ATTR amyloidosis is a protein-misfolding disorder of the transthyretin (TTR) protein1
THE SOURCE OF THE DISEASE IS PRODUCED IN THE LIVER3,4
Liver
(where 90% of TTR is produced)
Transthyretin
tetramer destabilizes
tetramer destabilizes
Tetramer dissociates
into monomers
into monomers
Monomers misfold
and
aggregate into
amyloid fibrils
and
aggregate into
amyloid fibrils
Amyloid deposits
throughout the body
throughout the body
WATCH THIS VIDEO TO LEARN MORE ABOUT THE MECHANISM OF DISEASE FOR ATTR
The disease is classified as hereditary or wild type4
Hereditary ATTR (hATTR): Instability of TTR is due to mutations in the TTR gene1,4
Wild-type ATTR (ATTRwt): Instability of TTR may be due to unknown environmental and age-related factors4
hATTR CAN PROGRESS RAPIDLY
Walking without assistance
STAGE 1
Walking with assistance
STAGE 2
Confined to a wheelchair or bed
STAGE 3
LIFE EXPECTANCY IS 5 TO 15 YEARS FROM DIAGNOSIS7
Early clinical HF
Arrhythmias
Arrhythmias
Restrictive CM
HF hospitalizations
HF hospitalizations
End-stage HF
LIFE EXPECTANCY IS 2.6 TO 6 YEARS FROM DIAGNOSIS9
Walking without assistance
STAGE 1
Walking with assistance
STAGE 2
Confined to a wheelchair or bed
STAGE 3
LIFE EXPECTANCY IS 5 TO 15 YEARS FROM DIAGNOSIS7
Early clinical HF
Arrhythmias
Arrhythmias
Restrictive CM
HF hospitalizations
HF hospitalizations
End-stage HF
LIFE EXPECTANCY IS 2.6 TO 6 YEARS FROM DIAGNOSIS9
Increased clinical suspicion of hATTR is important for your patients
Low clinical suspicion and nonspecific symptoms result in underdiagnosis, misdiagnosis, and/or delayed treatment.1,10
Patients with hATTR may face a diagnostic delay of
>
3YEARS5
50% of patients saw
≥
3PHYSICIANS
before receiving the correct diagnosis of hATTR11
ATTR-CM, cardiomyopathy of transthyretin-mediated amyloidosis; ATTRwt, wild-type transthyretin-mediated amyloidosis; CM, cardiomyopathy; hATTR, hereditary transthyretin-mediated amyloidosis; hATTR-PN, polyneuropathy of hereditary transthyretin-mediated amyloidosis; HF, heart failure.
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