Cardiac amyloidosis (transthyretin, ATTR-CM)
A misfolded blood protein called transthyretin builds up as stiff deposits inside the heart muscle, making it thicken and stop relaxing properly. A bone-scanning tracer that also sticks to these deposits can diagnose it without a heart biopsy.
Overview
Transthyretin amyloid cardiomyopathy (ATTR-CM) is caused by misfolded transthyretin (wild-type or a hereditary variant) depositing as amyloid fibrils in the myocardium, producing a restrictive, thick-walled heart failure phenotype that mimics hypertensive heart disease on echocardiography. It is distinct from AL (light-chain) cardiac amyloidosis, which needs haematology-led treatment, so excluding a plasma cell clone (serum/urine immunofixation and free light chains) alongside imaging is mandatory.
Bone-avid Tc-99m bisphosphonate tracers (pyrophosphate, or DPD/HMDP outside the US) bind ATTR amyloid deposits, apparently via calcium co-deposition, and are read against rib (bone) uptake on a 0-3 visual grade. Gillmore et al. (2016, JAMA Cardiology, n=1,217) showed grade 2-3 uptake, combined with the absence of a monoclonal protein, had 100% specificity and positive predictive value for ATTR-CM, avoiding endomyocardial biopsy in most patients. Multisociety expert consensus (ASNC/AHA/ASE/EANM/HFSA/ISA/SCMR/SNMMI, with a 2021 addendum) now requires SPECT or SPECT/CT confirmation of myocardial uptake; planar grading or the heart-to-contralateral ratio alone is no longer sufficient for diagnosis.
The test matters clinically because ATTR-specific therapies (TTR stabilisers and gene-silencing agents) are now available, so a confident non-invasive diagnosis changes management; this is outside Nuclide's therapeutic scope but is the reason demand for pyrophosphate scanning has grown sharply since the mid-2010s.
State of the art
Tc-99m pyrophosphate (or DPD/HMDP) SPECT/CT grade 2-3 myocardial uptake plus exclusion of a monoclonal light-chain clone
Subtypes & biomarkers
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Dated changes read from the records linked to this indication: approvals, regulatory steps, reported trials, guideline versions and milestones. Newest first; no date is inferred.
All 3 changes by month →- 2026-09-22This recordCardiac amyloidosis (transthyretin, ATTR-CM)Facts on this page last checked
When this page itself was last checked or edited.
- 1976ApprovalTechnetium Tc-99m pyrophosphateTechnetium Tc-99m pyrophosphate approved in US
Skeletal imaging to demonstrate areas of altered osteogenesis
- 1976ApprovalTechnetium Tc-99m pyrophosphateTechnetium Tc-99m pyrophosphate approved in US
Cardiac imaging as an adjunct in the diagnosis of acute myocardial infarction
What is in development for Cardiac amyloidosis (transthyretin, ATTR-CM), drawn from the whole corpus: 1 items. Drugs are grouped by the most advanced trial phase they have reached anywhere; approved treatments sit under standard of care. Technologies are the methods being tested for this cancer, trials are the studies recorded here, and ideas are proposals not yet in a trial.
Drugs in emerging · 1
Open problems and what is being done
Trials
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Direct links plus the targets, companies, and technologies of this cancer's products.
Latest papers
topQuery for this indication: (TITLE:"Cardiac amyloidosis" OR ABSTRACT:"Cardiac amyloidosis" OR TITLE:"transthyretin, ATTR-CM" OR ABSTRACT:"transthyretin, ATTR-CM") AND (treatment OR therapy OR trial OR survival OR diagnosis). Results are unfiltered search hits about Cardiac amyloidosis (transthyretin, ATTR-CM), not a curated reading list.