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Background: Neovascularization (NV) within plaques is widely recognized as an important indicator of plaque vulnerability; however, the relationship between NV and plaque rupture in patients with acute myocardial infarction (AMI) has not been extensively evaluated. The purpose of this study was to investigate the association between NV of culprit lesions and plaque rupture in patients with AMI.
Methods: This study included 384 patients diagnosed with AMI. All patients were divided into Non-NV and NV groups according to whether NV was present in the optical coherence tomography (OCT) images of the preoperative culprit lesions.
Results: Patients with NV lesions had thinner minimal fibrous cap thickness, smaller minimal lumen area and symmetry, longer lesion length, and larger plaque volume and plaque burden than patients with AMI without NV lesions ( < 0.05). Patients with both AMI and NV had a higher incidence of thin-cap fibroatheroma, cholesterol crystals, macrophages, thrombus, calcific plaque, lipid-rich plaque, and plaque rupture ( < 0.01). After adjusting for covariates, NV is independently associated with plaque rupture (OR 3.21, 95% CI 2.00-5.14; < 0.001). For the evaluation of the model after adjusting the covariates, the receiver operating characteristic (ROC) curve, clinical calibration curve, and decision curve analysis (DCA) of the model show good discriminative ability, prediction accuracy, and clinical utility.
Conclusions: In patients with AMI, NV of culprit lesions is significantly correlated with plaque growth, formation of unstable plaque phenotypes, and plaque rupture. NV may be an effective predictor of plaque rupture in AMI patients.
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http://dx.doi.org/10.1186/s12872-025-04995-z | DOI Listing |
Rev Cardiovasc Med
August 2025
Cardiology Department, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, CIBERCV, 28007 Madrid, Spain.
Stress cardiomyopathy/Takotsubo syndrome (TTS) is a transient cardiac condition characterized by sudden and reversible left ventricular dysfunction, typically triggered by emotional or physical stress. The international TTS (InterTAK) score predicts the probability of suffering from TTS. However, the diagnostic algorithm includes three mutually exclusive diagnoses: acute coronary syndrome (ACS), TTS, and acute infectious myocarditis.
View Article and Find Full Text PDFRev Cardiovasc Med
August 2025
Department of Cardiology, Shandong Key Laboratory for Diagnosis and Treatment of Cardiovascular Diseases, Jining Key Laboratory of Precise Therapeutic Research of Coronary Intervention, Affiliated Hospital of Jining Medical University, 272029 Jining, Shandong, China.
Coronary heart disease (CHD) is associated with increased morbidity and mortality. Acute cardiovascular events frequently occur in patients with coronary artery stenoses exceeding 70%. Although coronary revascularization can significantly improve ischemic symptoms, the inflection point for reducing mortality from CHD has yet to be reached.
View Article and Find Full Text PDFJ Geriatr Cardiol
August 2025
Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.
Curr Opin Lipidol
August 2025
Cardiometabolic Immunity Laboratory, Department of Physiology, Monash Biomedicine Discovery Institute (BDI) and Victorian Heart Institute (VHI), Monash University, Melbourne, Victoria, Australia.
Purpose Of Review: This review explores the evolving understanding of efferocytosis - the clearance of dead or dying cells by phagocytes - in the context of atherosclerosis. It highlights recent discovers in cell death modalities, impaired clearance mechanisms and emerging therapeutic strategies aimed at restoring efferocytosis to stabilize plaques and resolve inflammation.
Recent Findings: Recent studies have expanded the scope of efferocytosis beyond apoptotic cells to include other pro-inflammatory cell death modes, including pyroptosis, necroptosis and ferroptosis, revealing context-dependent clearance efficiency and immunological outcomes.
Front Cardiovasc Med
August 2025
Department of Biomedical Engineering, Thorax Center Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands.
Atherosclerotic plaque rupture can lead to thrombotic cardiovascular events such as stroke and myocardial infarction. Computational models have shown that microcalcifications (calcified particles with a diameter < 50 μm) in the atherosclerotic plaque cap can increase cap tissue stresses and consequently contribute to plaque rupture. Microcalcification characteristics, such as particle size and volume fraction, have been implicated to affect cap stresses.
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