Recognizing
ATTR‑CM

Learn about this unrelenting, progressive heart disease

ATTR‑CM can diminish quality of life, cause recurrent hospitalization, and lead to premature death.1

ATTR-CM Diagnosis

Early diagnosis enables early interventions that may help slow disease progression.2-4 A noninvasive diagnostic algorithm is available to facilitate timely identification of patients with ATTR-CM.5

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Explore the steps to confirm an ATTR‑CM diagnosis

Delayed diagnosis prevents timely intervention and contributes to premature death.1,2,6

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>4 years median diagnostic delay1

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3–5 years median survival1

in untreated patients following diagnosis

Although ATTR‑CM has become an increasingly recognized cause of heart failure and arrhythmia, misdiagnosis is common.4,6

Patient Populations Considered At-Risk for ATTR‑CM3

patient populations considered at-risk for attr-cm infographic

There are 2 subtypes of ATTR-CM2:

  • Wild-type (ATTRwt-CM) comes from age-related changes to the TTR protein
  • Variant (ATTRv-CM) occurs through variants in the TTR gene*

*Also known as hereditary ATTR-CM (ATTRh-CM).

80% of patients9

20%9†

Wild-type ATTR-CM2,8,10

  • Sporadic disease
  • TTR gene has normal sequence; TTR protein becomes unstable with age
  • Reduced symptom severity at diagnosis
  • Typically manifests later in life (70-75 years of age)

Variant ATTR-CM1,10,11

  • Autosomal dominant pattern of inheritance
  • Variant sequence in TTR gene destabilizes the TTR protein
  • More severe disease at diagnosis (poorer survival, EF, renal function, and performance status)
  • Typical age of onset is >60 years of age

†In a study of 879 people with ATTR-CM.9

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A prevalent pathogenic TTR gene variant is V122I, which affects 3%-4% of all Black Americans and has been found in 10% of those aged 65 years or older with severe congestive heart failure12

Although predominantly diagnosed ​in men, ATTR-CM is becoming increasingly recognized in women13

On average, women are 3.3 years older than men at diagnosis.13

Both sexes have similar mortality rates, 1-year disease progression rates, and overall structure and function when accounting for body size13

sex differences in attr-cm infographic

‡In a study of 1732 consecutive patients, comprising 1095 with wild-type ATTR-CM and 637 with variant ATTR-CM.13

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References:
1.

Lane T, Fontana M, Martinez-Naharro A, et al. Natural history, quality of life, and outcome in cardiac transthyretin amyloidosis. Circulation. 2019;140(1):16-26. 2. Rozenbaum MH, Large S, Bhambri R, et al. Impact of delayed diagnosis and misdiagnosis for patients with transthyretin amyloid cardiomyopathy (ATTR-CM): a targeted literature review. Cardiol Ther. 2021;10(1):141-159. 3. Kittleson MM, Maurer MS, Ambardekar AV, et al. Cardiac amyloidosis: evolving diagnosis and management: a scientific statement from the American Heart Association. Circulation. 2020;142(1):e7-e22. 4. Griffin JM, Rosenthal JL, Grodin JL, Maurer MS, Grogan M, Cheng RK. ATTR amyloidosis: current and emerging management strategies: JACC: CardioOncology state-of-the-art review. JACC CardioOncol. 2021;3(4):488-505. 5. Witteles RM, Bokhari S, Damy T, et al. Screening for transthyretin amyloid cardiomyopathy in everyday practice. JACC Heart Fail. 2019;7(8): 709-716. 6. Gillmore JD, Maurer MS, Falk RH, et al. Nonbiopsy diagnosis of cardiac transthyretin amyloidosis. Circulation. 2016;133(24): 2404-2412. 7. Gertz M, Adams D, Ando Y, et al. Avoiding misdiagnosis: expert consensus recommendations for the suspicion and diagnosis of transthyretin amyloidosis for the general practitioner. BMC Fam Pract. 2020;21(1):198. 8. Reynolds MM, Veverka KK, Gertz MA, et al. Ocular manifestations of familial transthyretin amyloidosis. Am J Ophthalmol. 2017;183:156-162. 9. Law S, Bezard M, Petrie A, et al. Characteristics and natural history of early-stage cardiac transthyretin amyloidosis. Eur Heart J. 2022;43(27):2622-2632. 10. Ruberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin amyloid cardiomyopathy: JACC state-of-the-art review. J Am Coll Cardiol. 2019;73(22):2872-2891. 11. Michels da Silva D, Langer H, Graf T. Inflammatory and molecular pathways in heart failure-ischemia, HFpEF and transthyretin cardiac amyloidosis. Int J Mol Sci. 2019;20(9):2322. 12. Buxbaum JN, Ruberg FL. Transthyretin V122I (pV142I)* cardiac amyloidosis: an age-dependent autosomal dominant cardiomyopathy too common to be overlooked as a cause of significant heart disease in elderly African Americans. Genet Med. 2017;19(7):733-742. 13. Patel RK, Ioannou A, Razvi Y, et al. Sex differences among patients with transthyretin amyloid cardiomyopathy – from diagnosis to prognosis. Eur J Heart Fail. 2022;24(12):2355-2363.