracellular factors involved in the activation and modulation of the NLRP3 inflammasome, together with its main effects. ASC, adaptor apoptosis-associated speck-like protein containing a caspase-recruitment domain; ATP, adenosine triphosphate; DAMPs, damage/danger-associated molecular patterns; ER, endoplasmic reticulum; IL-1R, interleukin-1 receptor; NFkB, nuclear factor-kB; NLRP3, nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3; oxLDL, oxide low-density lipoprotein; PAMPs, pathogen-associated molecular patterns; PTMs, post-translational modification; TLR, toll-like receptor; TNFR, tumor-necrosis factor receptor.

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  Figure 3. Interplay between clinical manifestations, pathophysiological mechanisms and main actors related to atherosclerosis in acute coronary syndromes. In the left column are the three main clinical steps of acute coronary syndrome: pre-clinical atherosclerosis progression, acute event occurrence and post-event management. In the center column are the principal signaling pathways and underlying pathological aspects. In the right column are the key elements and substances mediating the pathophysiological process. Lp(a), lipoprotein(a); Lp-PLA2, lipoprotein associated-phospholipase A2; NETosis, neutrophil extracellular traps (NETs) formation; NLRP3, nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3.