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Patients with idiopathic pulmonary fibrosis, patients tolerated [68Ga]CBP8 without adverse effects, and there was a strong correlation between high collagen tracer signal and fibrotic lung regions established by chest computed tomography scan findings in preliminary studies, as shown by a strong correlation. Extracellular collagen deposition in the myocardium may also contribute to myocardial stiffness in patients with cardiac amyloidosis. Collagen deposition findings in adverse cardiac remodeling using identical mechanisms as amyloidosis and may precipitate heart failure in patients with cardiac amyloidosis. In addition, amyloid fibrils therapies, directed against amyloid fibrils, have differing response rates in cardiac amyloidosis patients with or without coexistent fibrosis. Magnetic resonance imaging is a common method of measuring extracellular mass in conditions where myocardial fibrosis is the primary cause of ECV increase. ECV may not be a good predictor of myocardial fibrosis in patients with cardiac amyloidosis, where ECV is already elevated as a result of myocardial amyloid infiltration. To determine differences in radiotracer uptake, if any, the investigators would like to study 15 patients with light-chain cardiac amyloidosis and 15 patients with transthyretin cardiac amyloidosis and 15 patients with transthyretin cardiac amyloidosis. The investigators will also enroll 15 patients with recent myocardial infarction and 15 patients with hypertrophic cardiomyopathy as positive controls for fibrosis, and 15 patients with chronic myocardial infarction as positive controls for fibrosis, and 15 patients with hypertrophic cardiomyopathy will be recruited as positive controls for fibrosis, and 5 people without cardiovascular disease will be included as negative controls. The aim of this research was to compare [68Ga]CBP8 PET uptake in patients with cardiac amyloidosis with standard MRI techniques.
Source link: https://clinicaltrials.gov/ct2/show/NCT05619302
Approximately 1. 5 million of the 44 million Blacks in the United States are users of the vaping-to-isoleucine substitution at position 122 in the transthyretin protein. The overall goal of this study is to determine the presence of subclinical hATTR-CA and to identify biomarkers that indicate amyloid migration in V122I TTR carriers. The central hypothesis will be tested by two specific objectives: Aim 1 determines the connection of V122I TTR carrier status with CMRI evidence of amyloid infiltration; Sub-aim 2 establish the connection between amyloid-specific biomarkers and V122I TTR carrier status; and Sub-aim 2 determines the connection between amyloid-specific biomarkers and V122I TTR carrier status; and Sub-aim 2 determine the connection between amyloid-specific biomarkers In Aim 1, CMRI will be used to analyze measurements related to cardiac amyloid infiltration in a cohort of V122I TTR carriers without HF that were not filtered by cascade genetic testing and age-, sex-, and race-matched non-carrier controls. Aim 1's sub-sample of carriers and non-carrier controls will be assessed and compared cardiac systolic and diastolic reserve by using CMRI. Both from Aim 1 and individuals with symptomatic V122I hATTR-CA from our clinical sites, with measurements matched non-carriers in V122I TTR carriers without HF. These biomarkers identify and quantify various aspects of TTR amyloidogenesis, including circulating TTR, retinol binding protein 4, TTR kinetic stability, and misfolded TTR oligomers.
Source link: https://clinicaltrials.gov/ct2/show/NCT05489549
Transthyretin cardiac amyloidosis is a chronic heart disease that is often ignored. Amyloid deposits can damage the heart muscle because the fragile, unfurled amyloid proteins fold up into large pieces that stick together between layers of tissue, causing amyloid deposits. Transthyretin Amyloidosis, a common disease that deposits in the heart, but in which PYP Scintigraphy did not find it in there; and People with Amyloidosis that usually deposits outside the heart, to see if this compound can detect them outside the heart; and People who have found Amyloid deposits in the heart to see if this compound can detect it in the heart; and People with a type of Amyloidosis that usually deposits in people with Amyloidos.
Source link: https://clinicaltrials.gov/ct2/show/NCT05635045
This research will determine whether this drug could reduce the signs of a heart disease caused by TTR amyloidosis, such as heart disease. NNC6019-0001 is a new drug developed for people with TTR amyloidosis. Participants will be infused with the study medicine 13 times, once every 4 weeks. Participants are unable to participate in this investigation if they have a heart disease other than a heart disease due to TTR amyloidosis.
Source link: https://clinicaltrials.gov/ct2/show/NCT05442047
During the 18-month Treatment Period, participants will be given vutrisiran subcutaneous injection every 3 months or the reference comparator patisiran intravenous injection every three weeks. In the Randomized Treatment Extension Period, all participants will be randomly assigned to receive vutrisiran SC injections every 6 months or q3M.
Source link: https://clinicaltrials.gov/ct2/show/NCT03759379
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