Background Several imaging parameters and biomarkers provide diagnostic and prognostic information for wild-type transthyretin amyloid cardiomyopathy. However, the relevance of these parameters and their association with cardiac amyloid load requires further substantiation. We aimed to elucidate the association of imaging parameters obtained using Tc-labeled pyrophosphate scintigraphy, cardiovascular magnetic resonance imaging, global longitudinal strain (GLS), and cardiac biomarkers with cardiac amyloid load in patients with wild-type transthyretin amyloid cardiomyopathy. Methods and Results Eighty-eight patients with wild-type transthyretin amyloid cardiomyopathy who underwent Tc-labeled pyrophosphate scintigraphy and cardiovascular magnetic resonance were retrospectively evaluated. Quantitative cardiac amyloid load was obtained from 61 patients after myocardial biopsy. Correlations were assessed using Pearson's correlation coefficient applied to medical record data. The mean heart to contralateral ratio, native T1, extracellular volume, and GLS were 1.91±0.36, 1419.4±56.4 ms, 56.5±13.6%, and -9.4±2.5%, respectively. Median high-sensitivity cardiac troponin T (hs-cTnT) and BNP (B-type natriuretic peptide) levels were 0.0478 (0.0334-0.0691) ng/mL and 213.8 (125.8-392.7) pg/mL, respectively. The mean cardiac amyloid load was 22.9±15.0%. The heart to contralateral ratio correlated significantly with native T1 (=0.397), extracellular volume (=0.477), GLS (=0.363), cardiac amyloid load (=0.379), and Ln (hs-cTnT) (=0.247). Further, cardiac amyloid load correlated significantly with native T1 (=0.509), extracellular volume (=0.310), GLS (=0.446), and Ln (hs-cTnT) (=0.354). Compared with BNP, hs-cTnT levels better correlated with several imaging parameters and cardiac amyloid load. Conclusions Increased cardiac amyloid load correlated with increased Tc-labeled pyrophosphate positivity, native T1, extracellular volume, and hs-cTnT levels, and an impaired GLS, suggesting that imaging parameters and cardiac biomarkers may reflect histological and functional changes attributable to amyloid deposition in the myocardium.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9238652PMC
http://dx.doi.org/10.1161/JAHA.121.024717DOI Listing

Publication Analysis

Top Keywords

amyloid load
36
cardiac amyloid
32
wild-type transthyretin
16
transthyretin amyloid
16
amyloid cardiomyopathy
16
imaging parameters
16
extracellular volume
16
amyloid
14
tc-labeled pyrophosphate
12
cardiac
11

Similar Publications

Purpose: This study aimed to develop a deep learning (DL) model for brain region parcellation using CT data from PET/CT scans to enable accurate amyloid quantification in 18F-FBB PET/CT without relying on high-resolution MRI.

Patients And Methods: A retrospective dataset of PET/CT and T1-weighted MRI pairs from 226 individuals (157 with mild cognitive impairment or dementia and 69 healthy controls) was used. The dataset was split into training/validation (60%) and test (40%) sets.

View Article and Find Full Text PDF

Determining causal pathogens and inflammatory state of mastitis in dairy cows via Gram staining of precipitates in milk.

Front Vet Sci

January 2025

Graduate School of Integrated Sciences for Life, Hiroshima University, Higashihiroshima, Hiroshima, Japan.

Early detection of bovine mastitis-causing pathogens is necessary for treatment. As culturing methods are time-consuming, a more rapid detection technique is required. This study investigated the sensitivity, specificity, and detection limit of Gram staining of milk precipitates (milk Gram stain, MGS) to detect bovine mastitis-causing pathogens in milk, as well as the potential of MGS to diagnose inflammation by counting polymorphonuclear leukocytes (PMN).

View Article and Find Full Text PDF

Tracing TMEM106B fibril deposition in aging and Parkinson's disease with dementia brains.

Life Med

February 2024

Department of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai 200040, China.

Transmembrane protein 106B (TMEM106B), previously identified as a risk factor in frontotemporal lobar degeneration, has recently been detected to form fibrillar aggregates in the brains of patients with various neurodegenerative diseases (NDs) and normal elders. While the specifics of when and where TMEM106B fibrils accumulate in human brains, as well as their connection to aging and disease progression, remain poorly understood. Here, we identified an antibody (NBP1-91311) that directly binds to TMEM106B fibrils extracted from the brain and to Thioflavin S-positive TMEM106B fibrillar aggregates in brain sections.

View Article and Find Full Text PDF

Mild behavioral impairment and its relation to amyloid load in isolated REM sleep behavior disorder.

Parkinsonism Relat Disord

January 2025

Department of Nuclear Medicine, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul, Republic of Korea. Electronic address:

Introduction: In isolated REM sleep behavior disorder (iRBD), the evidence of cognitive impairment and co-existing amyloid pathology suggests that mild behavioral impairment (MBI) may be associated with disease progression. In this study, we investigated MBI and its association with cognitive function, brain amyloid load and glucose metabolism in iRBD patients to evaluate the utility of MBI as a predictive marker of disease progression.

Methods: Patients with iRBD underwent a neuropsychological evaluation, F-florbetaben (FBB) PET, and F-fluorodeoxyglucose (FDG) PET.

View Article and Find Full Text PDF

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.

Mol Neurodegener

January 2025

Department of Neurobiology and Behavior, Charlie Dunlop School of Biological Sciences, University of California, Irvine, CA, 92697-4545, USA.

Background: Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer's Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects.

View Article and Find Full Text PDF

Want 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!