Heart failure with preserved ejection fraction (HFpEF) is a highly complex and heterogeneous syndrome that causes substantial morbidity and mortality, positioning this disease as one of the biggest unmet medical needs today.
The past years have seen great scientific and clinical efforts on elucidating the driving mechanisms, but much remains unknown and successful therapies at still largely absent.
One of the biggest challenges to treating HFpEF is the heterogeneous nature of the syndrome. Risk assessment by conventional biomarkers has not led to any significant therapies, but selection of a more homogenous patient population might be the way forward.
Fibrosis is a hallmark feature of HFpEF pathology, acting as a driver of outcome. Understanding the intricate pathways that lead to fibrogenesis, and how they ultimately impact pathogenesis, is important for understanding how to treat HFpEF. We have developed a biomarker of fibroblast activity, PRO-C6, which independently and with high precision can identify a subset of HFpEF patients with a very elevated risk of adverse outcome.
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