Background: To evaluate the feasibility of non-invasive fractional flow reserve (FFR) estimation using histologically-validated assessment of plaque morphology on coronary CTA (CCTA) as inputs to a predictive model further validated against invasive FFR.
Methods: Patients (n = 113, 59 ± 8.9 years, 77% male) with suspected coronary artery disease (CAD) who had undergone CCTA and invasive FFR between August 2013 and May 2018 were included. Commercially available software was used to extract quantitative plaque morphology inclusive of both vessel structure and composition. The extracted plaque morphology was then fed as inputs to an optimized artificial neural network to predict lesion-specific ischemia/hemodynamically significant CAD with performance validated by invasive FFR.
Results: A total of 122 lesions were considered, 59 (48%) had low FFR values. Plaque morphology-based FFR assessment achieved an area under the curve, sensitivity and specificity of 0.94, 0.90 and 0.81, respectively, versus 0.71, 0.71, and 0.50, respectively, for an optimized threshold applied to degree of stenosis. The optimized ridge regression model for continuous value estimation of FFR achieved a cross-correlation coefficient of 0.56 and regression slope of 0.59 using cross validation, versus 0.18 and 0.10 for an optimized threshold applied to degree of stenosis.
Conclusions: Our results show that non-invasive plaque morphology-based FFR assessment may be used to predict lesion-specific ischemia resulting in hemodynamically significant CAD. This substantially outperforms degree of stenosis interpretation and has a comparable level of sensitivity and specificity relative to publicly reported results from computational fluid dynamics-based approaches.
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http://dx.doi.org/10.1016/j.ijcard.2021.01.040 | DOI Listing |
Acta Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFJ Neurochem
January 2025
Center for Protein Diagnostics (PRODI) Biospectroscopy, Ruhr University Bochum, Bochum, Germany.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) plaques in the brain, contributing to neurodegeneration. This study investigates lipid alterations within these plaques using a novel, label-free, multimodal approach. Combining infrared (IR) imaging, machine learning, laser microdissection (LMD), and flow injection analysis mass spectrometry (FIA-MS), we provide the first comprehensive lipidomic analysis of chemically unaltered Aβ plaques in post-mortem human AD brain tissue.
View Article and Find Full Text PDFJ Oral Biosci
January 2025
Department of Biochemistry, Nihon University School of Dentistry, Tokyo, Japan; Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, Tokyo, Japan. Electronic address:
Objectives: Exposure of gingival epithelial cells to butyrate, a short-chain fatty acid produced by dental plaque bacteria, cause cell death and subsequent damage-associated molecular pattern (DAMP) release. We investigated the effects of curcumin, a polyphenol extracted from turmeric, on butyrate-induced human gingival epithelial Ca9-22 cell death and DAMP release.
Methods: Ca9-22 cells were pretreated with curcumin before butyrate exposure.
Neurology
February 2025
Departments of Child Neurology and General Practice, University of Turku and Turku University Hospital, Finland.
Background And Objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE).
View Article and Find Full Text PDFTheranostics
January 2025
Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Vulnerable plaques, which are high-risk features of atherosclerosis, constitute critical elements in the disease's progression due to their formation and rupture. Macrophages and macrophage-derived foam cells are pivotal in inducing vulnerability within atherosclerotic plaques. Thus, understanding macrophage contributions to vulnerable plaques is essential for advancing the comprehension of atherosclerosis and devising novel therapeutic and diagnostic strategies.
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