Key result
ATTRibute-CM evaluates acoramidis effects on quality-of-life outcomes across genotypes in ATTR-CM.
Why the study?
Transthyretin amyloid cardiomyopathy causes progressive heart failure, impaired health-related quality of life, and high mortality, with hereditary disease progressing more rapidly than wild-type disease.
May warrant closer surveillance for ATTRv-CM; leaves open whether genotype-specific interventions improve outcomes.
Transthyretin amyloid cardiomyopathy (ATTR-CM) causes progressive heart failure (HF), functional limitation, impaired health-related quality of life (HRQoL), and high mortality in the absence of therapy.1 ATTR-CM occurs as wild-type disease (ATTRwt-CM), typically presenting in older adults, and hereditary disease (ATTRv-CM) caused by genetic mutations in transthyretin (TTR). ATTRv-CM progresses more rapidly than ATTRwt-CM, evidenced by worse functional status, faster health status deterioration, and reduced survival in these patients.
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Joyce et al. (2026) studied Transthyretin amyloid cardiomyopathy (ATTR-CM). Acoramidis was evaluated on KCCQ and EQ-5D-5L outcomes.
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