From biology to imaging: Rethinking vulnerable plaques in coronary artery disease

Area of Science:

• Cardiovascular Medicine
• Medical Imaging
• Pathophysiology

Background:

• Coronary artery disease (CAD) is a major global health burden, driven by atherosclerosis.
• Atherosclerosis is increasingly understood as a chronic, inflammatory, and panvascular disorder.
• Plaque rupture was initially thought to be the primary trigger for acute coronary syndromes (ACS), but plaque erosion and calcific nodules are also recognized contributors.

Purpose of the Study:

• To critically review current evidence on plaque vulnerability and destabilization using intravascular imaging (IVI) findings.
• To assess the utility of IVI-derived features in predicting cardiovascular events and guiding treatment decisions.
• To explore the role of medical therapies in plaque stabilization and regression.

Main Methods:

• Review of current evidence focusing on intravascular imaging (IVI) techniques.
• Analysis of in vivo characterization of high-risk plaque phenotypes using optical coherence tomography, intravascular ultrasound, and near-infrared spectroscopy.
• Evaluation of studies associating IVI-derived vulnerability features with major cardiovascular events and treatment outcomes.

Main Results:

• High-resolution IVI allows detailed in vivo characterization of vulnerable plaque phenotypes (e.g., thin-cap fibroatheromas, lipid-rich cores, macrophage infiltration, microcalcifications, intraplaque hemorrhage).
• While IVI improves pathophysiological understanding, its translation into reliable prognostic tools for lesion-specific prediction remains uncertain.
• Studies show associations between imaging-derived vulnerability features and cardiovascular events, but preventive percutaneous treatments lack clear survival or myocardial infarction reduction benefits.

Conclusions:

• Vulnerable plaques identified by IVI are markers of global patient risk, not definitive predictors of culprit lesions.
• Current evidence does not support routine preemptive intervention on non-culprit vulnerable plaques.
• Optimized medical therapy is the cornerstone of management, with intensive lipid-lowering and anti-inflammatory strategies promoting plaque stabilization and regression.