A new technique that stimulates heart muscle cells with low-energy light raises the possibility of a future light-controlled pacemaker, researchers reported in Circulation: Arrhythmia & Electrophysiology, a journal of the American Heart Association.
"Electronic cardiac pacemakers and defibrillators are well established and successful technologies, but they are not without problems, including the breakage of metal leads, limited battery life and interference from strong magnetic fields," said Emilia Entcheva, Ph.D., senior author of the study and associate professor of biomedical engineering at Stony Brook University in Stony Brook, New York. "Eventually, optical stimulation may overcome some of these problems and offer a new way of controlling heart function."
The research is part of a new field called optogenetics that introduces light-sensitive proteins into "excitable" cells, making it possible to control specific activities within cells. Excitable cells can actively generate electrical signals such as nerve cells and muscle cells.
The main appeal of control by light is the unprecedented ability to remotely, without contact, turn on/off a single cell or a cell type, not possible by electrical or other means of stimulation.
Several years ago, investigators discovered that brain cells could be stimulated using light if they were genetically altered to produce a light-sensitive protein called channelrhodopsin 2 (ChR2).
In the new study, researchers created cells expressing the ChR2 protein and coupled them with heart muscle cells from animals, creating heart tissue stimulated by light. They found light-triggered heart muscle contractions and electrical waves were indistinguishable from electrically-triggered waves.
Rather than directly modifying heart cells, the researchers coupled donor cells optimized for light responsiveness with the heart cells. The new technique uses much lower energy than in prior studies and doesn't require the use of viruses or the introduction of genes from other organisms into heart cells. Instead, cells from a person's bone marrow or skin can be cultured and modified to respond to light, reducing the possibility that the immune system will reject the light-sensitive cells.
"Our method of non-viral cell delivery may overcome some hurdles toward potential clinical use by harvesting cells from the patient, making them light-responsive and using them as donor cells in the same patient," Entcheva said.
The approach may someday improve pacemakers and defibrillators. Instead of metal leads, a light-controlled pacemaker would use biocompatible, flexible plastic optic fibers.
In preliminary calculations, a light-based system might require only one-tenth the energy, meaning that a battery could last 50 years rather than five. The more immediate application of the technique will likely be to aid heart research.
"Optical stimulation is a great tool to selectively probe and control different parts of the electrical circuitry of the heart to better understand where the vulnerable sites are or what gives rise to lethal arrhythmias," Entcheva said.
The technique might also be used to test new drugs for possible cardiac side effects.
Co-authors are: Zhiheng Jia, M.S.; Virginijus Valiunas, Ph.D.; Zongju Lu, Ph.D.; Harold Bien, M.D., Ph.D.; Huilin Liu, M.S.; Hong-Zhang Wang, Ph.D.; Barbara Rosati, Ph.D.; Peter R. Brink, Ph.D.; and Ira S. Cohen, M.D., Ph.D. Author disclosures and sources of funding are on the manuscript.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by American Heart Association.
Friday, August 12, 2011
Why the Human Heart Can't Regenerate Itself
Stem cell researchers at UCLA have uncovered for the first time why adult human cardiac myocytes have lost their ability to proliferate, perhaps explaining why the human heart has little regenerative capacity.
The study, done in cell lines and mice, may lead to methods of reprogramming a patient's own cardiac myocytes within the heart itself to create new muscle to repair damage, said Dr. Robb MacLellan, a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and senior author of the study.
Unlike newts and salamanders, human adults cannot spontaneously regrow damaged organs such as the heart. However, recent research suggests that mammals do have the ability to regenerate the heart for a very brief period, about the first week of life. But that ability is quickly lost. But if we had it once, MacLellan said, maybe it is possible to regain that ability.
Published in the Aug. 8 issue of the peer-reviewed Journal of Cell Biology, MacLellan's study suggests it might be possible to turn back the cellular clock to a time when cardiac myocytes had the ability to proliferate and re-grow heart muscle.
"These salamanders and other lower organisms have the ability to de-differentiate cardiac myocytes, or take them back to an earlier, more primitive state, which allows them to re-enter the cell cycle, creating new heart muscle," said MacLellan, who also is an associate professor of cardiology and physiology. "In mammals, we've lost that potential. If we knew how to restore that, or knew the reason why adult myocytes can't do it, we could try to figure out a way to use nature's methods to regenerate the heart."
During human development, cardiac myocytes are made by progenitor stem cells and proliferate to form the heart. Once the heart is formed, the myocytes transform from immature cells into mature cells that cannot proliferate. That's not so for newts and salamanders, whose cardiac myocytes can go back and forth between immature, or primitive, states to proliferate and repair damage and then revert back into mature cells once the damage is repaired.
MacLellan believes the reason adult human cardiac myocytes can't do this is quite simple -- when the myocytes are in a more primitive state, they are not as good at contracting, which is vital for proper heart function. Because humans are much larger than newts and salamanders, we needed more heart contraction to maintain optimum blood pressure and circulation.
"The way we evolved, in order to maintain blood pressure and flow we had to give up the ability to regenerate the heart muscle," MacLellan said. "The up side is we got more efficient cardiac myocytes and better hearts. But it was a trade-off."
MacLellan said that by temporarily knocking down the proteins that block the cell cycle mechanism, it may be possible to get adult cardiac myocytes to re-enter the cell cycle and revert to a state where they can again proliferate. These therapies would need to be reversible so that the effects of the protein manipulation eventually wear off once the damage is repaired. Then myocytes would become mature again and aid in contracting the regenerated heart muscle. MacLellan currently is looking into using nanoparticles to deliver small interfering RNA to the heart to knock out the proteins that are keeping the myocytes mature.
When a heart attack occurs, oxygen is cut off to part of the heart, causing the cardiac myocytes to die and resulting in scar tissue. It's easy to locate the damaged area of the heart, and if a way could be developed to reprogram a patient's own myocytes, the protein manipulation system could be injected into the damaged area, reverting the myocytes to their primitive state and replacing the dead muscle with new, living muscle, MacLellan said.
"People have been talking about the regenerative potential of these lower organisms for a long time and why this does not occur in humans" MacLellan said. "This is the first paper that provided a rationale and mechanism for why this happens."
There has been much talk of using human embryonic stem cells or reprogrammed induced pluripotent stem cells to regenerate the heart. However, it's unknown how much regeneration is possible and how much benefit would come from it.
"From my point of view, this is a potential mechanism to regenerate heart muscle without having to harvest or expand stem cells," MacLellan said. "Each person would be their own source for cells for regeneration."
The five-year study was funded by the National Institutes of Health.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by University of California - Los Angeles Health Sciences, via EurekAlert!, a service of AAAS.
The study, done in cell lines and mice, may lead to methods of reprogramming a patient's own cardiac myocytes within the heart itself to create new muscle to repair damage, said Dr. Robb MacLellan, a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and senior author of the study.
Unlike newts and salamanders, human adults cannot spontaneously regrow damaged organs such as the heart. However, recent research suggests that mammals do have the ability to regenerate the heart for a very brief period, about the first week of life. But that ability is quickly lost. But if we had it once, MacLellan said, maybe it is possible to regain that ability.
Published in the Aug. 8 issue of the peer-reviewed Journal of Cell Biology, MacLellan's study suggests it might be possible to turn back the cellular clock to a time when cardiac myocytes had the ability to proliferate and re-grow heart muscle.
"These salamanders and other lower organisms have the ability to de-differentiate cardiac myocytes, or take them back to an earlier, more primitive state, which allows them to re-enter the cell cycle, creating new heart muscle," said MacLellan, who also is an associate professor of cardiology and physiology. "In mammals, we've lost that potential. If we knew how to restore that, or knew the reason why adult myocytes can't do it, we could try to figure out a way to use nature's methods to regenerate the heart."
During human development, cardiac myocytes are made by progenitor stem cells and proliferate to form the heart. Once the heart is formed, the myocytes transform from immature cells into mature cells that cannot proliferate. That's not so for newts and salamanders, whose cardiac myocytes can go back and forth between immature, or primitive, states to proliferate and repair damage and then revert back into mature cells once the damage is repaired.
MacLellan believes the reason adult human cardiac myocytes can't do this is quite simple -- when the myocytes are in a more primitive state, they are not as good at contracting, which is vital for proper heart function. Because humans are much larger than newts and salamanders, we needed more heart contraction to maintain optimum blood pressure and circulation.
"The way we evolved, in order to maintain blood pressure and flow we had to give up the ability to regenerate the heart muscle," MacLellan said. "The up side is we got more efficient cardiac myocytes and better hearts. But it was a trade-off."
MacLellan said that by temporarily knocking down the proteins that block the cell cycle mechanism, it may be possible to get adult cardiac myocytes to re-enter the cell cycle and revert to a state where they can again proliferate. These therapies would need to be reversible so that the effects of the protein manipulation eventually wear off once the damage is repaired. Then myocytes would become mature again and aid in contracting the regenerated heart muscle. MacLellan currently is looking into using nanoparticles to deliver small interfering RNA to the heart to knock out the proteins that are keeping the myocytes mature.
