Unveiling wild-type transthyretin cardiac amyloidosis as a significant and potentially modifiable cause of heart failure with preserved ejection fraction

This editorial refers to ‘Wild-type transthyretin amyloidosis as a cause of heart failure with preserved ejection fraction’, by F. Gonzalez-Lopez et al ., on page doi:10.1093/eurheartj/ehv338. Heart failure with a normal or preserved ejection fraction (HFnEF/HFpEF) is a heterogeneous clinical syndrome without proven treatments. Numerous biological mechanisms have been implicated in the genesis of HFnEF/HFpEF and include intrinsic cardiomyocyte stiffness related to abnormal calcium homeostasis, and cytoskeletal and extracellular matrix (ECM) abnormalities. Given the lack of efficacy of pharmacological therapies, there is a growing emphasis on how co-morbidities influence the development of this clinical syndrome,1 with an emerging hypothesis that co-morbidities drive its phenotypic expression.2 Characterization of HFnEF/HFpEF stratified by aetiological subgroups may therefore identify relevant cohorts for investigation and treatable pathophysiological mechanisms.3 Figure 1 Screening and treatment paradigm for unveiling transthyretin amyloid (ATTR) as a potentially modifiable cause of heart failure with preserved ejection fraction (HFpEF). The diagnosis of TTR cardiac amyloidosis among patients hospitalized with heart failure ( A ) can be ascertained using technetium 99 m bone tracers ( B ) so that emerging therapies may …