The aim of this study was to assess the association between the spatial location of plaque rupture and remodeling pattern of culprit lesions in acute anterior myocardial infarction (MI). Positive remodeling suggests a potential surrogate marker of plaque vulnerability, whereas plaque rupture causes thrombus formation followed by coronary occlusion and MI. Intravascular ultrasound (IVUS) can determine the precise spatial orientation of coronary plaque formation. We studied 52 consecutive patients with acute anterior MI caused by plaque rupture of the culprit lesion as assessed by preintervention IVUS. The plaques were divided into those with and without positive remodeling. We divided the plaques into three categories according to the spatial orientation of plaque rupture site: myocardial (inner curve), epicardial (outer curve), and lateral quadrants (2 intermediate quadrants). Among 52 plaque ruptures in 52 lesions, 27 ruptures were oriented toward the epicardial side (52%), 18 toward the myocardial side (35%), and 7 in the 2 lateral quadrants (13%). Among 35 plaques with positive remodeling, plaque rupture was observed in 21 (52%) on the epicardial side, 12 (34%) on the myocardial side, and 2 (6%) on the lateral side. However, among 17 plaques without positive remodeling, plaque rupture was observed in 6 (35%), 6 (35%), and 5 (30%), respectively (p = 0.047). Atherosclerotic plaques with positive remodeling showed more frequent plaque rupture on the epicardial side of the coronary vessel wall in anterior MI than those without positive remodeling.
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http://dx.doi.org/10.1007/s00380-011-0184-7 | DOI Listing |
Immunity
January 2025
Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilian-University (LMU), Munich, Germany; Deutsches Zentrum für Neurodegenerative Erkrankungen e. V. (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance (MHA), Munich, Germany. Electronic address:
Common genetic variants in a conserved cis-regulatory element (CRE) at histone deacetylase (HDAC)9 are a major risk factor for cardiovascular disease, including stroke and coronary artery disease. Given the consistency of this association and its proinflammatory properties, we examined the mechanisms whereby HDAC9 regulates vascular inflammation. HDAC9 bound and mediated deacetylation of NLRP3 in the NACHT and LRR domains leading to inflammasome activation and lytic cell death.
View Article and Find Full Text PDFCurr Opin Hematol
January 2025
Department of Pathology, Section of Oncopathology and Morphological Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Purpose Of Review: This review aims to summarize the histological differences among thrombi in acute myocardial infarction, ischemic stroke, venous thromboembolism, and amniotic fluid embolism, a newly identified thrombosis.
Recent Findings: Acute coronary thrombi have a small size, are enriched in platelets and fibrin, and show the presence of fibrin and von Willebrand factor, but not collagen, at plaque rupture sites. Symptomatic deep vein thrombi are large and exhibit various phases of time-dependent histological changes.
J Atheroscler Thromb
January 2025
Department of Neurology, National Cerebral and Cardiovascular Center.
Aim: Branch atheromatous disease (BAD), characterized by the occlusion of perforating branches near the orifice of a parent artery, often develops early neurological deterioration because the mechanisms underlying BAD remain unclear. Abnormal wall shear stress (WSS) is strongly associated with endothelial dysfunction and plaque growth or rupture. Therefore, we hypothesized that computational fluid dynamics (CFD) modeling could detect differences in WSS between BAD and small-vessel occlusion (SVO), both of which result from perforating artery occlusion/stenosis.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China.
Coronary obstruction following plaque rupture is a critical pathophysiological change in the progression of stable angina (SAP) to acute coronary syndrome (ACS). The accumulation of platelets and various inflammatory cells on apoptotic endothelial cells is a key factor in arterial obstruction after plaque rupture. Through single-cell sequencing analysis (scRNA-seq) of plaques from SAP and ACS patients, we identified significant changes in the annexin V and P-selectin glycoprotein ligand 1 pathways.
View Article and Find Full Text PDFActa Biomater
January 2025
Department of Cardiology, Biomedical Engineering, Cardiovascular Institute, Thorax Center, Erasmus MC, Rotterdam, The Netherlands.
Many cardiovascular events are triggered by fibrous cap rupture of an atherosclerotic plaque in arteries. However, cap rupture, including the impact of the cap's structural components, is poorly understood. To obtain better mechanistic insights in a biologically and mechanically controlled environment, we previously developed a tissue-engineered fibrous cap model.
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