When a heart attack occurs, oxygen is cut off to part of the heart, causing the cardiac myocytes to die and resulting in scar tissue. It's easy to locate the damaged area of the heart, and if a way could be developed to reprogram a patient's own myocytes, the protein manipulation system could be injected into the damaged area, reverting the myocytes to their primitive state and replacing the dead muscle with new, living muscle, MacLellan said.
"People have been talking about the regenerative potential of these lower organisms for a long time and why this does not occur in humans" MacLellan said. "This is the first paper that provided a rationale and mechanism for why this happens."
There has been much talk of using human embryonic stem cells or reprogrammed induced pluripotent stem cells to regenerate the heart. However, it's unknown how much regeneration is possible and how much benefit would come from it.
"From my point of view, this is a potential mechanism to regenerate heart muscle without having to harvest or expand stem cells," MacLellan said. "Each person would be their own source for cells for regeneration."
The five-year study was funded by the National Institutes of Health.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by University of California - Los Angeles Health Sciences, via EurekAlert!, a service of AAAS.
No Proof Fibrate Drugs Reduce Heart Risk in Diabetes Patients On Statins, Experts Say
Type 2 diabetes patients, who face higher risk of cardiovascular disease, often take a combination of medications designed to lower their LDL or "bad" cholesterol and triglyceride levels while raising their HDL or "good" cholesterol because doctors long have thought that taken together, the drugs offer protection from heart attacks and improve survival.
But in a commentary in the current New England Journal of Medicine, a trio of doctors who served on a recent Food and Drug Administration panel that evaluated the drugs' effectiveness says the commonly prescribed medications have not been proven successful at preventing heart attacks in Type 2 diabetes patients with elevated cholesterol.
The drugs, called fibrates, seek to lower blood triglyceride levels and raise the amount of HDL cholesterol. They often are prescribed to diabetes patients as an add-on to statins, drugs that lower LDL cholesterol. Annual sales in the U.S. for the three fibrates now approved by the FDA -- gemfibrozil (Lopid), fenofibrate (Tricor) and fenofibric acid (Trilipix) -- amount to billions of dollars.
"There have been few studies regarding the clinical outcome efficacy of fibrates," said Sanjay Kaul, MD, a commentary author and director of the Cardiology Fellowship Training Program at the Cedars-Sinai Heart Institute. "Thousands and thousands of Americans take fibrates every day but so far, there are no long-term studies showing that fibrates lower cardiovascular risk or improve survival among diabetes patients who are also on statins."
The commentary calls for more studies. Meantime, the authors suggest that doctors prescribe the statin-fibrate combination only to diabetic patients at high risk for a heart attack and only after optimal control of LDL cholesterol has been achieved with statin treatment.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Cedars-Sinai Medical Center, via EurekAlert!, a service of AAAS.
But in a commentary in the current New England Journal of Medicine, a trio of doctors who served on a recent Food and Drug Administration panel that evaluated the drugs' effectiveness says the commonly prescribed medications have not been proven successful at preventing heart attacks in Type 2 diabetes patients with elevated cholesterol.
The drugs, called fibrates, seek to lower blood triglyceride levels and raise the amount of HDL cholesterol. They often are prescribed to diabetes patients as an add-on to statins, drugs that lower LDL cholesterol. Annual sales in the U.S. for the three fibrates now approved by the FDA -- gemfibrozil (Lopid), fenofibrate (Tricor) and fenofibric acid (Trilipix) -- amount to billions of dollars.
"There have been few studies regarding the clinical outcome efficacy of fibrates," said Sanjay Kaul, MD, a commentary author and director of the Cardiology Fellowship Training Program at the Cedars-Sinai Heart Institute. "Thousands and thousands of Americans take fibrates every day but so far, there are no long-term studies showing that fibrates lower cardiovascular risk or improve survival among diabetes patients who are also on statins."
The commentary calls for more studies. Meantime, the authors suggest that doctors prescribe the statin-fibrate combination only to diabetic patients at high risk for a heart attack and only after optimal control of LDL cholesterol has been achieved with statin treatment.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Cedars-Sinai Medical Center, via EurekAlert!, a service of AAAS.
How Estrogen Could Help Protect Women from Cardiovascular Disease
The sex hormone estrogen could help protect women from cardiovascular disease by keeping the body's immune system in check, new research from Queen Mary, University of London has revealed.
The study has shown that the female sex hormone works on white blood cells to stop them from sticking to the insides of blood vessels, a process which can lead to dangerous blockages.
The results could help explain why cardiovascular disease rates tend to be higher in men and why they soar in women after the menopause.
The researchers compared white blood cells from men and pre-menopausal women blood donors. They found that cells from premenopausal women have much higher levels of protein called annexin-A1 on the surface of their white blood cells.
The scientists also found that annexin-A1 and estrogen levels were strongly linked throughout the menstrual cycle.
White blood cells play a vital role in protecting the body from infections. When they are activated they stick to the walls of blood vessels. This process normally helps the cells to tackle infection but if it happens too much, it can lead to blood vessel damage, which in turn can lead to cardiovascular disease. However, when annexin-A1 is on the surface of these white blood cells, it prevents them from sticking to the blood vessel wall.
The new research shows that estrogen can move annexin-A1 from inside the white blood cell, where it is normally stored, to the surface of the cells, thereby preventing the cells from sticking to blood vessel walls and causing vascular damage. This may have important implications in cardiovascular disease.
Dr Suchita Nadkarni from the William Harvey Research Institute, Queen Mary, University of London, who led the research, said: "We've known for a long time that estrogen protects pre-menopausal women from heart disease, but we don't know exactly why. This study brings us a step closer to understanding how natural estrogen might help protect our blood vessels.
"We've shown a clear relationship between estrogen levels and the behaviour of these white blood cells. Our results suggest that estrogen helps maintain the delicate balance between fighting infections, and protecting arteries from damage that can lead to cardiovascular disease.
"Understanding how the body fights heart disease naturally is vital for developing new treatments."
The study was co-funded by the British Heart Foundation, the Wellcome Trust and the National Institutes of Health Research (NIHR).
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
The study has shown that the female sex hormone works on white blood cells to stop them from sticking to the insides of blood vessels, a process which can lead to dangerous blockages.
The results could help explain why cardiovascular disease rates tend to be higher in men and why they soar in women after the menopause.
The researchers compared white blood cells from men and pre-menopausal women blood donors. They found that cells from premenopausal women have much higher levels of protein called annexin-A1 on the surface of their white blood cells.
The scientists also found that annexin-A1 and estrogen levels were strongly linked throughout the menstrual cycle.
White blood cells play a vital role in protecting the body from infections. When they are activated they stick to the walls of blood vessels. This process normally helps the cells to tackle infection but if it happens too much, it can lead to blood vessel damage, which in turn can lead to cardiovascular disease. However, when annexin-A1 is on the surface of these white blood cells, it prevents them from sticking to the blood vessel wall.
The new research shows that estrogen can move annexin-A1 from inside the white blood cell, where it is normally stored, to the surface of the cells, thereby preventing the cells from sticking to blood vessel walls and causing vascular damage. This may have important implications in cardiovascular disease.
Dr Suchita Nadkarni from the William Harvey Research Institute, Queen Mary, University of London, who led the research, said: "We've known for a long time that estrogen protects pre-menopausal women from heart disease, but we don't know exactly why. This study brings us a step closer to understanding how natural estrogen might help protect our blood vessels.
"We've shown a clear relationship between estrogen levels and the behaviour of these white blood cells. Our results suggest that estrogen helps maintain the delicate balance between fighting infections, and protecting arteries from damage that can lead to cardiovascular disease.
"Understanding how the body fights heart disease naturally is vital for developing new treatments."
The study was co-funded by the British Heart Foundation, the Wellcome Trust and the National Institutes of Health Research (NIHR).
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
Depression Linked to Increased Risk of Stroke in Women
Depressed women may face an increased risk of stroke, according to new research reported in Stroke: Journal of the American Heart Association.
In six years of follow-up of women in the Nurses' Health Study, researchers found that a history of depression was associated with a 29 percent increased risk of total stroke -- even after considering other stroke risk factors. Women who used anti-depressant medication -- particularly selective serotonin reuptake inhibitors -- had a 39 percent increased risk of stroke. Examples of these drugs are Prozac, Zoloft, and Celexa.
Anti-depressant medication use may be an indicator of depression severity, said Kathryn Rexrode, M.D., the study's senior author and Associate Physician at Brigham and Women's Hospital in Boston, Mass. "I don't think the medications themselves are the primary cause of the risk. This study does not suggest that people should stop their medications to reduce the risk of stroke."
