Editorial: Novel phenotyping and risk stratification strategies for heart failure

Abstract

Editorial on the Research Topic Novel phenotyping and risk stratification strategies for heart failure Since its designation as an emerging epidemic in 1997, heart failure (HF) has remained a major public health problem (1). With an estimated 64.3 million people living with HF worldwide, it is a common cause of hospitalizations and contributes significantly to healthcare costs, morbidity, and mortality (2). Although recent decades have seen massive leaps in the understanding and management of HF, much remains to be explored and the frontiers of HF research continue to be pushed, as is evident from the 15 excellent articles presented in this Research Topic.Pathophysiological understanding is critically important in all medical conditions, and HF is no exception. Here, Meng et al. presented a prospective cohort of 84 consecutive patients with acute decompensation of HF who, compared to 83 patients without HF, had higher CD4 + /CD8 + expression of T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3), a unique inhibitory co-receptor expressed on the surface of immune cells and mediates immune tolerance; Tim-3 expression was also independently associated with major adverse cardiac and cerebrovascular events. These highlighted the importance of inflammation in acute decompensation of HF. Meanwhile, Li N. et al. provided a comprehensive review of the role of RNA binding motif protein 20 (RBM20) and other splicing factors in titin isoform ratio modification, myocardial stiffness, and thus pathophysiology of HF with preserved ejection fraction (HFpEF). Aside from pathophysiological insights, the authors suggested that RBM20 may be a therapeutic target for mitigating myocardial stiffness in HFpEF, which, given the relative paucity of efficacious treatments for HFpEF (3), may be an exciting prospect warranting further exploration.