ATTR amyloidosis is a protein-misfolding disorder of the transthyretin (TTR) protein1

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THE SOURCE OF THE DISEASE IS PRODUCED IN THE LIVER3,4

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Liver

(where 90% of TTR is produced)

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Transthyretin tetramer destabilizes
Transthyretin
tetramer destabilizes
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Tetramer dissociates into monomers
Tetramer dissociates
into monomers
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Monomers Misfold And Aggregate Into Amyloid Fibrils
Monomers misfold
and
aggregate into
amyloid fibrils
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Amyloid deposits throughout the body
Amyloid deposits
throughout the body

WATCH THIS VIDEO TO LEARN MORE ABOUT THE MECHANISM OF DISEASE FOR ATTR

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The disease is classified as hereditary or wild type4

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Hereditary ATTR (hATTR): Instability of TTR is due to mutations in the TTR gene1,4

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Wild-type ATTR (ATTRwt): Instability of TTR may be due to unknown environmental and age-related factors4

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hATTR CAN PROGRESS RAPIDLY

hATTR-PN5,6

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Stage 1: Walking Without Assistance
Walking without assistance
STAGE 1
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Stage 2: Walking With Assistance
Walking with assistance
STAGE 2
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Stage 3: Confined To A Wheelchair Or Bed
Confined to a wheelchair or bed
STAGE 3
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MORTALITY

ATTR-CM8

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Early Clinical HF And Arrhythmias
Early clinical HF
Arrhythmias
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Restrictive HF and HF Hospitalizations
Restrictive CM
HF hospitalizations
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End Stage HF
End-stage HF
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MORTALITY

Configure Accordion Item: - See how hATTR-PN progresses to mortality as soon as 5 years from diagnosis7
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Configure Accordion Item: - See how hATTR-PN progresses to mortality as soon as 5 years from diagnosis7

hATTR-PN5,6

Stage 1: Walking Without Assistance
Walking without assistance
STAGE 1
Stage 2: Walking With Assistance
Walking with assistance
STAGE 2
Stage 3: Confined To A Wheelchair Or Bed
Confined to a wheelchair or bed
STAGE 3

MORTALITY

Configure Accordion Item: - See how ATTR-CM progresses to mortality as soon as 2.6 years from diagnosis9
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Configure Accordion Item: - See how ATTR-CM progresses to mortality as soon as 2.6 years from diagnosis9

ATTR-CM8

Early Clinical HF And Arrhythmias
Early clinical HF
Arrhythmias
Restrictive HF and HF Hospitalizations
Restrictive CM
HF hospitalizations
End Stage HF
End-stage HF

MORTALITY

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

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Patients with hATTR may face
a diagnostic delay of

>

3

YEARS5

50% of patients saw

3

PHYSICIANS

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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