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.”

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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.

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Inflammation may be the reason high blood sugar levels damage blood vessels

Inflammation may be the reason high blood sugar levels damage blood vessels, raising the possibility that anti-inflammatory medications might someday be used to lower the risk of blood vessel disease in people with diabetes, according to a study presented at the American Heart Association’s High Blood Pressure Research Scientific Sessions 2014.

“These findings may explain why good blood sugar control is not sufficient to avoid the development of diabetes-induced cardiovascular diseases,” said Carlos F. Sánchez-Ferrer, M.D., Ph.D., study author and professor of pharmacology at the Universidad Autónoma de Madrid, Spain. “We need to find new medications focused on reducing inflammation.”

Using cultured smooth muscle cells from the main human artery (aorta), researchers found:

• In the absence of inflammation, excess glucose in the culture fluid didn’t enter the cells.
• When extra glucose was forced into the cells, no harm was done in the absence of inflammation.
• When the inflammation-stimulating protein interleukin-1 (IL-1) was introduced, more glucose entered the cells.
• With IL-1, the glucose entering the cells was metabolized via chemical pathways that spur escalating inflammation, overwhelming the cells’ ability to counteract it.
• In the presence of the anti-inflammatory drug anakinra, which blocks the activity of IL-1, the deleterious changes didn’t occur.

“We need to reduce the inflammatory environment associated with diabetes,” Sánchez-Ferrer said. “Changes in life-style, such as physical exercise and weight reduction, are important not only because they reduce blood sugar but because they reduce inflammation.”

The researchers plan to test whether the effect is similar in cultured cells from the lining of blood vessels and explore the blood sugar/inflammation connection in animals.

http://www.medicalnewstoday.com/releases/282447.php