Why the study?
Despite extensive scientific breakthroughs in HF research, questions persist regarding the ideal therapeutic targets to achieve maximum benefit.
This review evaluates the mechanisms of action of current heart failure therapies, suggesting that interventions targeting multiple pathophysiological pathways may be more effective.
May support multi-pathway HF strategies; hypothesis-generating and requires prospective validation.
Heart failure (HF) is a complex, multifactorial and heterogeneous syndrome with substantial mortality and morbidity. Over the last few decades, numerous attempts have been made to develop targeted therapies that may attenuate the known pathophysiological pathways responsible for causing the progression of HF. However, therapies developed with this objective have sometimes failed to show benefit. The pathophysiological construct of HF with numerous aetiologies suggests that interventions with broad mechanisms of action which simultaneously target more than one pathway maybe more effective in improving the outcomes of patients with HF. Indeed, current therapeutics with clinical benefits in HF have targeted a wider range of intermediate phenotypes. Despite extensive scientific breakthroughs in HF research recently, questions persist regarding the ideal therapeutic targets which may help achieve maximum benefit. In this review, we evaluate the mechanism of action of current therapeutic strategies, the pathophysiological pathways they target and highlight remaining knowledge gaps regarding the mode of action of these interventions.
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Khan et al. (2022) studied this question.
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