Inflammation during Percutaneous Coronary Intervention-Prognostic Value, Mechanisms and Therapeutic Targets

Bradley Tucker, Kaivan Vaidya, Blake J Cochran, Sanjay Patel, Bradley Tucker, Kaivan Vaidya, Blake J Cochran, Sanjay Patel

Abstract

Periprocedural myocardial injury and myocardial infarction (MI) are not infrequent complications of percutaneous coronary intervention (PCI) and are associated with greater short- and long-term mortality. There is an abundance of preclinical and observational data demonstrating that high levels of pre-, intra- and post-procedural inflammation are associated with a higher incidence of periprocedural myonecrosis as well as future ischaemic events, heart failure hospitalisations and cardiac-related mortality. Beyond inflammation associated with the underlying coronary pathology, PCI itself elicits an acute inflammatory response. PCI-induced inflammation is driven by a combination of direct endothelial damage, liberation of intra-plaque proinflammatory debris and reperfusion injury. Therefore, anti-inflammatory medications, such as colchicine, may provide a novel means of improving PCI outcomes in both the short- and long-term. This review summarises periprocedural MI epidemiology and pathophysiology, evaluates the prognostic value of pre-, intra- and post-procedural inflammation, dissects the mechanisms involved in the acute inflammatory response to PCI and discusses the potential for periprocedural anti-inflammatory treatment.

Keywords: angioplasty; atherosclerosis; cardiovascular disease; inflammation; myocardial infarction; percutaneous coronary intervention; periprocedural myocardial infarction.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The inflammatory response to PCI. Balloon inflation and/or stent deployment (A) causes direct endothelial injury. In response the endothelium upregulates its expression of proinflammatory cytokines, chemokines and adhesion molecules, which drive platelet and leukocyte recruitment and activation (B). This process is further enhanced by reperfusion-induced ROS. Balloon inflation and/or stent deployment also causes microembolisation of plaque material, which travels downstream and contributes to microvascular obstruction. Moreover, the liberation of cholesterol crystals and NETs facilitates activation of the NLRP3 inflammasome, ultimately resulting in the production of IL-1β and IL-6 (C). IL-1β, Interleukin-1β; IL-6, Interleukin-6; MAPK, Mitogen-activated protein kinase; NETs, Neutrophil extracellular traps; NF-κB, Nuclear factor-κB; NLRP3, NOD-like receptor protein 3.

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