Researchers followed 80,574 women 54 to 79 years old in the Nurses' Health Study from 2000-06 without a prior history of stroke. They assessed depressive symptoms multiple times with a Mental Health Index. Anti-depressant use was reported every two years beginning in 1996, and physicians diagnosed depression beginning in 2000.
Depression was defined as currently reporting or having a history of depression.
The reported prevalence of depression at baseline in the women was 22 percent, and 1,033 stroke cases were documented during six years of follow-up.
Compared to women without a history of depression, depressed women were more likely to be single, smokers and less physically active. They were also slightly younger, had a higher body mass index and more coexisting conditions such as high blood pressure, heart disease and diabetes.
"Depression can prevent individuals from controlling other medical problems such as diabetes and hypertension, from taking medications regularly or pursuing other healthy lifestyle measures such as exercise," said Rexrode, who is also Assistant Professor of Medicine at Harvard Medical School. "All these factors could contribute to increased risk."
Depression may be associated with an increased risk of stroke through a variety of mechanisms. It may be linked to inflammation, which increases the risk of stroke as well as other conditions or underlying vascular disease in the brain, said An Pan, Ph.D., lead author of the study and a research scientist at the Harvard School of Public Health. "Regardless of the mechanism, recognizing that depressed individuals may be at a higher risk of stroke may help the physician focus on not only treating the depression, but treating stroke risk factors such as hypertension, diabetes and elevated cholesterol as well as addressing lifestyle behaviors such as smoking and exercise."
Among limitations of the study, the participants were predominantly white registered nurses, it excluded women without detailed information on depression measures and the participants with onset of stroke at a young age.
"We cannot infer cause or fully exclude the possibility that the results could be explained by other unmeasured unknown factors," Pan said. "Although the underlying mechanisms remain unclear, recognizing that depressed women may be at a higher risk of stroke merits additional research into preventive strategies in this group."
Other co-authors are Olivia I. Okereke, M.D.; Qi Sun, M.D., Sc.D.; Giancarlo Logroscino, M.D., Ph.D.; JoAnn E. Manson, M.D.; Walter C.Willett, M.D.; Alberto Ascherio, M.D.; and Frank B. Hu, M.D., Ph.D. Author disclosures are on the manuscript.
The National Institutes of Health/National Heart, Blood, Lung Institute funded the study.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by American Heart Association, via EurekAlert!, a service of AAAS.
In six years of follow-up of women in the Nurses' Health Study, researchers found that a history of depression was associated with a 29 percent increased risk of total stroke -- even after considering other stroke risk factors. Women who used anti-depressant medication -- particularly selective serotonin reuptake inhibitors -- had a 39 percent increased risk of stroke. Examples of these drugs are Prozac, Zoloft, and Celexa.
Anti-depressant medication use may be an indicator of depression severity, said Kathryn Rexrode, M.D., the study's senior author and Associate Physician at Brigham and Women's Hospital in Boston, Mass. "I don't think the medications themselves are the primary cause of the risk. This study does not suggest that people should stop their medications to reduce the risk of stroke."
Researchers followed 80,574 women 54 to 79 years old in the Nurses' Health Study from 2000-06 without a prior history of stroke. They assessed depressive symptoms multiple times with a Mental Health Index. Anti-depressant use was reported every two years beginning in 1996, and physicians diagnosed depression beginning in 2000.
Depression was defined as currently reporting or having a history of depression.
The reported prevalence of depression at baseline in the women was 22 percent, and 1,033 stroke cases were documented during six years of follow-up.
Compared to women without a history of depression, depressed women were more likely to be single, smokers and less physically active. They were also slightly younger, had a higher body mass index and more coexisting conditions such as high blood pressure, heart disease and diabetes.
"Depression can prevent individuals from controlling other medical problems such as diabetes and hypertension, from taking medications regularly or pursuing other healthy lifestyle measures such as exercise," said Rexrode, who is also Assistant Professor of Medicine at Harvard Medical School. "All these factors could contribute to increased risk."
Depression may be associated with an increased risk of stroke through a variety of mechanisms. It may be linked to inflammation, which increases the risk of stroke as well as other conditions or underlying vascular disease in the brain, said An Pan, Ph.D., lead author of the study and a research scientist at the Harvard School of Public Health. "Regardless of the mechanism, recognizing that depressed individuals may be at a higher risk of stroke may help the physician focus on not only treating the depression, but treating stroke risk factors such as hypertension, diabetes and elevated cholesterol as well as addressing lifestyle behaviors such as smoking and exercise."
Among limitations of the study, the participants were predominantly white registered nurses, it excluded women without detailed information on depression measures and the participants with onset of stroke at a young age.
"We cannot infer cause or fully exclude the possibility that the results could be explained by other unmeasured unknown factors," Pan said. "Although the underlying mechanisms remain unclear, recognizing that depressed women may be at a higher risk of stroke merits additional research into preventive strategies in this group."
Other co-authors are Olivia I. Okereke, M.D.; Qi Sun, M.D., Sc.D.; Giancarlo Logroscino, M.D., Ph.D.; JoAnn E. Manson, M.D.; Walter C.Willett, M.D.; Alberto Ascherio, M.D.; and Frank B. Hu, M.D., Ph.D. Author disclosures are on the manuscript.
The National Institutes of Health/National Heart, Blood, Lung Institute funded the study.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by American Heart Association, via EurekAlert!, a service of AAAS.
Lasers Stimulate Stem Cells and Reduce Heart Scarring After Heart Attack, Study Suggests
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 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 percent.
Prof. Oron's innovative method, which was recently reported in the journal Lasers in Surgery and Medicine, is ready for clinical trial.
Sending an SOS signal into the bone marrow
Though the heart is known to contain some stem cells, they have a very limited ability to repair damage caused by a heart attack, says Prof. 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.
Prof. 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.
But he was determined to find a simpler method. After a low-level laser was "shined" into a person's bone marrow -- an area rich in stem cells -- the stem cells took to the blood stream, moving through the body and responding to the heart's signals of distress and harm, Prof. Oron discovered. 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, Prof. 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.
In the longer run, Prof. Oron sees this as a way to make cell therapy simpler. Without the need to remove the stem cells from the body, 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, he notes.
A safe and painless procedure
Although stem cells naturally heed the call to heal throughout the body, says Prof. Oron, their success tends to be limited without this laser treatment. But with treatment, the cells' effectiveness become much more highly enhanced.
"After we stimulate the cells with the laser and enhance their proliferation in the bone marrow, it's likely that more cells will migrate into the bloodstream. The cells that eventually reach the heart secrete growth factors to a higher extent, and new blood vessel formation is encouraged," Prof. Oron theorizes.
Through these animal models, Prof. Oron's non-invasive procedure has been proven safer and quicker than other options. He says that his team, including TAU's Dr. Hana Tuby and Lidya Maltz, has also done a series of safety studies to rule out the possibility that the stimulation of the stem cells by laser could encourage the growth of abnormal tissues. Under the specific and low doses of energy applied in this technique, no such dangers were found.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by American Friends of Tel Aviv University, via EurekAlert!, a service of AAAS.
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 percent.
Prof. Oron's innovative method, which was recently reported in the journal Lasers in Surgery and Medicine, is ready for clinical trial.
Sending an SOS signal into the bone marrow
Though the heart is known to contain some stem cells, they have a very limited ability to repair damage caused by a heart attack, says Prof. 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.
Prof. 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.
But he was determined to find a simpler method. After a low-level laser was "shined" into a person's bone marrow -- an area rich in stem cells -- the stem cells took to the blood stream, moving through the body and responding to the heart's signals of distress and harm, Prof. Oron discovered. 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, Prof. 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.
In the longer run, Prof. Oron sees this as a way to make cell therapy simpler. Without the need to remove the stem cells from the body, 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, he notes.
A safe and painless procedure
Although stem cells naturally heed the call to heal throughout the body, says Prof. Oron, their success tends to be limited without this laser treatment. But with treatment, the cells' effectiveness become much more highly enhanced.
"After we stimulate the cells with the laser and enhance their proliferation in the bone marrow, it's likely that more cells will migrate into the bloodstream. The cells that eventually reach the heart secrete growth factors to a higher extent, and new blood vessel formation is encouraged," Prof. Oron theorizes.
Through these animal models, Prof. Oron's non-invasive procedure has been proven safer and quicker than other options. He says that his team, including TAU's Dr. Hana Tuby and Lidya Maltz, has also done a series of safety studies to rule out the possibility that the stimulation of the stem cells by laser could encourage the growth of abnormal tissues. Under the specific and low doses of energy applied in this technique, no such dangers were found.
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by American Friends of Tel Aviv University, via EurekAlert!, a service of AAAS.
Wednesday, May 18, 2011
Simple Surgical Procedure May Help Prevent Heart Damage in Children
Removing enlarged tonsils and adenoids may help prevent high blood pressure and heart damage in children who suffer from obstructive sleep apnea (OSA), according to a study conducted at Cincinnati Children's Hospital Medical Center. In some children with OSA, adenotonsillectomy can result in significantly lower blood pressure within 24 months of the procedure.
