Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI
Chao Fang1, Yanwei Yin1, Senqing Jiang1
1Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China; Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China.
Insights
ST-segment elevation myocardial infarction (STEMI) patients exhibit greater pancoronary plaque vulnerability and distinct layered phenotypes compared to non-STEMI (NSTEMI) patients. These findings highlight differences in plaque characteristics between STEMI and NSTEMI, impacting acute myocardial infarction presentation.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Pathology
Background:
- Pancoronary plaque vulnerability and layered phenotypes are crucial for understanding acute myocardial infarction (AMI) presentations.
- Layered plaques signify prior coronary destabilization and thrombosis, influencing clinical outcomes.
Purpose of the Study:
- To investigate pancoronary plaque vulnerability and layered phenotypes in ST-segment elevation myocardial infarction (STEMI) versus non-STEMI (NSTEMI) patients.
- To identify plaque characteristics associated with STEMI presentation.
Main Methods:
- 464 AMI patients underwent 3-vessel optical coherence tomography (OCT) imaging.
- Patients were categorized into STEMI (318) and NSTEMI (146) groups.
- Follow-up was conducted for a median of 2 years.
Main Results:
- STEMI culprit lesions showed more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels than NSTEMI.
- Nonculprit lesions in STEMI also had higher prevalence of plaque rupture, microvessels, and calcification.
- Culprit lesion layer area, TCFA, thrombus, and non-left circumflex artery location predicted STEMI presentation.
Conclusions:
- STEMI patients demonstrate increased plaque vulnerability and distinct layered phenotypes in both culprit and nonculprit lesions compared to NSTEMI patients.
- Culprit lesion features like large layer area, TCFA, thrombus, and specific location are predictive of STEMI.
- While AMI type didn't affect outcomes, specific plaque features predicted major adverse cardiovascular events.
Objectives:
This study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI).
Background:
Pancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis.
Methods:
A total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years.
Results:
Compared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non-left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI.
Conclusions:
Patients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non-left circumflex artery location predicted the clinical presentation of STEMI.
More Related Videos
13:07Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
09:06Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Related Concept Videos
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
01:30Acute Coronary Syndrome I: Introduction
01:30Acute Coronary Syndrome III: Diagnostic Studies
01:26Coronary Artery Disease II: Pathophysiology
01:30Atherosclerosis I: Introduction
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...