Keeping you up to date in recent developments in cardiology

Tel Aviv researcher uses laser-treated bone marrow stem cells to reduce heart attack scarring . . . After a heart attack or stroke, heart scarring can lead to dangerously paper-thin heart walls and a decreased ability to pump blood through the body. Although the heart is unable to completely heal itself, a new treatment developed at Tel Aviv University (TAU) uses laser-treated bone marrow stem cells to help restore heart function and health. Combining the therapeutic benefits of low-level lasers – a process called shining – and bone marrow stem cells, Prof. Uri Oron of the Department of Zoology at TAU's George S. Wise Faculty of Life Sciences has developed an effective, non-invasive procedure that significantly reduces heart scarring after an ischemic event, in which the heart is injured by a lack of blood supply. When the laser is applied to these cells a few hours after a heart attack, scarring can be reduced by up to 80%. Oron's method, which was recently reported in the journal Lasers in Surgery and Medicine, is ready for clinical trial, TAU says. Though the heart is known to contain some stem cells, they have a very limited ability to repair damage caused by a heart attack, according to Oron, and researchers have had to look elsewhere. One of the first efforts to use stem cells to reduce heart scarring involved harvesting them from the bone marrow and inserting them back into the heart muscle, close to the heart's blood supply, but this had limited success. Oron, who has long used low level lasers to stimulate stem cells to encourage cell survival and the formation of blood vessels after a heart attack, was inspired to test how laser treatments could also work to heal the heart. He and his fellow researchers tried different methods, including treating the heart directly with low level lasers during surgery, and shining harvested stem cells before injecting them back into the body. After a low-level laser was shined into a person's bone marrow the stem cells took to the blood stream, moving through the body and responding to the heart's signals of distress and harm. Once in the heart, the stem cells used their healing qualities to reduce scarring and stimulate the growth of new arteries, leading to a healthier blood flow. To determine the success of this method, Oron performed the therapy on an animal model. Following the flow of bone marrow stem cells through the use of a fluorescent marker, the researchers saw an increase in stem cell population within the heart, specifically in the injured regions of the heart. The test group that received the shining treatment showed a vastly higher concentration of cells in the injured organ than those who had not been treated with the lasers. This treatment stimulates a whole variety of stem cells to help heal the body - a cocktail ultimately more efficient than single-cell type treatments. This could prove to be beneficial to the repair of other human organs such as the kidney or the liver, Oron notes.

Study of tricuspid valves points to causes of leakage . . . A new study into the causes of leakage in one of the heart's most complex valve structures could lead to improved diagnosis and treatment of the condition. An estimated 1.6 million Americans suffer moderate to severe leakage through their tricuspid valve, a complex structure that closes off the heart's right ventricle from the right atrium. Most people have at least some leakage in the valve, but what causes the problem is not well understood. A new study, published online in the journal Circulation, found that either dilating the tricuspid valve opening or displacing the papillary muscles that control its operation can cause the valve to leak. A combination of the two actions can increase the severity of the leakage, which is called tricuspid regurgitation. “We think this is the first in vitro investigation into the mechanics of the tricuspid valve, and that our findings into the mechanisms that cause tricuspid regurgitation could lead to improved diagnosis and treatment,“ said Ajit Yoganathan, Regents professor and Wallace H. Coulter Distinguished Faculty Chair in Biomedical Engineering in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University (both Atlanta). The tricuspid valve consists of three flaps that open to allow blood to flow from the heart's upper right chamber to the ventricle. To close the valve, the flaps re-cover the opening, keeping blood from flowing back into the chamber it just left. When the valve is leaky or doesn't close tightly enough, blood flows backward into the chamber just after the heart contracts. Tricuspid regurgitation has been increasingly recognized as a source of disease in patients with chronic mitral valve regurgitation, but surgical repair of the tricuspid valve alone is recommended only in rare cases. If an individual suffers from severe tricuspid regurgitation, surgeons will sometimes repair the tricuspid valve during a surgery to repair other leaky heart valves. With funding from the American Heart Association (Dallas), Yoganathan and Coulter Department graduate student Erin Spinner conducted experiments with porcine tricuspid valves to determine possible causes of tricuspid regurgitation. The valves were attached to a plate designed to create physiological dilation and then placed inside a right heart simulator. The researchers first investigated the effect of dilating the opening of the tricuspid valves. When the openings stretched to an area 40% larger than their normal size, a hole appeared in the central region of the valve. The hole caused leakage, and increased in size with further dilatation. This finding surprised the researchers because similar studies using the same method had shown that the heart's mitral valve could withstand dilation of 75% before leaking. The research team also investigated the effect of displacing the valve's three papillary muscles, which attach to the valve via threads. Contraction of the papillary muscles opens the valve and relaxation of the muscles closes the valve. The study showed that papillary displacement alone resulted in significant tricuspid leakage.

AF linked to greater risk of dementia, including Alzheimer's . . . The most common kind of chronically irregular heartbeat, atrial fibrillation, is associated with a greater risk of dementia, including Alzheimer's disease. This discovery by scientists at Group Health Research Institute (Seattle) and their collaborators was published online in advance of print on in the Journal of the American Geriatrics Society. “Both atrial fibrillation and dementia increase with age,“ said Sascha Dublin, MD, PhD, a Group Health Research Institute assistant investigator who led the research. “Before our prospective cohort study, we knew that atrial fibrillation can cause stroke, which can lead to dementia. Now we've learned that atrial fibrillation may increase dementia risk in other, more subtle ways as well.“ The results of Dublin's study suggest a relationship between atrial fibrillation and dementia beyond the connection through stroke. The people in the study had a mean age of 74 years when the study began. None had dementia or a history of stroke. At the beginning of the study, 4.3% had atrial fibrillation, and an additional 12.2% developed it during the study. In the course of the study, 18.8% developed some type of dementia. People with atrial fibrillation were more likely to have other cardiovascular risk factors and disease than were those without the condition. So the researchers looked to see if atrial fibrillation increased dementia risk more than just through its association with other kinds of heart disease. Participants were followed for an average of seven years. Over this time, those with atrial fibrillation had a 40% to 50% higher risk of developing dementia of any type, including probable Alzheimer's disease, compared to those without atrial fibrillation. This was true even for people who did not also have a stroke during the follow-up period. The research was part of Adult Changes in Thought (ACT), an ongoing joint project of the Group Health and University of Washington (Seattle) studying risk factors for dementia in older adults. Dublin's study, which ran from 1994 to 2008, followed 3,045 people. The researchers relied on Group Health's advanced electronic data systems to determine whether participants had atrial fibrillation. The cognitive function of all study participants was evaluated every two years with tests and interviews as part of ACT. Patients whose ACT tests indicated possible dementia had additional tests including physical, neurological, and psychological exams, and many also had brain scans. A panel of experts determined the correct diagnosis for patients with cognitive problems. Dublin said an important next step is studying whether any treatments for atrial fibrillation reduce the risk of developing dementia. The researchers also hope their results reach primary care providers, who are often the main doctors caring for people with atrial fibrillation, dementia, or both. “Right now, we think we are protecting our patients' brains as long as they don't have a stroke, but tiny insults over time can add up,“ said Dublin, who is a primary care physician at Group Health. “This paper is a wakeup call, telling us that we need to learn more about how to protect brain function, while continuing to give patients with atrial fibrillation the best possible care.“

– Compiled by Amanda Pedersen, MDD