The results were presented at the ATS 2011 International Conference in Denver.
Children with enlarged tonsils and adenoids are particularly prone to developing OSA, said study lead author Lisa Burns, MD, (Pulmonary Fellow at Cincinnati Children's Hospital Medical Center). And, in children and adults, OSA has been linked with elevations in both daytime and nighttime blood pressure. OSA can also interfere with the normal "dip" in blood pressure levels that occur during sleep. Persistent elevations in blood pressure can result in organ damage, including heart damage.
"Our study emphasizes the importance of treating severe sleep apnea in order to prevent persistent elevation in blood pressure and end-organ damage," Dr. Burns said. "We also show that during sleep, diastolic blood pressure, the measurement of your blood pressure when the heart is relaxing, is more sensitive to the effects of sleep apnea than other measures of blood pressure."
Dr. Burns and colleagues evaluated 115 children between the ages of 7 and 13 years, including 28 patients with mild OSA, 27 with severe OSA and 60 healthy controls. The subjects were evaluated for level of OSA using polysomnography, a diagnostic test used to measure breathing during periods of sleep. All OSA subjects had enlarged adenoids and tonsils and underwent adenotonsillectomy. Blood pressure, rest and activity levels, and heart size were measured at the beginning of the study and during follow-up at 12 to 24 months.
At follow-up, researchers found blood pressure levels during sleep decreased following adenotonsillectomy when compared with measurements at baseline. The procedure also restored the normal nighttime "dip" in blood pressure relative to daytime blood pressure, Dr. Burns said.
In addition, in a subset of children with moderate to severe sleep apnea, there was a decrease in heart size after adenotonsillectomy.
Dr. Burns said the results are similar to those obtained from studies of adults with OSA.
"We expected to see changes based on what we know about adults with sleep apnea and its effect on blood pressure," she said. "We know that children with sleep apnea tend to have higher blood pressures than children without sleep apnea, even if these elevations still fall within a normal range. However this is the first study to evaluate how treatment of sleep apnea impacts blood pressure and heart size in a pediatric population who are free from other diseases, which may also contribute to elevations in blood pressure.
Treating OSA in childhood is especially critical, Dr. Burns noted.
"Children who have elevated blood pressure throughout childhood will often go on to develop high blood pressure in adulthood," she said. "Adults with high blood pressure are at risk for other cardiovascular diseases, such as heart attacks, stroke, and heart failure. By identifying and treating elevations in blood pressure at an earlier age through treatment of OSA, we hope to prevent development of cardiovascular disease in childhood and later in life."
Future studies should investigate the mechanisms leading to blood pressure changes with sleep apnea, she added.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Thoracic Society, via EurekAlert!, a service of AAAS.
The results were presented at the ATS 2011 International Conference in Denver.
Children with enlarged tonsils and adenoids are particularly prone to developing OSA, said study lead author Lisa Burns, MD, (Pulmonary Fellow at Cincinnati Children's Hospital Medical Center). And, in children and adults, OSA has been linked with elevations in both daytime and nighttime blood pressure. OSA can also interfere with the normal "dip" in blood pressure levels that occur during sleep. Persistent elevations in blood pressure can result in organ damage, including heart damage.
"Our study emphasizes the importance of treating severe sleep apnea in order to prevent persistent elevation in blood pressure and end-organ damage," Dr. Burns said. "We also show that during sleep, diastolic blood pressure, the measurement of your blood pressure when the heart is relaxing, is more sensitive to the effects of sleep apnea than other measures of blood pressure."
Dr. Burns and colleagues evaluated 115 children between the ages of 7 and 13 years, including 28 patients with mild OSA, 27 with severe OSA and 60 healthy controls. The subjects were evaluated for level of OSA using polysomnography, a diagnostic test used to measure breathing during periods of sleep. All OSA subjects had enlarged adenoids and tonsils and underwent adenotonsillectomy. Blood pressure, rest and activity levels, and heart size were measured at the beginning of the study and during follow-up at 12 to 24 months.
At follow-up, researchers found blood pressure levels during sleep decreased following adenotonsillectomy when compared with measurements at baseline. The procedure also restored the normal nighttime "dip" in blood pressure relative to daytime blood pressure, Dr. Burns said.
In addition, in a subset of children with moderate to severe sleep apnea, there was a decrease in heart size after adenotonsillectomy.
Dr. Burns said the results are similar to those obtained from studies of adults with OSA.
"We expected to see changes based on what we know about adults with sleep apnea and its effect on blood pressure," she said. "We know that children with sleep apnea tend to have higher blood pressures than children without sleep apnea, even if these elevations still fall within a normal range. However this is the first study to evaluate how treatment of sleep apnea impacts blood pressure and heart size in a pediatric population who are free from other diseases, which may also contribute to elevations in blood pressure.
Treating OSA in childhood is especially critical, Dr. Burns noted.
"Children who have elevated blood pressure throughout childhood will often go on to develop high blood pressure in adulthood," she said. "Adults with high blood pressure are at risk for other cardiovascular diseases, such as heart attacks, stroke, and heart failure. By identifying and treating elevations in blood pressure at an earlier age through treatment of OSA, we hope to prevent development of cardiovascular disease in childhood and later in life."
Future studies should investigate the mechanisms leading to blood pressure changes with sleep apnea, she added.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Thoracic Society, via EurekAlert!, a service of AAAS.
Novel Gene Linked to Aging Hearts
Researchers at the University of Ottawa Heart Institute (UOHI) have identified a novel gene in the nucleus of muscle and brain cells that affects heart development and the aging process. Their investigation brings the promise of new treatments for an old, failing heart.
"We know that aging is the greatest predictor of cardiovascular disease and heart failure. So we have been working backward in time, looking at the fetal heart to understand changes in the process as it ages, grows frail and fails," said molecular biologist Patrick Burgon, PhD.
A research team led by Burgon discovered the gene in the cell's nucleus -- the site where hereditary information or DNA is housed -- suggesting that it may control the behavior of other genes important in heart development.
The researchers, who focus on the fetal heart as it grows into an adult heart, named the gene MLIP for Muscle enriched A-type Lamin Interacting Protein. Mutations in the Lamin gene family are associated with muscular dystrophy and other degenerative heart muscle diseases.
Their findings have been reported electronically in the Journal of Biological Chemistry and are scheduled for formal publication in June. Researchers now will investigate how animal models respond when the MLIP gene is removed to gain greater knowledge into its function.
"Greater knowledge of this gene and how it works will help us understand loss of cardiac function. Our research opens up new avenues relevant to the characteristics of cardiac development," said Burgon.
At the Heart Institute, studies to identify complex cardiovascular mechanisms are part of a world-wide effort among a core of leading scientific organizations. The Heart Institute collaborates with an international consortium that has already discovered 13 new genes that increase the risk of coronary artery disease (CAD).
Heart Institute researchers previously identified gene 9p21 -- the first genetic risk factor recognized for heart disease and the first major new cardiovascular risk factor since the discovery of cholesterol. The Institute has also located a variety of other genes influencing diseases such as atrial fibrillation and biological processes such as obesity.
Research by Burgon's group was funded by the Heart institute and Canadian Institutes of Health Research.
Story Source:The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by University of Ottawa Heart Institute.
"We know that aging is the greatest predictor of cardiovascular disease and heart failure. So we have been working backward in time, looking at the fetal heart to understand changes in the process as it ages, grows frail and fails," said molecular biologist Patrick Burgon, PhD.
A research team led by Burgon discovered the gene in the cell's nucleus -- the site where hereditary information or DNA is housed -- suggesting that it may control the behavior of other genes important in heart development.
The researchers, who focus on the fetal heart as it grows into an adult heart, named the gene MLIP for Muscle enriched A-type Lamin Interacting Protein. Mutations in the Lamin gene family are associated with muscular dystrophy and other degenerative heart muscle diseases.
Their findings have been reported electronically in the Journal of Biological Chemistry and are scheduled for formal publication in June. Researchers now will investigate how animal models respond when the MLIP gene is removed to gain greater knowledge into its function.
"Greater knowledge of this gene and how it works will help us understand loss of cardiac function. Our research opens up new avenues relevant to the characteristics of cardiac development," said Burgon.
At the Heart Institute, studies to identify complex cardiovascular mechanisms are part of a world-wide effort among a core of leading scientific organizations. The Heart Institute collaborates with an international consortium that has already discovered 13 new genes that increase the risk of coronary artery disease (CAD).
Heart Institute researchers previously identified gene 9p21 -- the first genetic risk factor recognized for heart disease and the first major new cardiovascular risk factor since the discovery of cholesterol. The Institute has also located a variety of other genes influencing diseases such as atrial fibrillation and biological processes such as obesity.
Research by Burgon's group was funded by the Heart institute and Canadian Institutes of Health Research.
Story Source:The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by University of Ottawa Heart Institute.
