Plaques Do Not Act Alone: Time to Redefine Coronary Vulnerability from Lesion to Phenotype

TL;DR

This paper argues that coronary vulnerability should be redefined by combining plaque biology, inflammation, and blood flow factors for better risk prediction.

Contribution

Proposes a new framework for coronary vulnerability integrating plaque biology, systemic inflammation, and haemodynamics.

Findings

Traditional plaque morphology fails to reliably predict clinical risk.

Multidimensional assessment using imaging and biomarkers improves risk stratification.

A dynamic, patient-specific phenotype is essential for personalized prevention strategies.

Abstract

The classical concept of plaque vulnerability, centred on specific morphological features, has failed to deliver reliable risk prediction in clinical practice. Recent evidence highlights the need to redefine coronary vulnerability as a dynamic, patient-specific phenotype shaped by plaque biology, systemic inflammation, and haemodynamic forces. Advanced imaging modalities, artificial intelligence, and circulating biomarkers now enable a multidimensional assessment of this complex phenotype. This integrative approach may offer a more precise framework for risk stratification and personalised prevention in coronary artery disease.

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