Targeting Inflammation Across the Myocardial Infarction Continuum: Biomarkers, Imaging, and Emerging Therapies

Figures

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  Figure 1. Cellular and molecular mechanisms linking vascular inflammation to plaque vulnerability and coronary thrombosis. Retention and oxidative modification of low-density lipoproteins (LDLs) within the arterial intima generate damage-associated molecular patterns (DAMPs), promoting endothelial activation, leukocyte recruitment, and differentiation of monocytes into macrophages and foam cells. Progressive lipid accumulation, defective efferocytosis, and cholesterol crystal formation activate the NLRP3 inflammasome, leading to the release of pro-inflammatory cytokines, including IL-1β and IL-18, and amplification of local immune responses through chemokines and T-cell activation. Smooth muscle cell migration and fibrous cap remodeling determine plaque stability, whereas persistent inflammation favors fibrous cap thinning, plaque rupture or erosion, and subsequent coronary thrombosis. CCL—C-C motif chemokine ligand; CXCL—C-X-C motif chemokine ligand; DAMPs—damage-associated molecular patterns; IFN-γ—interferon gamma; IL—interleukin; LDL—low-density lipoprotein; NLRP3—nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3; oxLDL—oxidized…

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  Figure 2. Inflammation across the continuum of atherosclerosis, acute myocardial infarction, and residual inflammatory risk. Traditional cardiovascular risk factors promote endothelial dysfunction, characterized by reduced nitric oxide bioavailability, oxidative stress, and endothelial activation, thereby initiating vascular inflammation. Activation of the NLRP3 inflammasome and the downstream IL-1/IL-6 signaling axis amplifies innate immune responses, driving atherosclerotic plaque progression toward a vulnerable phenotype prone to rupture or erosion. Sex and hormonal status may modulate this continuum through effects on endothelial function, vascular inflammation, microvascular function, and coronary vasomotion, particularly in relation to the loss of estrogen-mediated vascular protection after menopause. Plaque disruption results in acute myocardial infarction (AMI), followed by myocardial inflammation, ventricular remodeling, and persistent residual inflammatory risk, which contributes to recurrent cardiovascular events. Biomarkers of systemic inflammation, multimodality cardiovascular imaging, and emerging anti-inflammatory therapies provide complementary tools for risk stratification…