Heart Drugs Ineffective in Treating Pulmonary Arterial Hypertension, Study Finds
Despite their beneficial effects in treating heart disease, neither aspirin nor simvastatin appear to offer benefit to patients suffering from pulmonary artery hypertension (PAH), according to a National Institutes of Health (NIH)-funded study conducted at four U.S. medical centers. This was the first NIH-funded randomized clinical trial (RCT) in PAH.
The results of the study were presented at the ATS 2011 International Conference in Denver.
PAH is a progressive, incurable disease characterized by increased blood pressure in the arteries of the lungs, which causes shortness of breath, dizziness and fatigue, and can lead to heart failure and death. PAH can occur on its own or be associated with other conditions, such as connective tissue diseases and congenital heart disease.
Although both aspirin and simvastatin are effective in many types of cardiovascular disease, these drugs have not been well-studied in the treatment of PAH, said Steven Kawut, MD, MS lead author and associate professor of medicine and epidemiology at the University of Pennsylvania School of Medicine. The study was designed to determine if the drugs could be effective in the treatment of patients with PAH.
"Surprisingly, we found no evidence that aspirin or simvastatin had beneficial clinical effects in this population, and the study was terminated early by the National Heart Lung and Blood Institute upon the recommendation of the Data and Safety Monitoring Board (DSMB)," said Dr. Kawut, who is also director of the university's Pulmonary Vascular Disease Program. "The results of this study do not support the routine treatment of PAH with these medications."
Researchers enrolled 65 patients in this placebo-controlled trial and randomized them into four groups: one in which patients received aspirin, one in which patients received simvastatin, one in which patients received both drugs, and one in which patients received neither drug. The main outcome, six-minute walk distance (6MWD) (a measure of how far a person can walk in six minutes), tended to be lower in the group taking simvastatin at six months. Based on these early results, the DSMB recommended stopping the study since there was a low probability of demonstrating a beneficial effect of simvastatin even if the study enrolled the planned number of subjects (92). There was no significant difference in the 6MWD between the group taking aspirin and the group taking placebo.
"Multiple animal studies have suggested that simvastatin would be effective in PAH, and aspirin has biologic effects which would be expected to benefit PAH patients," Dr. Kawut said. "This study demonstrates that federally-funded, investigator-initiated RCTs in PAH and other pulmonary vascular diseases are feasible. The findings show the importance of subjecting traditional cardiovascular therapies and drugs which appear effective in the laboratory to placebo-controlled RCTs in humans before recommending their use."
"Aspirin and simvastatin may be prescribed for usual clinical indications in patients with PAH, but should not be administered specifically to treat PAH," he added.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Thoracic Society, via EurekAlert!, a service of AAAS.
The results of the study were presented at the ATS 2011 International Conference in Denver.
PAH is a progressive, incurable disease characterized by increased blood pressure in the arteries of the lungs, which causes shortness of breath, dizziness and fatigue, and can lead to heart failure and death. PAH can occur on its own or be associated with other conditions, such as connective tissue diseases and congenital heart disease.
Although both aspirin and simvastatin are effective in many types of cardiovascular disease, these drugs have not been well-studied in the treatment of PAH, said Steven Kawut, MD, MS lead author and associate professor of medicine and epidemiology at the University of Pennsylvania School of Medicine. The study was designed to determine if the drugs could be effective in the treatment of patients with PAH.
"Surprisingly, we found no evidence that aspirin or simvastatin had beneficial clinical effects in this population, and the study was terminated early by the National Heart Lung and Blood Institute upon the recommendation of the Data and Safety Monitoring Board (DSMB)," said Dr. Kawut, who is also director of the university's Pulmonary Vascular Disease Program. "The results of this study do not support the routine treatment of PAH with these medications."
Researchers enrolled 65 patients in this placebo-controlled trial and randomized them into four groups: one in which patients received aspirin, one in which patients received simvastatin, one in which patients received both drugs, and one in which patients received neither drug. The main outcome, six-minute walk distance (6MWD) (a measure of how far a person can walk in six minutes), tended to be lower in the group taking simvastatin at six months. Based on these early results, the DSMB recommended stopping the study since there was a low probability of demonstrating a beneficial effect of simvastatin even if the study enrolled the planned number of subjects (92). There was no significant difference in the 6MWD between the group taking aspirin and the group taking placebo.
"Multiple animal studies have suggested that simvastatin would be effective in PAH, and aspirin has biologic effects which would be expected to benefit PAH patients," Dr. Kawut said. "This study demonstrates that federally-funded, investigator-initiated RCTs in PAH and other pulmonary vascular diseases are feasible. The findings show the importance of subjecting traditional cardiovascular therapies and drugs which appear effective in the laboratory to placebo-controlled RCTs in humans before recommending their use."
"Aspirin and simvastatin may be prescribed for usual clinical indications in patients with PAH, but should not be administered specifically to treat PAH," he added.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Thoracic Society, via EurekAlert!, a service of AAAS.
Simple Fitness Test Could Predict Long-Term Risk for Heart Attack, Stroke in Middle-Aged People
If you're middle-aged, the answer could provide a strong predictor of your risk of heart attack or stroke over the next decade or more.
In two separate studies, UT Southwestern Medical Center researchers have found that how fast a middle-age person can run a mile can help predict the risk of dying of heart attack or stroke decades later for men and could be an early indicator of cardiovascular disease for women.
In one recent study in the Journal of the American College of Cardiology, researchers analyzed the heart disease risk of 45-, 55- and 65-year-old men based on their fitness level and traditional risk factors, such as age, systolic blood pressure, diabetes, total cholesterol and smoking habits. The scientists found that low levels of midlife fitness are associated with marked differences in the lifetime risk for cardiovascular disease.
For example, a 55-year-old man who needs 15 minutes to run a mile has a 30 percent lifetime risk of developing heart disease. In contrast, a 55-year-old who can run a mile in eight minutes has a lifetime risk of less than 10 percent.
"Heart disease tends to cluster at older ages, but if you want to prevent it, our research suggests that the prescription for prevention needs to occur earlier -- when a person is in his 40s and 50s," said Dr. Jarett Berry, assistant professor of internal medicine and a corresponding author on both studies.
Researchers in this study found that a higher fitness level lowered the lifetime risk of heart disease even in people with other risk factors.
In a separate study in Circulation, UT Southwestern researchers found that the same treadmill test predicts how likely a person is to die of heart disease or stroke more accurately than assessing the risk using only typical prediction tools such as blood pressure and cholesterol levels.
Heart disease is a leading killer in industrialized nations and the No. 1 killer of women in the U.S. Women younger than 50 are particularly difficult to assess for long-term cardiovascular risk.
"Nearly all women under 50 years of age are at low risk for heart disease," Dr. Berry said. "However, as women get older, their risk increases dramatically. In our study, we found that low levels of fitness were particularly helpful in identifying women at risk for heart disease over the long term."
For decades, scientists have tried to improve their ability to determine which patients are at highest cardiovascular disease risk. Blood-based and imaging techniques have been used to try to improve risk prediction, but fitness has not been examined until now, Dr. Berry said.
For both studies, researchers collected information from thousands of participants who underwent a comprehensive clinical exam and a treadmill exercise test at the Cooper Clinic in Dallas between 1970 and 2006.
In the JACC study, researchers evaluated more than 11,000 men tested before 1990 -- women were excluded because of the low number of participants and cardiovascular death rates -- and found 1,106 who died of heart attack or stroke during the study period. They measured participant fitness levels and traditional risk factors for heart disease. Within each age group, higher levels of fitness were associated with lower levels of traditional risk factors.
For the Circulation study, researchers examined more than 66,000 participants without cardiovascular disease, ages 20 to 90. They were then followed until death or the end of the study period; follow-up lasted up to 36 years. There were 1,621 cardiovascular deaths during the study. The researchers found that by adding fitness to the traditional risk factors, they significantly improved their ability to classify participants' short-term (10 years) and long-term (25 years) risk.
Researchers next will try to extend the JACC investigation parameters to women.
Other UT Southwestern researchers involved in the Circulation study were Dr. Sachin Gupta, a postdoctoral trainee in internal medicine and lead author; Dr. Anand Rohatgi, assistant professor of internal medicine; Colby Ayers, faculty associate in internal medicine; Dr. Amit Khera, assistant professor of internal medicine; Dr. Mark Drazner, professor of internal medicine and medical director of the Heart Failure, Left Ventricular Assist Devices and Cardiac Transplant Program; and Dr. James de Lemos, associate professor of internal medicine. Researchers from the Cooper Clinic in Dallas and Stanford University also participated in the research.
Other UT Southwestern researchers involved in the JACC study were Drs. Susan Lakoski, assistant professor of internal medicine; and Drs. de Lemos, Gupta, Khera and Rohatgi. Researchers from the Cooper Clinic, Stanford and Northwestern universities also participated.
The National Institutes of Health and the American Heart Association funded the studies.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by UT Southwestern Medical Center.
