Session 2: Histopathology and Imaging in CAD 5. Characterizing vulnerable plaques – Elaaha Anwari

Introduction to Acute Coronary Syndromes and Imaging Techniques

Speaker Introduction

• Elahan Vari introduces himself as a resident doctor at Charité, discussing his work in circular imaging and acute coronary syndromes.

• He mentions that Dr. Abdul Vahed was supposed to present but is unable to attend.

Case Presentation

• A 76-year-old patient presents with sudden chest pain radiating to the left arm; ECG shows ST elevation in inferior leads.

• The circumflex artery appears markedly aneurysmal and filled with thrombus, leading the team to suspect a proximal culprit lesion.

Imaging Insights and Treatment Strategy

Initial Treatment Plan

• The initial plan involves thrombus aspiration, gentle balloon dilation, and possibly administering a GP IIb/IIIa inhibitor.

OCT Findings

• Optical Coherence Tomography (OCT) reveals that the true culprit lesion is not in the aneurysm but rather in a distal segment of the circumflex artery.

• This finding shifts their strategy from treating an inappropriate site to focusing on the actual culprit lesion.

Pathophysiology of Vulnerable Plaques

Understanding Vulnerable Plaques

• The case illustrates how OCT can distinguish between true lesions and secondary thrombus propagation, avoiding unnecessary interventions.

• Vulnerable plaques are discussed as being characterized by plaque rupture due to underlying pathophysiological factors.

Importance of In Vivo Imaging

• Histology cannot be performed on living patients; thus, in vivo imaging like OCT is essential for understanding plaque characteristics.

Mechanisms of Plaque Vulnerability

How OCT Works

• OCT uses light transmission through vessel walls; lipid-rich areas absorb light appearing dark while fibrous tissue reflects it appearing bright.

Key Indicators of Vulnerability

• Cap thickness under 65 micrometers indicates vulnerability; other features include macrophage accumulation and lipid core burden index assessed by different imaging techniques.

Preventive Strategies Against ACS

Detecting Non-flow Limiting Lesions

• Studies show that non-flow limiting lesions can be detected early using imaging techniques for preemptive treatment strategies.

Biological Modification of Plaque Stability

• High-dose statins or PCSK9 inhibitors may biologically alter plaque stability by thickening fibrous caps and reducing lipid content.

Different Pathophysiologies of Acute Coronary Syndromes

Mechanisms Leading to ACS

• Various mechanisms such as classic plaque rupture, intact fibrous cap erosion, calcified nodules, and spontaneous coronary artery dissection are discussed as causes of ACS.

Visual Representation

• Diagrams illustrate these mechanisms: ruptured plaques lead to STEMI while intact caps can still result in significant thrombus formation.

Research Focus at Charité

Investigating Vulnerable Plaques

Optico ACS: Insights into Acute Coronary Syndrome

Overview of the Study

• The Optico ACS study was a prospective translational multicenter research project involving patients with acute coronary syndrome (ACS), including both STEMI and non-STEMI cases. High-resolution optical coherence tomography (OCT) was utilized to analyze carpet lesions during percutaneous coronary intervention (PCI).

• In addition to imaging, intravascular blood sampling was performed at the lesion site to investigate local immune signatures, enhancing understanding beyond mere visual assessment.

Distinct Immune Signatures

• Analysis revealed that lesions classified as IFCASS exhibited a significant enrichment of CD4 and CD8 T cells at the culprit site compared to RFCS lesions, indicating a varied immune microenvironment even within the same artery. This suggests that plaque vulnerability is influenced by surrounding immune responses rather than just morphological characteristics.

Mechanisms of Plaque Rupture

• A detailed examination of rupture points in carpet lesions showed that these often occurred in segments where lipid and calcium coexisted, rather than in purely lipid or poorly calcified areas. This finding highlights the biomechanical fragility created by lipid-induced stress combined with calcium's role as a stress concentrator.

• The study emphasizes that identifying specific rupture hotspots can provide insights into why certain plaques are more vulnerable than others, moving beyond general assessments of plaque stability.

Key Takeaways from Findings

• The case study of a 76-year-old STEMI patient exemplifies typical presentations of vulnerable plaques leading to rupture and thrombosis; it illustrates how clinical manifestations are merely the final stages in an ongoing pathological process.

• Advanced imaging techniques like OCT allow for precise evaluations beyond traditional angiographic methods, enabling targeted interventions based on detailed anatomical and physiological insights. This approach supports personalized treatment strategies for patients with ACS.

Future Directions

• The findings suggest opportunities for integrating morphological, biological, and mechanical data to better select patients who would benefit from localized therapies such as drug-coated balloons (DCB). This holistic view could enhance treatment efficacy in managing vulnerable plaques associated with ACS.