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Heart failure: An Important link with cognitive impairment.

Heart failure: An Important link with cognitive impairment.

Heart failure affects more than 64 million people globally. One of the most frequent complications in heart failure patients is cognitive impairment.

Heart failure may cause cognitive decline because, according to Columbia University researchers, there is a little calcium leak inside the brain’s neurons.

Additionally, researchers have created an investigational medication that aims to ‘plug’ the calcium leak and halt the course of heart failure.

Heart failure, an incurable cardiovascular disorder where the heart cannot effectively pump blood throughout the body, affects about 64 million people globally.

Complications include shortness of breath, arrhythmia, and kidney problems. Also, fluid retention in the lungs, belly, feet, and legs is more common in those with heart failure.

Additionally, one frequent complication in persons with heart disease is cognitive impairment.

A little calcium leak inside the brain’s neurons, according to Columbia University researchers, may be the reason heart failure can result in cognitive impairment.

In addition, researchers have created an experimental medication to “plug” the calcium leak and perhaps reduce the development of heart failure.

What is cognitive dysfunction?

Cognitive impairment is also known as mild cognitive impairment. It happens when a person struggles to perform routine tasks that call for mental abilities like memory and thought.

Cognitive disability examples include:

  • forgetfulness
  • missing events on the calendar
  • not knowing how to travel to frequented locations
  • difficulty understanding a talk
  • decision-making challenges
  • failure to follow through on commitments or directions

People who have modest cognitive impairment could also go through emotional changes like despair, anxiety, and rage.

Cognitive impairment can be brought on by a variety of conditions, including infections, prescription drugs, and other diseases.

A increased chance of developing other types of dementia, such as Alzheimer’s disease, exists in those with mild cognitive impairment.

How does brain dysfunction may affect cognition?

The team decided to investigate a potential link between heart failure and cognitive decline. Based on what they already knew about the ryanodine receptor type 2 (RyR2)/intracellular Ca2+ (calcium release channel), Dr. Andrew R. Marks, chair of the Department of Physiology & Cellular Biophysics at Columbia University Vagelos College of Physicians and Surgeons and lead researcher of this study explained.

Both the heart and the brain have the RyR2 channel, thus he said, “I reasoned that since the channel is leaky in the heart due to systemic stress of heart failure it might also be leaky in the brain.”

In heart muscle, there is an encoded protein called RyR2. It contributes to the delivery of that specific mineral to the cardiac muscles as a component of the intracellular calcium channel.

Calcium is essential for both heart and brain function, Dr. Marks noted. “Calcium is required to activate muscle contraction in the heart and for signaling in the brain.”

Testing the theory of the heart-brain relationship

Dr. Marks and his team tested their theory in this study using a mouse model. Researchers discovered that calcium leakage in the brain’s neurons caused cognitive impairment in rats with heart failure.

Scientists also looked at the brains of heart failure victims who had passed away. They looked at those brains and discovered leaky calcium channels, which may have contributed to cognitive impairment in those people.

Since heart failure is progressive, clinicians may want to closely examine their heart failure patients for cognitive impairment and keep track of this, according to Dr. Marks’ research. “The doctors could determine whether their patient’s cognitive impairment is affecting their capacity to comply with medical advice and take their medications.”

Are calcium leaks treatable by doctors?

Dr. Marks and his team discovered throughout the study that an investigational medication called Rycals created by Marks’ group. It could be used to “plug” the calcium leak and possibly delay the onset of heart failure.

Rycals fix the leak in RyR channels and are in clinical trials at the Mayo Clinic and at the AMC in Amsterdam for an inherited form of exercise-induced sudden death,” stated Dr. Marks. In a year or two, depending on the outcome of this experiment, they might be available.

A broad unifying hypothesis?

About this study, Dr. Richard Wright, a cardiologist at Providence Saint John’s Health Centre in Santa Monica, California, who was not involved in the study, remarked.

He applauded the researchers for finally developing a comprehensive, all-encompassing theory of various disease states after years of research.

Dr. Wright said, “People with chronic heart failure are weak and have respiratory problems; this has long been known. As this article noted, they frequently exhibit cognitive impairment in comparison to their classmates.”

Here, Dr. Marks’ team is attempting to develop a unified theory to account for all these many changes that take place in heart failure patients, and I believe they have done so. Dr. Richard Wright stated, “I believe this idea that calcium excess is a unifying mechanism to explain not only the heart’s dysfunction but skeletal muscle dysfunction, diaphragm dysfunction, and as the article’s main thesis, brain dysfunction as well.”

The beginning of a new era is upon us.

Dr. Wright remarked that he was thrilled to learn of a substance created in the lab of the study team that has been demonstrated to favourably effect these alterations.

We are at the beginning of a new era, which I would refer to as the period of designer molecules, he remarked. “We’ve seen it in hypertrophic cardiomyopathy and amyloidosis already, where you can design molecules that change pathologic changes of proteins.”

They have compounds created in their lab to prevent alterations that help prevent calcium excess in neurons, heart cells, and skeletal muscle cells. This could have a significant impact on the results of our research.

Dr. Wright did point out that additional research is still required because the majority of the results in this article came from a mouse model.

Humans are not mice, he continued, so “sometimes we get misled.” However, they’ve done a great job of avoiding that and gone to the bother of using chunks of autopsied brains to support their claim, which I think is quite real.”

