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Abstract
AimsThe HERMES (HEart failure Molecular Epidemiology for Therapeutic targetS) consortium aims to identify the genomic and molecular basis of heart failure.Methods and resultsThe consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome‐wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow‐up following heart failure diagnosis ranged from 2 to 116 months. Forty‐nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34–90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of ≥1.10 for common variants (allele frequency ≥ 0.05) and ≥1.20 for low‐frequency variants (allele frequency 0.01–0.05) at P < 5 × 10−8 under an additive genetic model.ConclusionsHERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction.
Highlights
Heart failure (HF) is a complex clinical syndrome that imposes a substantial burden on public health; an estimated 30 million people worldwide are living with HF, and the prevalence is expected to rise with the aging of the global population.[1]
Human genetic and genomic studies provide unique opportunities to explore the causal biology in patients; the HERMES consortium provides a collaborative platform that enables these approaches
While this complexity is mirrored in other common cardiovascular diseases, such as coronary artery disease, heterogeneity is marked for HF
Summary
R. Thomas Lumbers1,2,3*, Sonia Shah[4,5], Honghuang Lin[6,7], Tomasz Czuba[8], Albert Henry[1,5], Daniel I. Holmes[14,15,16], Johan Ärnlöv[17,18], Per Svensson[19,20], Harry Hemingway[1,2,21], Neneh Sallah[1,2,22], Peter Almgren[23], Krishna G. Smith[95,99,100], Kari Stefansson[61,101], Steen Stender[102], David J. Taylor[96], Maris Teder-Laving[55], Alexander Teumer[53,58], Guðmundur Thorgeirsson[61,101], Unnur Thorsteinsdottir[61,101], Christian Torp-Pedersen[105,106,107], Stella Trompet[68,108], Danny Tuckwell[42], Benoit Tyl[56], Andre G. Uitterlinden[57,109], Felix Vaura[90,110], Abirami Veluchamy[51], Peter M.
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