The heart’s own immune cells can help it heal

The heart holds its own pool of immune cells capable of helping it heal after injury, according to new research in mice at Washington University School of Medicine in St. Louis.

Most of the time when the heart is injured, these beneficial immune cells are supplanted by immune cells from the bone marrow, which are spurred to converge in the heart and cause inflammation that leads to further damage. In both cases, these immune cells are called macrophages, whether they reside in the heart or arrive from the bone marrow. Although they share a name, where they originate appears to determine whether they are helpful are harmful to an injured heart.

In a mouse model of heart failure, the researchers showed that blocking the bone marrow’s macrophages from entering the heart protects the organ’s beneficial pool of macrophages, allowing them to remain in the heart, where they promote regeneration and recovery. The findings may have implications for treating heart failure in humans.

The study is now available in The Proceedings of the National Academy of Sciences Early Edition.

“Researchers have known for a long time that the neonatal mouse heart can recover well from injury, and in some cases can even regenerate,” said first author Kory J. Lavine, MD, PhD, instructor in medicine. “If you cut off the lower tip of the neonatal mouse heart, it can grow back. But if you do the same thing to an adult mouse heart, it forms scar tissue.”

This disparity in healing capacity was long a mystery because the same immune cells appeared responsible for both repair and damage. Until recently, it was impossible to distinguish the helpful macrophages that reside in the heart from the harmful ones that arrive from the bone marrow.

The new research and past work by the same group – led by Douglas L. Mann, MD, the Tobias and Hortense Lewin Professor of Medicine and cardiologist-in-chief at Barnes-Jewish Hospital – appear to implicate these immune cells of different origins as responsible for the difference in healing capacity seen in neonatal and adult hearts, at least in mice.

“The same macrophages that promote healing after injury in the neonatal heart also are present in the adult heart, but they seem to go away with injury,” Lavine said. “This may explain why the young heart can recover while the adult heart can’t.”

Because they are interested in human heart failure, Lavine and his colleagues developed a method to progressively damage mouse cardiac tissue in a way that mimicked heart failure. They compared the immune response to cardiac damage in neonatal and adult mouse hearts.

The investigators found that the helpful macrophages originate in the embryonic heart and harmful macrophages originate in the bone marrow and could be distinguished by whether they express a protein on their surface called CCR2. Macrophages without CCR2 originate in the heart; those with CCR2 come from the bone marrow, the research showed.

Lavine and his colleagues asked whether a compound that inhibits the CCR2 protein would block the bone marrow’s macrophages from entering the heart.

“When we did that, we found that the macrophages from the bone marrow did not come in,” Lavine said. “And the macrophages native to the heart remained. We saw reduced inflammation in these injured adult hearts, less oxidative damage and improved repair. We also saw new blood vessel growth. By blocking the CCR2 signaling, we were able to keep the resident macrophages around and promote repair.”

Some CCR2 inhibitors are being tested in phase 1 and 2 clinical trials for treating rheumatoid arthritis. But before these drugs can be evaluated in people with heart failure, more work must be done to find out whether the same mechanisms are at work in human hearts, according to the researchers.

“We have identified similar immune cell subtypes that are present in the human heart,” Lavine said. “We need to find out more about their roles in heart failure in patients and understand more about how macrophages that reside in the heart promote repair.”

http://www.medicalnewstoday.com/releases/284750.php

 

 

Heightened risk of anxiety, depression among women after heart attack

A new study by researchers from Lithuania claims women are more likely to experience anxiety and depression following a heart attack than men. Furthermore, patients with depression may be at much higher risk of death in the 6 months after a heart attack than those without depression.

 

Study author Prof. Pranas Serpytis and colleagues presented their findings at the annual meeting of the Acute Cardiovascular Care Association – a part of the European Society of Cardiology – in Geneva, Switzerland.

To reach their findings, the team analyzed 160 patients who were admitted to the Vilnius University Hospital Santariskiu Clinics in Vilnius, Lithuania, with a heart attack.

The researchers interviewed patients around 1 month after their heart attack to gather demographic information, such as age, sex education and marital status, and to determine whether they had a history of mental illness.

The team also collected clinical information from the patients – such as whether they had experienced a heart attack before and whether they had a history of high blood pressure or diabetes – and determined if they had any other risk factors for cardiovascular disease, including smoking and lack of physical activity.

The Hospital Anxiety and Depression Scale (HADS) was used to assess patients. Those who had a score of 0-7 had nodepression or anxiety, a score of 8-10 indicated possible depression and anxiety, while a score of 11 or more suggested mild to moderate levels of depression and anxiety.

The risks of anxiety, depression and death after heart attack

Almost 25% of patients were depressed, the researchers say, and 28.2% of these had used antidepressants.