In two separate studies, UT Southwestern Medical Center researchers have found that how fast a middle-age person can run a mile can help predict the risk of dying of heart attack or stroke decades later for men and could be an early indicator of cardiovascular disease for women.
In one recent study in the Journal of the American College of Cardiology, researchers analyzed the heart disease risk of 45-, 55- and 65-year-old men based on their fitness level and traditional risk factors, such as age, systolic blood pressure, diabetes, total cholesterol and smoking habits. The scientists found that low levels of midlife fitness are associated with marked differences in the lifetime risk for cardiovascular disease.
For example, a 55-year-old man who needs 15 minutes to run a mile has a 30 percent lifetime risk of developing heart disease. In contrast, a 55-year-old who can run a mile in eight minutes has a lifetime risk of less than 10 percent.
"Heart disease tends to cluster at older ages, but if you want to prevent it, our research suggests that the prescription for prevention needs to occur earlier -- when a person is in his 40s and 50s," said Dr. Jarett Berry, assistant professor of internal medicine and a corresponding author on both studies.
Researchers in this study found that a higher fitness level lowered the lifetime risk of heart disease even in people with other risk factors.
In a separate study in Circulation, UT Southwestern researchers found that the same treadmill test predicts how likely a person is to die of heart disease or stroke more accurately than assessing the risk using only typical prediction tools such as blood pressure and cholesterol levels.
Heart disease is a leading killer in industrialized nations and the No. 1 killer of women in the U.S. Women younger than 50 are particularly difficult to assess for long-term cardiovascular risk.
"Nearly all women under 50 years of age are at low risk for heart disease," Dr. Berry said. "However, as women get older, their risk increases dramatically. In our study, we found that low levels of fitness were particularly helpful in identifying women at risk for heart disease over the long term."
For decades, scientists have tried to improve their ability to determine which patients are at highest cardiovascular disease risk. Blood-based and imaging techniques have been used to try to improve risk prediction, but fitness has not been examined until now, Dr. Berry said.
For both studies, researchers collected information from thousands of participants who underwent a comprehensive clinical exam and a treadmill exercise test at the Cooper Clinic in Dallas between 1970 and 2006.
In the JACC study, researchers evaluated more than 11,000 men tested before 1990 -- women were excluded because of the low number of participants and cardiovascular death rates -- and found 1,106 who died of heart attack or stroke during the study period. They measured participant fitness levels and traditional risk factors for heart disease. Within each age group, higher levels of fitness were associated with lower levels of traditional risk factors.
For the Circulation study, researchers examined more than 66,000 participants without cardiovascular disease, ages 20 to 90. They were then followed until death or the end of the study period; follow-up lasted up to 36 years. There were 1,621 cardiovascular deaths during the study. The researchers found that by adding fitness to the traditional risk factors, they significantly improved their ability to classify participants' short-term (10 years) and long-term (25 years) risk.
Researchers next will try to extend the JACC investigation parameters to women.
Other UT Southwestern researchers involved in the Circulation study were Dr. Sachin Gupta, a postdoctoral trainee in internal medicine and lead author; Dr. Anand Rohatgi, assistant professor of internal medicine; Colby Ayers, faculty associate in internal medicine; Dr. Amit Khera, assistant professor of internal medicine; Dr. Mark Drazner, professor of internal medicine and medical director of the Heart Failure, Left Ventricular Assist Devices and Cardiac Transplant Program; and Dr. James de Lemos, associate professor of internal medicine. Researchers from the Cooper Clinic in Dallas and Stanford University also participated in the research.
Other UT Southwestern researchers involved in the JACC study were Drs. Susan Lakoski, assistant professor of internal medicine; and Drs. de Lemos, Gupta, Khera and Rohatgi. Researchers from the Cooper Clinic, Stanford and Northwestern universities also participated.
The National Institutes of Health and the American Heart Association funded the studies.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by UT Southwestern Medical Center.
Saturday, May 07, 2011
Increases in Peripheral Arterial Disease Revascularization Correlates With Screening Growth
Peripheral arterial disease (PAD) is an indicator for coronary and carotid arterial disease and carries inherent risks of claudication and amputation. PAD screening has increased dramatically, particularly among cardiologists, while vascular surgery has demonstrated the greatest growth in revascularization procedures treating PAD, according to research being presented at the 2011 American Roentgen Ray Society's annual meeting.
The study was performed at Rhode Island Hospital in Providence, RI. CPT codes were extracted for lower extremity vascular noninvasive physiologic studies and for peripheral arterial stent placement and transluminal angioplasty. Six years of data were examined from the Centers for Medicare and Medicaid Services Physician/Supplier Procedure Summary Master files over an eight year span from 2000 -- 2007.
Regarding non-invasive physiologic testing, cardiology has demonstrated nearly twice the compounded annual growth rate of vascular surgery and radiology. However, in endovascular therapy for PAD, vascular surgery has shown the greatest increase, with compounded growth rates more than twice that of cardiology. In contrast, radiology has experienced a net decline in endovascular PAD therapy.
"There has been a marked increase in volume of non-invasive physiologic testing, particularly within cardiology, a self-referring specialty, and this has been associated with tremendous growth in endovascular therapy for peripheral arterial disease," said Tyler Harris, MD, lead author of the study.
"Prior work has shown the majority of peripheral arterial stenting and angioplasty is performed for patients with intermittent claudication, particularly when performed by cardiologists," said Harris.
"However, non-invasive therapies such as supervised exercise programs have shown equivalent outcomes versus stenting and angioplasty in this population across multiple trials. Additionally, this growth has occurred in the absence of any major advance in the understanding of morbidity and mortality of peripheral arterial disease," he said.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Roentgen Ray Society, via EurekAlert!, a service of AAAS.
The study was performed at Rhode Island Hospital in Providence, RI. CPT codes were extracted for lower extremity vascular noninvasive physiologic studies and for peripheral arterial stent placement and transluminal angioplasty. Six years of data were examined from the Centers for Medicare and Medicaid Services Physician/Supplier Procedure Summary Master files over an eight year span from 2000 -- 2007.
Regarding non-invasive physiologic testing, cardiology has demonstrated nearly twice the compounded annual growth rate of vascular surgery and radiology. However, in endovascular therapy for PAD, vascular surgery has shown the greatest increase, with compounded growth rates more than twice that of cardiology. In contrast, radiology has experienced a net decline in endovascular PAD therapy.
"There has been a marked increase in volume of non-invasive physiologic testing, particularly within cardiology, a self-referring specialty, and this has been associated with tremendous growth in endovascular therapy for peripheral arterial disease," said Tyler Harris, MD, lead author of the study.
"Prior work has shown the majority of peripheral arterial stenting and angioplasty is performed for patients with intermittent claudication, particularly when performed by cardiologists," said Harris.
"However, non-invasive therapies such as supervised exercise programs have shown equivalent outcomes versus stenting and angioplasty in this population across multiple trials. Additionally, this growth has occurred in the absence of any major advance in the understanding of morbidity and mortality of peripheral arterial disease," he said.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by American Roentgen Ray Society, via EurekAlert!, a service of AAAS.
Animal Studies Reveal New Route to Treating Heart Disease
Scientists at Johns Hopkins have shown in laboratory experiments in mice that blocking the action of a signaling protein deep inside the heart's muscle cells blunts the most serious ill effects of high blood pressure on the heart. These include heart muscle enlargement, scar tissue formation and loss of blood vessel growth.
Specifically, the Johns Hopkins team found that their intervention halted transforming growth factor beta (TGF-beta) secretion at a precise location called cell receptor type 2 in cardiac muscle cells. Blocking its action in this cell type forestalled pathways for hypertrophy, fibrosis, and angiogenesis by stopping the unbridled TGF-beta signaling, which is typically observed in heart failure, in all other non-muscle types of cells in blood vessels and fibrous tissue. However, blocking TGF-beta signaling in non-muscle cells did not stop disease progression.
In several dozen different experiments, using genetically altered mice or chemicals to selectively block different TGF-beta pathways, researchers were able to pinpoint where the signaling protein had its greatest impact on heart function and determine how its unimpeded activity promoted heart disease.
"Now that we know about the pivotal and specific bad roles played by TGF-beta in a common form of heart disease, we can try to mimic our lab experiments to develop cell-specific drug therapies that stop the chain reactions in the heart muscle at the TGF-beta type 2 cell receptor location," says senior study investigator and cardiologist, David Kass, M.D. Kass is a professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute.
The Kass team study, to be published in the June edition of the Journal of Clinical Investigation, is believed to show the first evidence of how TGF-beta is stimulated differently by various cell types in the heart and which resulting pathways promote heart failure, the most common kind of heart disease. Nearly 6 million Americans are estimated to have the condition.
Kass says previous research showed TGF-beta played a mixed role in various heart diseases, reducing arterial inflammation in some while harming valve and blood vessel function in others, such as people with Marfan syndrome. Until now, however, no explanation existed as to why any of these differences occurred, which cells controlled the TGF-beta signal, and which enzymes are stimulated as a result.
