1,721,118 research outputs found
Biomarkers: monoclonal protein and indicators of cardiac damage.
No full textCardiac amyloidosis (CA) is a group of systemic disorders characterized by the deposition of abnormal protein fibrils in the heart, leading to progressive heart failure (HF) and poor prognosis. Early detection, accurate diagnosis, and effective risk stratification are critical for guiding treatment decisions and improving patient outcomes. Circulating biomarkers reflect the pathophysiology of amyloidosis (Fig. 11.1), and some of them have emerged as valuable tools in the management of CA, providing insights into organ involvement, disease progression, and response to therapy. This review paper aims to explore the role of biomarkers in CA, focusing on two major subtypes: biomarkers related to monoclonal protein and indicators of cardiac damage, namely natriuretic peptides (NPs) and troponin
Left ventricular ejection fraction and coronary artery disease in the era of precision medicine
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How a large registry can explain pathophysiology: The case of anemia in the heart failure syndromes
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High-Sensitivity Troponins and Prognosis in Heart Failure: Which Kind of Meta-Analysis Is Needed?
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PET-CT evaluation of amyloid systemic involvement with [18F]-florbetaben in patient with proved cardiac amyloidosis: a case report
No full textBackground: One of the most frequent disorders which lead to cardiac amyloidosis is transthyretin-related amyloidosis (ATTR). Some PET radio-pharmaceuticals for the detection of beta-amyloid deposits within the brain have shown to be able to detect also cardiac amyloid deposits. We present a case of a man with ATTR studied with [18F]-florbetaben PET-CT. Results: Total-body scan showed a moderate uptake in the bone marrow, especially in correspondence of the vertebral column, while no significant myocardial uptake was present. Cardiac-focused scans showed low mean cardiac SUV values confirming the absence of significant myocardial uptake. Brain scan showed a significant cortical brain uptake of the radio-pharmaceutical more evident in correspondence of frontal and temporal lobes. Conclusions: Distinct subtypes of amyloidosis show different uptake of the radiotracer. Brain amyloid deposition in the presence of a systemic disease could not be caused by the same amyloid precursor
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