Editorial
Grasp of Fate: Determining the Prognosis of Plaque Erosion?
2024 Volume 31 Issue 1 Pages 15-16
Details
2024 Volume 31 Issue 1 Pages 15-16
See article vol. 31: 23-35
Acute coronary syndrome (ACS) continues to be a common and highly fatal cardiovascular disease worldwide, and involves three underlying pathologies: plaque rupture, plaque erosion (PE), and calcified nodules1, 2). The incidence of PE accounts for more than one-third of ACS cases and appears to be increasing in association with the ongoing changes in patients’ cardiovascular risk profile, including aggressive lipid-lowering therapies and antihypertensive treatment3, 4). Recent advances in intracoronary imaging modalities, particularly optical coherence tomography (OCT), have provided valuable insights into the atherosclerotic plaque features that characterize PE in vivo.
In this issue of the Journal of Atherosclerosis and Thrombosis, Li et al. examined the distribution of lipid and calcium content in culprit lesions of PE in patients with STEMI using OCT5). The introduction of OCT have enabled us to distinguish PE in vivo, which also allows us to evaluate the clinical treatment strategies and outcomes in patients with PE. Li et al found that lipid and calcium contents were more likely to exist in the external erosion zone of the culprit lesions, particularly in the proximal region near the erosion site. A high level of lipid content in the proximal external erosion zone was significantly associated with plaque vulnerability and a higher incidence of major adverse cardiac events (MACEs).
These findings suggest that the distribution of lipid content in the proximal region of the external erosion zone can serve as a novel method for risk stratification and precise management in patients with PE. However, caution may be required in interpreting this study because there was no significant difference in MACE when the two groups were divided by total lipid content of the entire lesion or by high/low lipid content at each site, and no data were presented on what type of events had occurred with respect to the MACEs. In addition, although stenting was performed in most of all cases in this study, it would be of great interest to know how the stents were implanted using OCT guidance. The presence of LRP can lead to events such as in-stent plaque prolapse, incomplete stent apposition, stent edge dissection, and procedure-related myocardial infarction due to distal embolization.
Although our current strategy mandates immediate stenting for ST-elevation myocardial infarction (STEMI) and non-STEMI, given the diverse demographics and pathologies of PE, individualized treatment strategies are crucial. Other studies have shown that ACS patients with PE have better outcomes, and the feasibility and safety of less invasive management strategies (antithrombotic therapy without stenting) are being investigated in these patients6, 7). For instance, in the EROSION study, patients with PE may benefit from antithrombotic therapy without stenting during at least 4 years follow-up8). On the other hand, recent OCT studies have shown that PE patients with lipid-rich plaque (LRP) have more vulnerable plaques and higher inflammation throughout the coronary artery, including non-culprit lesions, compared to PE patients with fibrous plaques9). Pathologically, it has been shown that PE with LRP has more severe stenosis than PE without LRP, and that more severe luminal stenosis may also cause PE in LRP10). The study by Li et al. adds data on how different underlying plaques in PE affect prognosis.
The future perspective of this study is to establish risk stratification and precise treatment of patients with PE based on plaque characteristics. This may help to identify high-risk plaque features and implement targeted management strategies. While understanding the mechanism, morphology, and risk stratification of PE is an ongoing area of research, this study contributes to our understanding of the distribution and characteristics of PE, which will help in the risk stratification and management of patients with this phenotype of ACS. We look forward to further research to elucidate the mechanisms of PE and identify effective preventive strategies, including a potential role for antiplatelet agents.
SS has received honoraria from Terumo and Abbott vascular; research grant from Terumo and Abbott vascular. KN has received honoraria from AstraZeneca, Bayer Yakuhin, Boehringer Ingelheim Japan, Daiichi Sankyo, Eli Lilly Japan, Mitsubishi Tanabe Pharma, MSD, Novartis Pharma, Ono Pharmaceutical, and Otsuka; research grant from Asahi Kasei, Astellas, Boehringer Ingelheim Japan, Fuji Yakuhin, Mitsubishi Tanabe Pharma, Mochida Pharmaceutical, Novartis Pharma, and Teijin Pharma; scholarship from Bayer Yakuhin, Medtronic, and Teijin Pharma.