In the new study, researchers also found that in mice with hypertension-induced disease, blocking TGF-beta type 2 cell receptor stopped activities of another kind of regulating protein, called TGF-beta activated kinase (TAK-1). Its activation appears to play a key role in heart enlargement and in secreting proteins tied to scarring, as well as others tied to blood vessel formation.
Researchers began the study with injections of TGF-beta neutralizing antibodies to see if they could rein in heart-failing TGF-beta signaling. But the disease got worse in mice whose hearts had induced high blood pressure, and TGF-beta signaling persisted inside the muscle cells even though it was suppressed in other cells in the heart. The action of two other kinds of proteins closely tied to TGF-beta was similarly split, with the activity of Smad proteins suppressed only outside muscle cells, while TAK-1 production continued. This led Kass and his team to investigate what was happening differently inside muscle cells.
Subsequent testing in mice selectively bred to lack either one of the two TGF-beta receptors in the muscle cells revealed that blocking only the TGF-beta type 2 cell receptor shut down both Smad and TAK-1 activity, stalling enlargement and scarring. Blocking only the TGF-beta type 1 receptor, however, failed to block TAK-1 activity, and disease-accelerating TGF-beta signaling persisted in non-muscle heart cells.
Researchers plan further tests in animals of chemicals that block TAK-1 as potential treatments for heart failure or other kinds of heart disease.Funding for the study, which took three years to complete, was provided by the National Institutes of Health, with additional support from the American Heart Association, the Japan Heart Foundation, the Peter Belfer Laboratory Foundation, and the Fondation Leducq.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by Johns Hopkins Medical Institutions, via EurekAlert!, a service of AAAS.
Specifically, the Johns Hopkins team found that their intervention halted transforming growth factor beta (TGF-beta) secretion at a precise location called cell receptor type 2 in cardiac muscle cells. Blocking its action in this cell type forestalled pathways for hypertrophy, fibrosis, and angiogenesis by stopping the unbridled TGF-beta signaling, which is typically observed in heart failure, in all other non-muscle types of cells in blood vessels and fibrous tissue. However, blocking TGF-beta signaling in non-muscle cells did not stop disease progression.
In several dozen different experiments, using genetically altered mice or chemicals to selectively block different TGF-beta pathways, researchers were able to pinpoint where the signaling protein had its greatest impact on heart function and determine how its unimpeded activity promoted heart disease.
"Now that we know about the pivotal and specific bad roles played by TGF-beta in a common form of heart disease, we can try to mimic our lab experiments to develop cell-specific drug therapies that stop the chain reactions in the heart muscle at the TGF-beta type 2 cell receptor location," says senior study investigator and cardiologist, David Kass, M.D. Kass is a professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute.
The Kass team study, to be published in the June edition of the Journal of Clinical Investigation, is believed to show the first evidence of how TGF-beta is stimulated differently by various cell types in the heart and which resulting pathways promote heart failure, the most common kind of heart disease. Nearly 6 million Americans are estimated to have the condition.
Kass says previous research showed TGF-beta played a mixed role in various heart diseases, reducing arterial inflammation in some while harming valve and blood vessel function in others, such as people with Marfan syndrome. Until now, however, no explanation existed as to why any of these differences occurred, which cells controlled the TGF-beta signal, and which enzymes are stimulated as a result.
In the new study, researchers also found that in mice with hypertension-induced disease, blocking TGF-beta type 2 cell receptor stopped activities of another kind of regulating protein, called TGF-beta activated kinase (TAK-1). Its activation appears to play a key role in heart enlargement and in secreting proteins tied to scarring, as well as others tied to blood vessel formation.
Researchers began the study with injections of TGF-beta neutralizing antibodies to see if they could rein in heart-failing TGF-beta signaling. But the disease got worse in mice whose hearts had induced high blood pressure, and TGF-beta signaling persisted inside the muscle cells even though it was suppressed in other cells in the heart. The action of two other kinds of proteins closely tied to TGF-beta was similarly split, with the activity of Smad proteins suppressed only outside muscle cells, while TAK-1 production continued. This led Kass and his team to investigate what was happening differently inside muscle cells.
Subsequent testing in mice selectively bred to lack either one of the two TGF-beta receptors in the muscle cells revealed that blocking only the TGF-beta type 2 cell receptor shut down both Smad and TAK-1 activity, stalling enlargement and scarring. Blocking only the TGF-beta type 1 receptor, however, failed to block TAK-1 activity, and disease-accelerating TGF-beta signaling persisted in non-muscle heart cells.
Researchers plan further tests in animals of chemicals that block TAK-1 as potential treatments for heart failure or other kinds of heart disease.Funding for the study, which took three years to complete, was provided by the National Institutes of Health, with additional support from the American Heart Association, the Japan Heart Foundation, the Peter Belfer Laboratory Foundation, and the Fondation Leducq.
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by Johns Hopkins Medical Institutions, via EurekAlert!, a service of AAAS.
Rate of Coronary Artery Bypass Graft Surgeries Decreases Substantially
Between 2001 and 2008, the annual rate of coronary artery bypass graft surgeries performed in the United States decreased by more than 30 percent, but rates of percutaneous coronary interventions (PCI; procedures such as balloon angioplasty or stent placement used to open narrowed coronary arteries) did not change significantly, according to a study in the May 4 issue of JAMA.
"Coronary revascularization, comprising coronary artery bypass graft (CABG) surgery and PCI, is among the most common major medical procedures provided by the U.S. health care system, with more than 1 million procedures performed annually," according to background information in the article. Several innovations in coronary revascularization, such as drug-eluting stents (DES) and minimally invasive CABG surgery have been adopted widely in the past decade, with the promise of improved clinical outcomes compared with older revascularization technologies and techniques. "During this period of technological innovation, new published evidence, and updated guidelines, it is not well known whether or how the volume of coronary revascularization and its constituent types changed in the United States. Substantial changes in the overall volume of revascularizations or the relative use of CABG surgery vs. PCI would have important ramifications on clinical outcomes, health care costs, and the future organization and delivery of hospital-based cardiovascular care."
Andrew J. Epstein, Ph.D., of the Philadelphia Veterans Affairs Medical Center and University of Pennsylvania, Philadelphia, and colleagues conducted a study using a representative national sample of hospitalization claims to estimate trends in the annual volume of coronary revascularization procedures. The study included data on patients undergoing CABG surgery or PCIs between 2001 and 2008 at U.S. hospitals in the Healthcare Cost and Utilization Project's Nationwide Inpatient Sample, which reports inpatient coronary revascularizations. These data were supplemented by Medicare outpatient hospital claims.
The researchers found that there was a 15 percent decrease in the annual rate of coronary revascularizations from 2001-2002 to 2007-2008. There was a substantial decrease in the rate of CABG surgery, with approximately one-third fewer CABG surgeries being performed in 2008 compared with 2001. The annual CABG surgery rate decreased steadily from 1,742 CABG surgeries per million adults per year in 2001-2002 to 1,081 CABG surgeries per million adults per year in 2007-2008, but PCI rates did not significantly change (3,827 PCI per million adults per year in 2001-2002 vs. 3,667 PCI per million adults per year in 2007-2008).
"Between 2001 and 2008, the number of hospitals in the Nationwide Inpatient Sample providing CABG surgery increased by 12 percent, and the number of PCI hospitals increased by 26 percent. The median (midpoint) CABG surgery caseload per hospital decreased by 28 percent and the number of CABG surgery hospitals providing fewer than 100 CABG surgeries per year increased from 23 (11 percent) in 2001 to 62 (26 percent) in 2008," the authors write.
The researchers write that the findings of this study "suggest the possibility that several thousand patients who underwent PCI in 2008 would have undergone CABG surgery had patterns of care not changed markedly between 2001 and 2008. Our data imply a sizeable shift in cardiovascular clinical practice patterns away from surgical treatment toward percutaneous, catheter-based interventions."
"In conclusion, although the total rate of U.S. coronary revascularization decreased modestly between 2001 and 2008, there was a substantial decrease in the CABG surgery rate. Between 2001 and 2008, the rate of PCI did not significantly change; however, there were continual changes in the frequency of stent types used for PCI."
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by JAMA and Archives Journals.
"Coronary revascularization, comprising coronary artery bypass graft (CABG) surgery and PCI, is among the most common major medical procedures provided by the U.S. health care system, with more than 1 million procedures performed annually," according to background information in the article. Several innovations in coronary revascularization, such as drug-eluting stents (DES) and minimally invasive CABG surgery have been adopted widely in the past decade, with the promise of improved clinical outcomes compared with older revascularization technologies and techniques. "During this period of technological innovation, new published evidence, and updated guidelines, it is not well known whether or how the volume of coronary revascularization and its constituent types changed in the United States. Substantial changes in the overall volume of revascularizations or the relative use of CABG surgery vs. PCI would have important ramifications on clinical outcomes, health care costs, and the future organization and delivery of hospital-based cardiovascular care."
