What we are bringing to you this time is recent advances in heart disease research and we hope it will be useful to you.

 

1. NEJM: Influenza increases the probability of heart attack by 6 times!

 

Jeffrey C. Kwong et al.Acute myocardial infarction after laboratory-confirmed influenza.N Engl J Med 2018; 378:345-353 DOI: 10.1056/NEJMoa1702090 infection

 

 

According to a recent study completed by ICRS and PHO researchers, the probability of a heart attack in the first seven days after laboratory-confirmed influenza infection was increased by six times.

 

“Our research is very important because the relationship between influenza and acute myocardial infarction emphasizes the importance of developing vaccines,” said Jeff Kwong, ICRS and PHO scientist and author of the study.

 

In this study, published in the New England Journal of Medicine, the authors found a strong link between acute myocardial infarction and acute respiratory infections, especially influenza.

 

Among them, elderly people, people with influenza B, and those who have had a heart attack before have a higher risk. Researchers also found that infection with other respiratory viruses also increases this risk, although the risk is not high.

 

“Our findings and previous evidence that influenza vaccines reduce cardiovascular disease morbidity and mortality support an international guide: recommend patients with high-risk of heart disease to receive influenza vaccine,” Kwong said.

 

The researchers observed 20,000 adults who were laboratory confirmed flu in Ontario from 2009 to 2014 and found that 332 patients were hospitalized for a heart attack within one year of infection.

 

“Patients with high risk of heart disease should prevent respiratory infections, especially flu, by injecting vaccines and washing hands frequently,” Kwong said.

 

The researchers also added that patients should have an immediate cardiac assessment after an acute respiratory infection (especially within one week).

 

2. Breakthrough! The Science reports that nanomedicine can treat heart disease!

 

Michele Miragoli et al. Inhalation of peptide-loaded nanoparticles improves heart failure, Science Translational Medicine (2018). DOI: 10.1126/scitranslmed.aan6205

 

 

A team of researchers from Italy and Germany has developed an inhalable nanoparticle for people with heart disease. In their latest study published in Science Translational Medicine, researchers instructed how they developed nanomedicines, how they are used, and how they work in detail.

 

In recent years, nanoparticles have been used to deliver a variety of drugs to various tissues of the body, most of which are administered orally or intravenously, but none of these methods can effectively deliver drugs to the heart. Therefore, researchers have developed respirable nanomedicines that allow them to reach the heart faster and be absorbed by cardiomyocytes, ultimately improving cardiac function.

 

The team used material calcium phosphate, similar to teeth and bones, to prepare nanoparticles that are small enough to enter the heart tissue but large enough to hold the drug. They chose drugs that can repair calcium channels on the surface of heart cells, and repairing calcium channels is thought to restore the most critical part of normal heart activity.

 

After loading the drug on the nanoparticles, mice and rats whose hearts suffered similar damage from diabetic heart disease inhaled these drugs. At the same time, the researchers detected the animals’ heart health. Prior to treatment, these animals had a 17% lower heart health score than normal animals, and scores increased by 15% after treatment, with almost complete recovery.

 

After receiving these encouraging results, the researchers conducted a study on pigs. They wanted to see how fast the nanomedicine could reach the heart tissue. As expected, the enrichment of this drug in heart tissue was better than other drugs.

 

The research team also reported that the drug delivery system does not cause toxicity to heart tissue, but further studies of the toxicity of the drug delivery system are needed before conducting human experiments.

 

3. Nat Med: Explains why exercise is good for the heart and high blood pressure is bad for the heart

 

Lorenz H Lehmann, Zegeye H Jebessa, Michael M Kreusser et al. A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway. Nature Medicine, January 2018, 24:62-72, DOI:10.1038/nm.4452

 

 

It is considered healthy when the heart stress responds caused by exercise, however, it is detrimental to the heart when stress response caused by hypertension. Why? Is this always the case? In a new study, researchers from the cardiovascular research center of German (DZHK) and the Heidelberg University Hospital obtained new discoveries that indicate a previously undetected stress-type dependent signaling pathway cause or stop heart failure. Related research results were published in the January 2018 Nature Medicine.

