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This article has been peer reviewed. It was published in: Clinical Medicine Insights: Cardiology.

Volume 9, 2015, Article number A009, Pages 57-64.

The published version is available at DOI: 10.4137/CMC.S29735

Copyright © 2015 the author(s), publisher and licensee Libertas Academica Ltd.

This is an open-access article distributed under the terms of the Creative Commons CC-BY-NC 3.0 License.


Heart function fails when the organ is unable to pump blood at a rate proportional to the body's need for oxygen or when this function leads to elevated cardiac chamber filling pressures (cardiogenic pulmonary edema). Despite our sophisticated knowledge of heart failure, even so-called ejection fraction-preserved heart failure has high rates of mortality and morbidity. So, novel therapies are sorely needed. This review discusses current standard therapies for heart failure and launches an exploration into emerging novel treatments on the heels of recently-approved sacubitril and ivbradine. For example, Vasoactive Intestinal Peptide (VIP) is protective of the heart, so in the absence of VIP, VIP knockout mice have dysregulation in key heart failure genes: 1) Force Generation and Propagation; 2) Energy Production and Regulation; 3) Ca(+2) Cycling; 4) Transcriptional Regulators. VIP administration leads to coronary dilation in human subjects. In heart failure patients, VIP levels are elevated as a plausible endogenous protective effect. With the development of elastin polymers to stabilize VIP and prevent its degradation, VIP may therefore have a chance to satisfy the unmet need as a potential treatment for acute heart failure.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 3.0 License

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