ArticleCirculation. Heart failure2026
Proteomics Profiling Reveals Molecular Subtypes of Transthyretin Cardiac Amyloidosis.
Article in Circulation. Heart failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTransthyretin cardiac amyloidosis (ATTR-CA) may involve heterogeneity in biological mechanisms (ie, molecular subtypes). Molecular subtypes potentially lead to differences in prognosis and treatment response to tafamidis-the first disease-modifying therapy for ATTR-CA. We aimed to derive molecular subtypes of ATTR-CA through comprehensive plasma proteomics profiling and to examine their associations with prognosis and estimated treatment effect of tafamidis.
methodsWe applied unsupervised machine learning to comprehensive plasma proteomics profiling of 7289 proteins to identify molecular subtypes in our prospective cohort of patients with ATTR-CA enrolled at Columbia University. We compared all-cause mortality risk and estimated the treatment effect of tafamidis among the identified molecular subtypes, adjusting for age, sex, TTR genotype, and concomitant medication use. We also performed pathway analysis comparing the worst prognosis subtype with the other subtypes combined.
resultsAmong 142 patients eligible for analysis, 96 patients received tafamidis treatment. We identified 3 molecular subtypes (subtype A: n=49, subtype B: n=38, and subtype C: n=55) with different survival risks during a median follow-up of 5.2 years (log-rank
conclusionsOur prospective cohort study using comprehensive plasma proteomics profiling not only uncovered molecular ATTR-CA subtypes but also identified pathogenetic mechanisms associated with differential prognosis and estimated the treatment effect of tafamidis.
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