AI Article Synopsis
- * Despite advancements in understanding heart failure, even cases considered "ejection fraction-preserved" still result in high mortality and need for new treatments.
- * Research highlights the potential of Vasoactive Intestinal Peptide (VIP) as a protective agent in heart failure; new methods to stabilize VIP could make it a promising option for treating acute heart failure.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4603524 | PMC |
| http://dx.doi.org/10.4137/CMC.S29735 | DOI Listing |
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