Background: Transesophageal echocardiography (TEE) has been used to identify the potential risk for cardiogenic embolism in patients with atrial fibrillation (AF). However, ischemic stroke in patients with AF is not always attributable to embolism. Identification of the risk of embolic versus atherothrombotic stroke should lead to the optimal individualized management of patients with AF.
Hypothesis: The goal of the study was to determine the relation between cortical infarction and perforating infarction and TEE findings in patients with AF.
Methods: We investigated the clinical usefulness of TEE in the risk stratification of clinical subtyping of the cerebral infarctions which were divided into two territories of the cortical branch (cortical infarction due to embolism) and deep perforators (perforating infarction due to atherothrombosis). Left atrial spontaneous echo contrast, peak flow velocity in the left atrial appendage, and generalized atherosclerosis as estimated by the intima-media wall thickness of the thoracic aorta were assessed by TEE in 118 consecutive patients with either paroxysmal (n = 44) or chronic (n = 74) AF. All patients underwent either brain computed tomography or magnetic resonance imaging.
Results: Cortical and perforating infarction was found in 39 and 18% of patients, respectively. The grade of spontaneous echo contrast was higher in patients with than in those without cortical infarction (p < 0.05). In contrast, patients with perforating infarction showed significant increase in the aortic wall thickness when compared with patients without perforating infarction (p < 0.05). In addition, multivariate logistic analysis revealed that spontaneous echo contrast was an independent predictor of cortical infarction, while intima-media wall thickness of the aorta, hypertension, and age were useful in predicting the risk of perforating infarction.
Conclusions: Transesophageal echocardiography has a potential role in the risk stratification for cortical and perforating infarction in patients with AF.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6654812 | PMC |
| http://dx.doi.org/10.1002/clc.4960230710 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Incidence and Factors in Delayed Neurological Deficits after Subarachnoid Hemorrhage in Mice.
Brain Hemorrhages
June 2024
The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, Texas, USA.
Background: Delayed cerebral ischemia (DCI) is one of the most feared complications in aneurysmal subarachnoid hemorrhage (SAH). Animal models are crucial to studying the disease mechanisms and potential treatments. DCI in rodents was thought to not exist; herein we examine literature and our experience with DCI in rodents.
View Article and Find Full Text PDFInflammatory adhesion mediates myocardial segmental necroptosis induced by mixed lineage kinase domain-like protein in acute myocardial infarction.
Cell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
Intra-arterial tenecteplase after successful endovascular recanalisation in patients with acute posterior circulation arterial occlusion (ATTENTION-IA): multicentre randomised controlled trial.
BMJ
January 2025
Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Objective: To assess whether intra-arterial tenecteplase administered after successful endovascular recanalisation improves outcomes in patients with acute arterial occlusion of the posterior circulation.
Design: Multicentre randomised controlled trial.
Setting: 31 hospitals in China, 24 January 2023 to 24 August 2023.
Genistein-3'-sodium sulfonate suppresses NLRP3-mediated cell pyroptosis after cerebral ischemia.
Metab Brain Dis
January 2025
Key Laboratory of Prevention and treatment of cardiovascular and cerebrovascular diseases of Ministry of Education, Gannan Medical University, Ganzhou, 341000, China.
Cerebral ischemia-induced pyroptosis contributes to the dissemination of neuroinflammation, and Nod-like receptor protein-3 (NLRP3) inflammasome plays a key role in this process. Previous studies have indicated that Genistein-3'-sodiumsulfonate (GSS) can inhibit neuroinflammation caused by cerebral ischemia, exert cerebroprotective effects, but its specific mechanism has not been comprehensively understood. The aim of this study was to explore the effect of GSS on ischemic stroke-induced cell pyroptosis.
View Article and Find Full Text PDFAn autopsy case of TFE3-rearranged PEComa-like neoplasm with systematic embolization involving the heart.
Cardiovasc Pathol
January 2025
Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine, Japan. Electronic address:
A rare autopsy case of malignant transcription factor E3 (TFE3)-rearranged perivascular epithelioid cell tumor (PEComa)-like neoplasm is presented. An 84-year-old woman manifested multiple cerebral infarctions and repetitive embolic events in the supra mesenchymal artery (SMA), and the presence of a mobile mass in the heart's left ventricle was also revealed. Tumoral lesions were also found in a pelvic space and a right pleural cavity, and a biopsy was performed from one of the disseminated tumor masses in the right pleura.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!