Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease

Figures

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  Figure 1. Overview of the inflammatory response in a COPD and AMI. The onset of either acute myocardial infarction (AMI) or chronic obstructive pulmonary disease (COPD) leads to cellular injury and necrosis of cardiac cells and pulmonary cells respectively, resulting in the release of intracellular content such as damage-associated molecular patterns (DAMPs), production of reactive oxygen species (ROS) and activation of the complement cascade. Once a DAMP (such as DNA, mitochondrial DNA (mtDNA), RNA, and the nuclear factor - high mobility group box 1 (HMGB1), and ATP) is recognised by toll-like receptors (TLRs), cytoplasmic myeloid differentiation factor 88 (MyD88) is activated. This in turn, stimulates the NF–κB pathway and through a signaling cascade and transcription, leads to the release of several inflammatory mediators such as pro-interleukin (IL)-1β. Additionally, in response to the release of DAMPs, inflammasomes (such as nucleotide-binding oligomerization domain receptor family protein 3, NLRP3) are activated to promote the cleavage of pro-Caspase-1 into Caspase-1, which in turn processes the pro-IL-1β into the active IL-1β form. As a result, pro-inflammatory mediators (IL-1β,…

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  Figure 2. Overview of how inflammation in COPD can “spill over” into the systemic circulation, increasing the risk of AMI. Long-term exposure to pollutants and frequent acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) can enhance and alter the inflammatory response in the lungs, resulting in a progressive and persistent inflammatory response. This COPD-related inflammatory response can promote systemic inflammation and oxidative stress through several inflammatory mediators (IL-1β, IL-6, IL-8, and TNF-α). Their actions can induce endothelial injury and vascular dysfunction through increased endothelial permeability and enhanced oxidative stress. Additionally, prolonged inflammation and oxidative stress can contribute to the development of atherosclerotic plaque and thrombosis, thereby increasing the risk of acute myocardial infarction (AMI). Patients with COPD exhibit a heightened platelet count and reactivity, ultimately increasing the risk of thrombotic events.