 

These researchers first studied a series of metabolic processes of histone deacetylase 4 (HDAC4) in the heart with an epigenetic switch. Epigenetics explores how environmental influences regulate genes. This newly discovered signaling pathway being up- or down-regulated depends on the type of stress in the mouse heart. They identified this is because at the end of this signaling pathway, a segment of HDAC4 is more prevalent in the heart of healthy mice after undergoing physiological stress (ie, after exercise). However, the mouse heart did not produce this fragment after suffering pathological stress (for example, permanent stress due to elevated blood pressure).

 

Temporary heart failure

 

These researchers aim to study this phenomenon further and to develop transgenic mice that do not produce this HDAC4 fragment. Surprisingly, when these mice suffer physiological stress, exercise no longer has a healthy effect on them. On the contrary, they suffer from transient heart failure after undergoing intensive exercise, so this intensive exercise leads to a significant decline in their performance. However, this heart failure will disappear after a short period of time.

 

Professor Johannes Backs, head of the Department of Molecular Cardiology and Epigenetics at Heidelberg University, professor of the Cardiovascular Research Center of Germany, said: “We have found a temporary heart fatigue,” according to Dr. Lorenz Lehmann from the Department of Cardiology at Heidelberg University, this syndrome is also found in patients. Lehmann claims that this condition can only be detected during exercise or within a few minutes after exercise.

 

It all depends on rest

 

Therefore, this HDAC4 fragment protects the heart from damage caused by temporary physiological stress. However, why cannot protect the heart from the stress response caused by hypertension or other types of pathological stress? Backs said, “Rest makes everything different.” During exercise, the heart often has a break. An enzyme called protein kinase A recovers during these breaks and then ensures that the healthy pathway activated and the HDAC4 fragment emerges at a critical stage in this series of metabolic processes.

 

On the other hand, during the permanent stress caused by severe hypertension, these signals in cardiac muscle cells are conducted along this newly discovered pathological path: the activity of protein kinase A is eventually significantly weakened under permanent stress. And this HDAC4 fragment disappears. Subsequently, the metabolism of these cardiomyocytes uses sugar molecules more than fat to generate energy. However, it is not the changes in energy that make the heart sick. On the contrary, this is because residual sugar is also attached to the protein. Some sugar-altered proteins eventually inhibit calcium metabolism, thereby inhibiting the contractile function of the heart muscle, which leads to insufficient pumping of the heart.

 

Backs said, “These findings are novel and have changed our thinking about how cardiac myocytes are dysfunctional. We were able to confirm that there is a metabolic link between epigenetics and cardiac contractility.” These researchers also confirmed that using this HDAC4 fragment can protect the mouse from the effect of pumping function lacking. Today, this new therapeutic principle is being thoroughly studied.

 

Extreme endurance sports can lead to heart damage

 

Even from an evolutionary point, this mechanism seems reasonable to these researchers. Our ancestors, who are collectors and hunters, often have to exercise for hours to find food and take it home. In this case, this newly discovered signal pathway may protect the heart. These results also explain why extreme endurance exercise without rest time can lead to heart damage. Backs claimed that “We all intuitively know that rest is important. Now, we may have discovered the molecular causes”.

 

The long-term stress that the heart suffers causes this signaling pathway to change, which may also be the cause of heartbreak syndrome (Takotsubo myocardial cardiomyopathy). In particular, in Takotsubo myocardial cardiomyopathy, transient heart failure is caused by emotion. Today, the researchers are studying this in detail.

 

(to be continued…)

 

Reference

1.Jeffrey C. Kwong et al.Acute myocardial infarction after laboratory-confirmed influenza.N Engl J Med 2018; 378:345-353 DOI: 10.1056/NEJMoa1702090 infection

2.Michele Miragoli et al. Inhalation of peptide-loaded nanoparticles improves heart failure, Science Translational Medicine (2018). DOI: 10.1126/scitranslmed.aan6205

3.Lorenz H Lehmann, Zegeye H Jebessa, Michael M Kreusser et al. A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway. Nature Medicine, January 2018, 24:62-72, DOI:10.1038/nm.4452