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Published on: June 14, 2016
Focusing Heart Failure Research on Myocardial Fibrosis to Prioritize Translation
Merry L Lindsey1, Kristine Y Deleon-Pennell2, Amy D Bradshaw2
1Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; Research Service, Nebraska-Western Iowa Health Care System, Omaha, Nebraska.
Insights
Heart failure (HF) classifications, including HF with reduced ejection fraction and HF with preserved ejection fraction, share common pathways like inflammation and extracellular matrix changes. Targeting these may offer new therapeutic strategies for heart failure patients.
Area of Science:
- Cardiology
- Biomedical Research
Background:
- Heart failure (HF) is traditionally defined by symptoms, but distinct classifications like HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF) have prognostic and therapeutic importance.
- HFrEF involves reduced left ventricular systolic function, while HFpEF involves abnormal left ventricular filling (diastolic dysfunction).
- HF is a significant issue within the US Department of Veterans Affairs (VA), representing a major research priority.
Purpose of the Study:
- To explore the myocardial extracellular matrix as a potential therapeutic target for both HFrEF and HFpEF.
- To identify common modifiable pathways and biological mediators shared by different forms of HF.
- To propose specific research directions for targeting myocardial fibrosis in heart failure.
Main Methods:
- A conference titled "Targeting Myocardial Fibrosis in Heart Failure" was convened, sponsored by the VA.
- The conference explored the hypothesis that HFrEF and HFpEF, despite distinct mechanisms, may share common pathways.
- Discussions focused on inflammation and extracellular matrix as converging themes.
Main Results:
- Inflammation and extracellular matrix changes were identified as major converging themes in both HFrEF and HFpEF.
- The extracellular matrix is proposed as a potential common therapeutic target.
- Specific research opportunities and unmet challenges were discussed.
Conclusions:
- Myocardial fibrosis, involving extracellular matrix changes, is a potential common therapeutic target for different forms of heart failure.
- Further research is needed to explore inflammation and extracellular matrix modulation as strategies to mitigate HF morbidity and mortality.
- Targeting shared pathways offers a promising avenue for developing novel treatments for the broad spectrum of heart failure patients.
Abstract:
Heart failure (HF) has traditionally been defined by symptoms of fluid accumulation and poor perfusion, but it is now recognized that specific HF classifications hold prognostic and therapeutic relevance. Specifically, HF with reduced ejection fraction is characterized by reduced left ventricular systolic pump function and dilation and HF with preserved ejection fraction is characterized primarily by abnormal left ventricular filling (diastolic failure) with relatively preserved left ventricular systolic function. These forms of HF are distributed equally among patients with HF and likely require distinctly different strategies to mitigate the morbidity, mortality, and medical resource utilization of this disease. In particular, HF is a significant medical issue within the US Department of Veterans Affairs (VA) hospital system and constitutes a major translational research priority for the VA. Because a common underpinning of both HF with reduced ejection fraction and HF with preserved ejection fraction seems to be changes in the structure and function of the myocardial extracellular matrix, a conference was convened sponsored by the VA, entitled, "Targeting Myocardial Fibrosis in Heart Failure" to explore the extracellular matrix as a potential therapeutic target and to propose specific research directions. The conference was conceptually framed around the hypothesis that although HF with reduced ejection fraction and HF with preserved ejection fraction clearly have distinct mechanisms, they may share modifiable pathways and biological mediators in common. Inflammation and extracellular matrix were identified as major converging themes. A summary of our discussion on unmet challenges and possible solutions to move the field forward, as well as recommendations for future research opportunities, are provided.
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