The team found, however, that women were more likely to be depressed and anxious than men after a heart attack. Men had an average depression score of 6.87, while women’s average score was 8.66. For anxiety, men had an average HADS score of 7.18 and women had an average score of 8.20.

The researchers say that further studies are needed to determine why women appear to be at higher risk of anxiety and depression following a heart attack than men.

Commenting on this finding, Prof. Serpytis says:

“Women are misrepresented in many clinical studies on myocardial infarction (heart attack) even though they often have worse outcomes. Our study shows that women are more likely to develop anxiety and depression after myocardial infarction than men but until now this issue has been largely unnoticed.

Clinicians should assess myocardial infarction patients, particularly women, for anxiety and depression so that timely treatment can be started.”

Earlier this year, Medical News Today reported on a study suggesting the reverse effect – that depressed women are at higher risk of heart attack.

The researchers of this latest study also found that patients with depression following a heart attack were almost six times more likely to die in the 6 months after a heart attack, compared with patients who were not depressed.

“Major depression follows myocardial infarction in approximately 18% of cases and is an important predictor of disability and poor quality of life in the year post-myocardial infarction,” notes Prof. Serpytis.

“The increased risk of death in patients with depression persists up to 18 months after the myocardial infarction. But despite the fact that post-myocardial infarction depression is common and burdensome, the condition remains under-recognised and undertreated.”

Smoking increases anxiety risk, while lack of physical activity linked to depression

Furthermore, the team found an increased risk of anxiety among patients who smoked; the average HADS score for anxiety among smoking patients was 10.16, compared with an average score of 7.3 for patients who had never smoked and 4.55 for patients who stopped smoking more than 2 years before.

No link was found between smoking and depression after a heart attack, the researchers say.

However, a small link was found between lack of physical activity and depression. The 64% of patients who were physically inactive had an average HADS depression score of 8.96.

Commenting on the team’s overall findings, Prof. Serpytis says:

“Our study suggests that encouraging patients to quit smoking and increase their physical activity levels should reduce their risks of anxiety and depression after myocardial infarction. More research is needed on the links between myocardial infarction and mental health problems.”

MNT recently reported on a study by researchers from Duke University Medical Center in Durham, NC, claiming theeffects of mental stress on the heart differ between men and women.

Written by Honor Whiteman

http://www.medicalnewstoday.com/articles/284082.php

 

 

Genetic test reveals risk of atrial fibrillation and stroke

Many of those who are genetically predisposed to develop atrial fibrillation, which dramatically raises the risk of stroke, can be identified with a blood test. This is shown by new research from Lund University in Sweden.

The number of people affected by atrial fibrillation is rising rapidly, partly as a result of the ageing population.

Over recent years, a research group at Lund University in Sweden, working with other universities and hospitals in Europe and the USA, has identified twelve genetic variants in the human genome that increase the risk of atrial fibrillation. The research group has now studied the possible clinical benefits of a DNA test:

“One in five people have a genetic weakness that means they have twice as high a risk of developing atrial fibrillation as those with a low genetic risk. This genetic risk is therefore one of the strongest risk factors for atrial fibrillation that we know of in people without overt cardiac disease. It increases the risk as much as high blood pressure, for example”, said Olle Melander, Professor of Internal Medicine, and Gustav Smith, Associate Professor in Cardiology, both from Lund University.

Since the symptoms of atrial flutter can be weak and unclear, they are sometimes difficult to pick up. However, even those with weak or absent symptoms of atrial flutter are at significantly higher risk of stroke.

“In patients who are suspected of having temporary but recurrent episodes of atrial fibrillation, or in people with high blood pressure, it can be important for doctors to look at their genetic predisposition using a blood test. The test can give guidance as to how often and how intensively doctors need to screen for presence of atrial fibrillation in these individuals. We also consider that more widespread treatment of high blood pressure may be justified in those with a high genetic risk of atrial fibrillation”, explained Professor Melander.

Patients already diagnosed with atrial fibrillation were also studied, and the researchers observed that if they had the risk genes, their risk of stroke was increased by a further 70-80 per cent.

If an individual with atrial fibrillation is regarded as having a sufficiently high stroke risk, lifelong treatment with anticoagulant drugs such as warfarin is required in order to lower the risk.

“There are also benefits of checking the genetic risk of those who have already been diagnosed with atrial fibrillation. The test makes it easier to correctly assess whether anticoagulant medication is necessary to prevent stroke, especially for those under 65”, said Olle Melander.

The research data was taken from a long-term follow-up of 27 400 participants in a population study.

“The present results are one of several examples of how genetics research is not only an effective way of identifying new disease mechanisms, but can also have clinical applications and help doctors and patients to decide on the right tests and treatment”, said Olle Melander.

http://www.medicalnewstoday.com/releases/283463.php