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

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.

Colchicine in atherosclerotic coronary artery disease: new challenges for an old drug

“…Although cardiac enzyme levels and infarct size by cardiac magnetic resonance imaging were significantly reduced (p=0.019), there was no reduction in adverse events. These results suggest a potential benefit of colchicine in AMI with ST -segment elevation (SLOBODNICK et al, 2018;TUCKER et al, 2021;KAO;HUANG, 2022).…”

“…al., 2018. Interacts with neutrophil function, inhibition of inflammasome receptor protein 3 (NLPR3), with suppression of Interleukin (IL)-1β, IL-18 and IL-6 release (OPSTAL et al, 2020;SLOBODNIK et al, 2018;GROSLAMBER;PY, 2018;ANDREIS;DE FERRARI, 2021 ;TUCKER et al, 2021).…”

Acute Coronary Syndromes (ACS)—Unravelling Biology to Identify New Therapies—The Microcirculation as a Frontier for New Therapies in ACS

“…This response, aiming to remove cellular debris and repair injured tissue, is mediated by the release of various cytokines and acute-phase proteins [ 31 , 32 ]. In particular, cellular debris activates the NLRP3 inflammasome—a macromolecular protein complex that regulates caspase 1 activation and subsequent production of potent pro-inflammatory cytokines IL-1ß and IL-18 [ 31 , 33 ]. The inflammasome potentiates the inflammatory response in ACS by amplifying tissue injury and leading to interstitial myocardial oedema, which compresses capillaries and arterioles in the coronary microcirculation, causes arteriolar spasm and other progressive endothelial abnormalities, and results in erythrocyte stasis and micothrombosis within the microvasculature, all of which contribute to MVO [ 34 , 35 ].…”

“…The inflammasome potentiates the inflammatory response in ACS by amplifying tissue injury and leading to interstitial myocardial oedema, which compresses capillaries and arterioles in the coronary microcirculation, causes arteriolar spasm and other progressive endothelial abnormalities, and results in erythrocyte stasis and micothrombosis within the microvasculature, all of which contribute to MVO [ 34 , 35 ]. Produced downstream of the inflammasome, IL-6 induces C-reactive protein (CRP) synthesis and acts as a secondary mediator of the inflammatory cascade [ 33 ]. There is growing evidence to suggest that CRP is not only a marker of atheroinflammation and cardiovascular risk, but is also a mechanistic proinflammatory mediator of myocardial damage and MVO.…”

Neutrophil Counts, Neutrophil-to-Lymphocyte Ratio, and Systemic Inflammatory Response Index (SIRI) Predict Mortality after Off-Pump Coronary Artery Bypass Surgery

“…Complex coronary artery disease can be treated by either coronary percutaneous or surgical revascularization [ 9 , 10 , 11 ]. The periprocedural inflammatory overreaction is one of the possible factors that indicate a worse long-term prognosis [ 12 , 13 , 14 , 15 , 16 ].…”