Other study limitations include the tiny number of human brains examined by the researchers and the fact that the study’s control group consisted of participants who were significantly younger than those who had suffered from heart failure and cognitive deterioration.


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Can the Hunger hormone help patients with heart failure?

Can the Hunger hormone help patients with heart failure?

A serious condition that affects how properly the heart can pump blood throughout the body is heart failure.

Heart failure is managed with a combination of medicines and lifestyle changes.

In a recent study, individuals with chronic heart failure were examined for the hormone acyl ghrelin.

Its discovery that acyl ghrelin could boost cardiac output may encourage more study into the therapeutic potential of this substance.

When the heart is unable to adequately pump blood throughout the body, heart failure can be hazardous. One area of research is discovering drugs that successfully enhance heart function.

Recently, a study on the use of the peptide hormone acyl ghrelin to increase cardiac output in persons with heart failure was published in the European Heart Journal.

Acyl ghrelin, which increases cardiac output, or the heart’s capacity to pump blood, was found to have no adverse impact on participants’ blood pressure or heart rhythms.

The impact of heart failure

When the heart cannot efficiently pump blood throughout the body, cardiac failure results. Many issues, including fluid retention and weariness, may result from this.

Serious side effects like kidney damage or unexpected cardiac arrest might also result from it. Almost 6 million adults in the US suffer from heart failure. Someone may be at risk of contracting the disorder if certain conditions exist.

For instance, those who have diabetes, high blood pressure, or coronary artery disease are more likely to develop heart failure. Risk can also be increased by lifestyle factors like inactivity or a diet high in salt.

Heart failure must be managed using a multifaceted strategy, frequently involving both medication and lifestyle modifications.

Cardiologist and medical director of the Deborah Heart and Lung Center’s Advanced Heart Failure Department, Dr. Kulpreet Barn, who was not involved in the current study.

More treatment options for heart failure

The authors of this study point out that certain drugs can improve cardiac output and the heart’s ability to contract. The quantity of blood that the heart pumps out is known as cardiac output.

Unfortunately, these drugs might have negative side effects and are frequently only taken temporarily. Ghrelin, a hormone that increases appetite, was tested to see if it might efficiently increase cardiac output. Acyl ghrelin, an active version of ghrelin, was used by the researchers.

The purpose of the study, according to study author Prof. Lars H. Lund of the Department of Medicine at Solna’s Karolinska Institute in Sweden, was “to test whether acyl ghrelin, a novel drug treatment, is safe and effective for patients with heart failure, and to test the mechanism of action in the laboratory.”

No adverse effects from ghrelin

There were roughly thirty individuals in the study who had heart failure and a low ejection fraction; it was a randomised, placebo-controlled, double-blind trial.

The amount of blood the heart pumps to the body with each contraction is measured by ejection fraction. To investigate the underlying mechanisms behind the effects of acyl ghrelin, researchers also examined the impact of the hormone on the heart muscle cells of mice.

Either the treatment group or the placebo group was selected from among the participants. The intervention group was given artificial human acyl ghrelin, while the control group received an intravenous saline infusion as a placebo.

The injections happened throughout a 2-hour period. Cardiac output significantly increased in the intervention group. A 28% increase in cardiac output was observed by researchers without any negative consequences.

Subjects did not experience low blood pressure, rapid heart rate, ischemia, or irregular heart rhythms. Participants from the intervention group continued to experience cardiac function that was higher than their pre-treatment baseline over the 2- to 5-day follow-up period.

Promising findings

The fundamental mechanisms of acyl ghrelin actions have been examined through research on the cardiac muscle cells of mice.

While more research is required, it’s possible that acyl ghrelin doesn’t cause any negative effects since calcium ions aren’t being mobilised. As a prospective therapy for persons with heart failure, acyl ghrelin appears to be promising.

Founder of Manhattan Cardiology and fellow of the American College of Cardiology (FACC) Dr. Robert Segal made the following observation although not participating in the study:

There is a need for additional clinical development because of the clinical benefit of acylated (activated) ghrelin that has been observed. It has always been difficult to treat heart failure caused by a low ejection fraction, but hopefully we can make progress with this terrible condition.

Optimal dose not yet clear

More investigation is necessary because this study has a number of shortcomings. First off, there were not many participants in the study, and there was little time for follow-up. Larger samples and a longer follow-up period may therefore be used in future studies.

Furthermore, there was no necessity for official reporting of adverse events because the inquiry concerned an endogenous peptide hormone rather than a novel chemical or medication. Nonetheless, the individuals were observed by the researchers both before and after the treatment.

The best dose of acyl ghrelin was not found by the researchers in their trial, they say. Also, there were some restrictions on how the researchers could measure cardiac function, and there might have been some variations between the intervention and placebo groups.

Potential conflicts of interest were also reported by some of the study’s authors. To comprehend the underlying mechanism for the enhancements in heart function observed by the researchers, more investigation is also required.

Future clinical trials

The present study “provides a framework for later phase trials with ghrelin-like therapies,” according to Prof. Lund.

Future studies could consist of “a larger clinical trial with extended treatment duration, to test whether this medication may be useful for chronic use,” the author continued.

According to D. R. Barn, this was “a terrific, early-phase study that shows tremendous potential as there are favourable changes to the heart function.”


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