What Is Heart Failure Therapy? 6 Potential Heart Failure Treatments
Cardiovascular disease resulting in heart failure is the leading cause of death for people living in developed countries. In an effort to find better ways to treat CVD, scientists have been researching a variety of heart failure therapies. Some of those are discussed in this article.
Omecamtiv mecarbil was developed as a safer alternative to inotropic agents while still having similar pharmacological effects. It specifically acts as a cardiac myosin activator. It binds to myosin and causes a shift in the equilibrium of ATP hydrolysis during a stroke.
Studies of omecamtiv mecarbil show that it was well tolerated by patients. Phase two trials had promising results as well, so expectations are high for phase three trials.
Elevated levels of a family of hormones called natriuretic peptides indicate heart failure. Three main natriuretic peptide receptors exist, NPR-A, NPR-B, and NPR-C. NPRs have been a component in the beneficial treatment of heart failure, so they are targeted for pharmacological therapies.
Ularitide is a synthetic version of urodilatin, a kidney peptide hormone. Ularitide binds with NPR-A, which causes diuresis and natriuresis to increase. Studies of ularitide therapy indicate that it can reduce cardiac wall stress and produce beneficial hemodynamic effects, but it doesn’t affect disease progression.
The location of the receptors in the body is important in cardiovascular therapy. Serelaxin is a synthetic version of relaxin; the peptides in relaxin have a structure similar to insulin. Currently, four relaxin receptors are known to be present in major body organs. These receptors exist in the kidney, blood cells, heart, and lungs.
Trials of Serelaxin have had mixed results. Tests with primarily Caucasian patients indicated that infusions of Serelaxin were more effective than oral doses. However, similar trials with Asian patients showed no significant improvement or change in mortality rates with Serelaxin therapy.
A consequence of heart failure is fluid retention. This fluid retention leads to edemas and pulmonary congestion. During heart failure, arginine vasopressin levels increase, and higher levels are part of the advanced stages of the disease. Sodium retention and neurohumoral abnormalities are the leading causes of fluid retention.
Loop diuretics are one of the common treatments for heart failure, but this therapy doesn’t work in approximately 30% of patients. Loop diuretics also cause hypotension or electrolyte imbalances in some patients. Tolvaptan is a treatment that is less likely to worsen kidney functions than typical diuretics.
The benefits of using tolvaptan to treat heart failure have been assessed in various studies. Results of one such study showed that symptoms of heart failure were decreased, but some patients developed hypernatremia at increased doses of tolvaptan.
CT-1 is connected to multiple heart-related issues. CT-1 is associated with myocardial fibrosis, the stimulation of fibroblasts, and heart valve disease, among others. CT-1 affects the entire cardiac muscle, not just single cardiomyocytes. The pathological changes created by CT-1 are similar to the physiological changes seen in athletes.
The physiological changes are not as beneficial as the ones brought about by CT-1. Another difference is the reversibility of the changes. The CT-1 changes are completely reversible.
Some doctors and scientists believe gene therapy is the best hope for rare congenital diseases. However, there hasn’t been a tremendous success with it, so many scientists think the expectations of success are unfounded. There is also hope that gene therapy could be of great benefit to the field of cardiology.
The main targets of gene therapy are proteins that regulate calcium levels. This is because people with CV (chronic venous) insufficiency often have imbalances when it comes to calcium regulation within the cardiomyocytes within their hearts. There are two main problems of gene therapy for cardiovascular diseases. They are the reaction of the patient’s immune system to the treatment and the effect of the treatment getting worse over a long time.
While there have been problems with gene therapy, scientists are still trying to improve the techniques. The continued gene therapy testing is a sign that the hope for its success continues to be justified.
Cardiovascular disease is the number one killer of people in developed countries. Scientists have been increasingly working on therapies for heart failure patients due to the increased number of people who suffer from cardiovascular disease. Continued progress means they have hope of finding a therapeutic solution for treating heart failure. All of the therapies discussed in this article show promise for success; however, they need continued research before they are deemed effective treatments.
Cardiovascular Research & Training Institute’s Heart Failure Research
Cardiovascular disease resulting in heart failure is the leading cause of death for people living in developed countries. In an effort to find better ways to treat CVD, scientists have been researching a variety of heart failure therapies. At the Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), researchers are interested in how cardiac muscle biology relates to the mechanistic basis of heart failure(HF). The CVRTI is committed to focusing on learning what drives heart muscle failure and how best to treat it.
Our Heart Failure Research in the Areas of Gene Therapy and Therapeutic Devices
Researchers are working on changing the standard of care for HF patients through drug therapy, gene therapy and therapeutic devices. Specifically, CVRTI investigators are trying to understand how the failing heart can recover in order to improve outcomes for HF patients. Our investigators are focused on identifying molecular and metabolic targets to develop new therapeutic tools for myocardial recovery. They also evaluate myocardial ultrastructure, microstructure, and function in normal, diseased, and aged hearts. Preserving and optimizing the cellular cytoskeleton and the mitochondrial function in the failing heart are major research interests of our investigators. Specifically, our investigators define the mechanisms by which the cytoskeleton delivers ion channels to their respective subregions on the cardiac membrane, and how delivery is changed during heart failure.
This work defined the paradigm of ‘targeted delivery’ which describes how the cytoskeleton delivers membrane proteins directly to their functional membrane subdomain and why there is less delivery in failing heart. Our CVRTI models involve exploration of Connexin43 gap junction trafficking to the cardiomyocyte intercalated disc and L-type calcium channel trafficking to cardiomyocyte T-tubules. In the process we identified that the mRNA of Cx43 is alternatively translated to generate endogenously up to six different truncated isoforms which are essential to trafficking. These isoforms we identified have a different biophysics and biology as Connexin43 and thus function as new proteins with important roles in basic cell biology.
A major current focus of our investigators is cardiac BIN1 which regulates L-type calcium channel trafficking, T-tubule folds and is also released into blood as T-tubule origin microparticles, and available as a biomarker of muscle remodeling. We have found that not only is cBIN1 important to calcium hemostasis and electrical stability in ventricular cells, but is reduced in acquired heart failure and is turned over into blood in levels that reflect cardiac content. We have helped developed a cBIN1 score (CS) as a first of its kind biomarker of cardiac muscle health that could be used as a screen for heart failure, prognosticate heart failure outcomes, and prognosticate the occurrence of ventricular arrhythmia. cBIN1 is now also tested by CVRTI investigators as potential gene therapy for chronic heart failure.
With these research programs in place, the CVRTI is committed to improving how acute and chronic heart failure patients are diagnosed and treated.