ArticleCureus2026
Transthyretin Cardiac Amyloidosis in an Older Athlete.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac amyloidosis is a clinical condition characterized by deposition of amyloid fibrils in the myocardium, leading to increased left ventricular wall thickness and ultimately heart failure. We present a case of a former athlete who was found to have severe left ventricular hypertrophy (LVH) on echocardiogram and was ultimately diagnosed with wild-type transthyretin (ATTR) cardiac amyloidosis, for which he was started on tafamidis. The recognition and diagnosis of cardiac amyloidosis are important given advances in the ability to diagnose and treat this condition, ideally before a patient develops heart failure symptoms. This report also emphasizes the differences between athletic cardiac remodeling of the heart and pathologic changes suggestive of cardiac disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.