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.