Objective: Determine plaque subtype and volume difference in male and female patients with obstructive and non-obstructive CAD using 320-row MDCTA.
Materials And Methods: 128 patients with suspected CAD underwent MDCTA. All studies were divided into two groups based on disease severity. 0-70% stenosis (non-obstructive CAD) & >70% (obstructive). All were compared for plaque quantity and subtypes by gender. Main arteries, RCA, LM, LAD and LCX were analyzed using Vitrea 5.2 software to quantify fatty, fibrous and calcified plaque. Thresholds for coronary plaque quantification (volume in mm(3)) were preset at 35 ± 12 HU for fatty, 90 ± 24 HU for fibrous and >130 HU for calcified/mixed plaque and analyzed using STATA software.
Results: Total plaque burden in 118 patients [65M: 53F] was significantly higher in all arteries in males compared to females with non-obstructive disease. Total plaque volume for males vs. females was: RCA: 10.10 ± 5.02 mm(3) vs. 6.89 ± 2.75 mm(3), respectively, p = 0.001; LAD: 7.21 ± 3.38 mm(3) vs. 5.89 ± 1.93 mm(3), respectively, p = 0.04; LCX: 9.13 ± 3.27 mm(3) vs. 7.16 ± 1.73 mm(3), respectively, p = 0.002; LM 15.13 ± 4.51 mm(3) vs. 11.85 ± 4.03 mm(3), respectively, p = 0.001. In sub-analyses, males had significantly more fibrous and fatty plaque in LM, LAD & LCX than females. However in the RCA, only fibrous plaque was significantly greater in males. Calcified plaque volume was not significantly different in both genders. Only 8% of patients had obstructive CAD (>70% stenosis); there was no significant difference in plaque volume or subtypes.
Conclusion: In patients with non-obstructive CAD, males were found to have significantly higher total coronary plaque volume with predominance of fibrous and fatty subtypes compared to females of the same age and BMI. There was no significant difference in plaque subtype or volume in patients with obstructive disease.
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http://dx.doi.org/10.1016/j.atherosclerosis.2012.11.033 | DOI Listing |
Alzheimers Dement
December 2024
Imaging Genetics Center, Mark and Mary Stevens Neuroimaging & Informatics Institute, University of Southern California, Marina del Rey, CA, USA.
Background: Amyloid-β (Aβ) plaques and tau pathogenesis in the brain precede cognitive decline in the progression of Alzheimer's dementia, yet the extent to which these measures can predict localized brain tissue atrophy has not been studied in a large, diverse population. Multisite studies offer robust statistical power with larger sample sizes but are confounded by variations in biomarker quantification across studies, including variations in MRI scanners, PET tracers, and CSF assays. Longitudinal data from N=1223 individuals from four independent AD studies were harmonized to assess localized brain tissue atrophy over 2 to 5 years.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Background: While magnetic resonance imaging (MRI) markers of neurodegeneration are nonspecific to Alzheimer's disease (AD) pathology, they have been correlated with cognitive dysfunction, and therefore, provide important information pertaining to disease staging. Neurodegeneration in AD is commonly assessed with macrostructural measures of brain atrophy, such as hippocampal volume. However, recent investigations have shown that markers of neural microstructure derived from diffusion MRI (DWI) may provide supplementary insight into the progression of AD pathophysiology.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Université Paris-Saclay, CEA, CNRS, Inserm, BioMaps, Orsay, France.
Background: Typical Alzheimer's disease (AD) and Limbic-predominant Age-related TDP-43 Encephalopathy (LATE) are two neurodegenerative diseases that present with a similar initial amnestic clinical phenotype but have distinct proteinopathies. AD is characterised by ß-amyloid plaques and intraneuronal neurofibrillary tangles, while LATE is characterised by abnormal neuronal TDP-43 protein. With reference to the prion-like hypothesis regarding the propagation of proteinopathies, investigating white matter fibre bundle alterations could provide new insights into the propagation pathways of specific proteinopathies.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology, Columbia University, New York, NY, USA.
Background: Adults with Down syndrome (DS) overproduce amyloid precursor protein, develop amyloid plaques at an early age, and are diagnosed with Alzheimer's disease (AD) dementia at a high frequency. There is emerging evidence that cerebrovascular disease is elevated across the AD continuum in older adults with DS, independent of age and vascular risk, around the same time as amyloid and tau, but the regional rates of accumulation within individuals are unknown.
Method: Adults with DS from the multisite Alzheimer's Biomarker Consortium-Down Syndrome study (ABC-DS; n=78; age=50±6; 40% women) have two timepoints of T2 FLAIR MRI (1.
Alzheimers Dement
December 2024
Institute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen, Guangdong, China.
Background: Previous cross-sectional studies suggest that higher educational attainment (EA) may mitigate cognitive decline in Alzheimer's disease (AD). This study systematically investigated the association between EA and longitudinal cognitive decline across various domains and explored its connections with β-amyloid (Aβ) plaque, tau tangle, gray matter volume (GMV) and glucose metabolism in AD.
Method: We analyzed Aβ-PET (A), tau-PET (T), and 3D T1-MRI images (N) from the ADNI cohort to identify 58 A+/T-, 77 A+/T+, and 84 cognitively unimpaired (CU) participants without evidence of AD pathology and neurodegeneration (A-/T-/N-/CU).
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