Key result
Targeting post-PCI residual inflammatory risk requires refined patient selection and clearer pathway timing.
Residual inflammatory risk is a clinically relevant post-PCI risk phenotype, but transitioning it from a prognostic marker to an actionable treatment target requires better definition of timing, inflammatory pathways, and patient selection.
Percutaneous coronary intervention (PCI) effectively treats flow-limiting coronary lesions but does not eliminate the systemic processes that drive atherosclerotic progression and recurrent events. Residual inflammatory risk (RIR), most commonly identified by persistent elevation of high-sensitivity C-reactive protein (hsCRP), has emerged as an important component of this remaining risk and frequently persists despite intensive lipid lowering. Its interpretation after PCI, however, requires attention to timing, since inflammation related to acute myocardial injury and procedural vascular damage must be distinguished from persistent inflammatory activity after clinical stabilisation. In this review, we examine the biological basis of RIR and its relationship with plaque vulnerability, vascular healing, and recurrent events after coronary intervention. We discuss the role of hsCRP and other circulating biomarkers in post-PCI phenotyping, together with cardiometabolic conditions—including obesity, diabetes, chronic kidney disease, atherogenic dyslipidaemia, and hyperuricaemia—that may sustain inflammatory activation despite successful revascularisation. We also critically appraise the therapeutic evidence. Although CANTOS established inflammation as a modifiable component of atherothrombotic risk and colchicine has shown benefit in selected coronary populations, neutral findings with hyperacute colchicine initiation and, more recently, IL-6 inhibition emphasise that biomarker reduction does not necessarily translate into fewer cardiovascular events. Current guidelines recognise anti-inflammatory therapy in selected settings but do not recommend hsCRP-guided treatment after PCI. RIR therefore represents a clinically relevant post-PCI risk phenotype, but its transition from prognostic marker to actionable treatment target will require better definition of timing, inflammatory pathways, and the patients most likely to benefit from intervention.
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Iliakis et al. (2026) conducted a review in Residual inflammatory risk after percutaneous coronary intervention. Anti-inflammatory therapy and hsCRP-guided phenotyping was evaluated. Residual inflammatory risk after PCI is a relevant risk phenotype, but using it as a treatment target requires better definition of timing, pathways, and target patients.
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