Why the study?
Despite substantial unmet needs in AF, drug development has been challenging and current drugs remain inadequate due to oversimplified patient classification and failure to target underlying disease mechanisms.
Proposes a new framework for atrial fibrillation drug development focusing on molecular pathophysiology and patient subsegmentation to improve clinical trial success.
Existing AF drugs remain inadequate; challenges oversimplified models and leaves open new therapeutic targets.
Atrial fibrillation (AF) is a highly prevalent cardiac arrhythmia and cause of significant morbidity and mortality. Its increasing prevalence in aging societies constitutes a growing challenge to global healthcare systems. Despite substantial unmet needs in AF prevention and treatment, drug developments hitherto have been challenging, and the current pharmaceutical pipeline is nearly empty. In this review, we argue that current drugs for AF are inadequate because of an oversimplified system for patient classification and the development of drugs that do not interdict underlying disease mechanisms. We posit that an improved understanding of AF molecular pathophysiology related to the continuous identification of novel disease-modifying drug targets and an increased appreciation of patient heterogeneity provide a new framework to personalize AF drug development. Together with recent innovations in diagnostics, remote rhythm monitoring, and big data capabilities, we anticipate that adoption of a new framework for patient subsegmentation based on pathophysiological, genetic, and molecular subsets will improve success rates of clinical trials and advance drugs that reduce the individual patient and public health burden of AF.
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Ang et al. (2020) studied this question.
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