Andrew J. Epstein, Ph.D., of the Philadelphia Veterans Affairs Medical Center and University of Pennsylvania, Philadelphia, and colleagues conducted a study using a representative national sample of hospitalization claims to estimate trends in the annual volume of coronary revascularization procedures. The study included data on patients undergoing CABG surgery or PCIs between 2001 and 2008 at U.S. hospitals in the Healthcare Cost and Utilization Project's Nationwide Inpatient Sample, which reports inpatient coronary revascularizations. These data were supplemented by Medicare outpatient hospital claims.
The researchers found that there was a 15 percent decrease in the annual rate of coronary revascularizations from 2001-2002 to 2007-2008. There was a substantial decrease in the rate of CABG surgery, with approximately one-third fewer CABG surgeries being performed in 2008 compared with 2001. The annual CABG surgery rate decreased steadily from 1,742 CABG surgeries per million adults per year in 2001-2002 to 1,081 CABG surgeries per million adults per year in 2007-2008, but PCI rates did not significantly change (3,827 PCI per million adults per year in 2001-2002 vs. 3,667 PCI per million adults per year in 2007-2008).
"Between 2001 and 2008, the number of hospitals in the Nationwide Inpatient Sample providing CABG surgery increased by 12 percent, and the number of PCI hospitals increased by 26 percent. The median (midpoint) CABG surgery caseload per hospital decreased by 28 percent and the number of CABG surgery hospitals providing fewer than 100 CABG surgeries per year increased from 23 (11 percent) in 2001 to 62 (26 percent) in 2008," the authors write.
The researchers write that the findings of this study "suggest the possibility that several thousand patients who underwent PCI in 2008 would have undergone CABG surgery had patterns of care not changed markedly between 2001 and 2008. Our data imply a sizeable shift in cardiovascular clinical practice patterns away from surgical treatment toward percutaneous, catheter-based interventions."
"In conclusion, although the total rate of U.S. coronary revascularization decreased modestly between 2001 and 2008, there was a substantial decrease in the CABG surgery rate. Between 2001 and 2008, the rate of PCI did not significantly change; however, there were continual changes in the frequency of stent types used for PCI."
Story Source: The above story is reprinted (with editorial adaptations by the Heart Smart Advice staff) from materials provided by JAMA and Archives Journals.
'Bad' Cholesterol Not as Bad as People Think, Study Shows
The so-called "bad cholesterol" -- low-density lipoprotein commonly called LDL -- may not be so bad after all, shows a Texas A&M University study that casts new light on the cholesterol debate, particularly among adults who exercise.
Steve Riechman, a researcher in the Department of Health and Kinesiology, says the study reveals that LDL is not the evil Darth Vader of health it has been made out to be in recent years and that new attitudes need to be adopted in regards to the substance. His work, with help from colleagues from the University of Pittsburgh, Kent State University, the Johns Hopkins Weight Management Center and the Northern Ontario School of Medicine, is published in the Journal of Gerontology.
Riechman and colleagues examined 52 adults from ages to 60 to 69 who were in generally good health but not physically active, and none of them were participating in a training program. The study showed that after fairly vigorous workouts, participants who had gained the most muscle mass also had the highest levels of LDL (bad) cholesterol, "a very unexpected result and one that surprised us.
"It shows that you do need a certain amount of LDL to gain more muscle mass. There's no doubt you need both -- the LDL and the HDL -- and the truth is, it (cholesterol) is all good. You simply can't remove all the 'bad' cholesterol from your body without serious problems occurring.
Cholesterol is found in all humans and is a type of fat around the body. A person's total cholesterol level comprises LDL (low-density lipoprotein) and HDL (high-density lipoprotein) cholesterol.
LDL is almost always referred to as the "bad" cholesterol because it tends to build up in the walls of arteries, causing a slowing of the blood flow which often leads to heart disease and heart attacks.
HDL, usually called the "good cholesterol," often helps remove cholesterol from arteries.
"But here is where people tend to get things wrong," Riechman says.
"LDL serves a very useful purpose. It acts as a warning sign that something is wrong and it signals the body to these warning signs. It does its job the way it is supposed to.
"People often say, 'I want to get rid of all my bad (LDL) cholesterol,' but the fact is, if you did so, you would die," the Texas A&M professor adds. "Everyone needs a certain amount of both LDL and HDL in their bodies. We need to change this idea of LDL always being the evil thing -- we all need it, and we need it to do its job."
According to the American Heart Association, about 36 million American adults have high cholesterol levels.
"Our tissues need cholesterol, and LDL delivers it," he notes. "HDL, the good cholesterol, cleans up after the repair is done. And the more LDL you have in your blood, the better you are able to build muscle during resistance training."
Riechman says the study could be helpful in looking at a condition called sarcopenia, which is muscle loss due to aging. Previous studies show muscle is usually lost at a rate of 5 percent per decade after the age of 40, a huge concern since muscle mass is the major determinant of physical strength. After the age of 60, the prevalence of moderate to severe sarcopenia is found in about 65 percent of all men and about 30 percent of all women, and it accounts for more than $18 billion of health care costs in the United States.
"The bottom line is that LDL -- the bad cholesterol -- serves as a reminder that something is wrong and we need to find out what it is," Riechman says.
"It gives us warning signs. Is smoking the problem, is it diet, is it lack of exercise that a person's cholesterol is too high? It plays a very useful role, does the job it was intended to do, and we need to back off by always calling it 'bad' cholesterol because it is not totally bad."
Story Source: The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Texas A&M University.
Steve Riechman, a researcher in the Department of Health and Kinesiology, says the study reveals that LDL is not the evil Darth Vader of health it has been made out to be in recent years and that new attitudes need to be adopted in regards to the substance. His work, with help from colleagues from the University of Pittsburgh, Kent State University, the Johns Hopkins Weight Management Center and the Northern Ontario School of Medicine, is published in the Journal of Gerontology.
Riechman and colleagues examined 52 adults from ages to 60 to 69 who were in generally good health but not physically active, and none of them were participating in a training program. The study showed that after fairly vigorous workouts, participants who had gained the most muscle mass also had the highest levels of LDL (bad) cholesterol, "a very unexpected result and one that surprised us.
"It shows that you do need a certain amount of LDL to gain more muscle mass. There's no doubt you need both -- the LDL and the HDL -- and the truth is, it (cholesterol) is all good. You simply can't remove all the 'bad' cholesterol from your body without serious problems occurring.
Cholesterol is found in all humans and is a type of fat around the body. A person's total cholesterol level comprises LDL (low-density lipoprotein) and HDL (high-density lipoprotein) cholesterol.
LDL is almost always referred to as the "bad" cholesterol because it tends to build up in the walls of arteries, causing a slowing of the blood flow which often leads to heart disease and heart attacks.
HDL, usually called the "good cholesterol," often helps remove cholesterol from arteries.
"But here is where people tend to get things wrong," Riechman says.
"LDL serves a very useful purpose. It acts as a warning sign that something is wrong and it signals the body to these warning signs. It does its job the way it is supposed to.
"People often say, 'I want to get rid of all my bad (LDL) cholesterol,' but the fact is, if you did so, you would die," the Texas A&M professor adds. "Everyone needs a certain amount of both LDL and HDL in their bodies. We need to change this idea of LDL always being the evil thing -- we all need it, and we need it to do its job."
According to the American Heart Association, about 36 million American adults have high cholesterol levels.
"Our tissues need cholesterol, and LDL delivers it," he notes. "HDL, the good cholesterol, cleans up after the repair is done. And the more LDL you have in your blood, the better you are able to build muscle during resistance training."
Riechman says the study could be helpful in looking at a condition called sarcopenia, which is muscle loss due to aging. Previous studies show muscle is usually lost at a rate of 5 percent per decade after the age of 40, a huge concern since muscle mass is the major determinant of physical strength. After the age of 60, the prevalence of moderate to severe sarcopenia is found in about 65 percent of all men and about 30 percent of all women, and it accounts for more than $18 billion of health care costs in the United States.
"The bottom line is that LDL -- the bad cholesterol -- serves as a reminder that something is wrong and we need to find out what it is," Riechman says.
"It gives us warning signs. Is smoking the problem, is it diet, is it lack of exercise that a person's cholesterol is too high? It plays a very useful role, does the job it was intended to do, and we need to back off by always calling it 'bad' cholesterol because it is not totally bad."
Story Source: The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Texas A&M University.
Age Alone Should Be Used to Screen for Heart Attacks and Strokes, Say Experts
Using age alone to identify those at risk of heart disease or stroke could replace current screening methods without diminishing effectiveness, according to a groundbreaking study published in the open access journal PLoS ONE.
Existing screening methods which include measuring cholesterol and blood pressure are expensive and time consuming. The authors of the new study from Barts and The London Medical School say that this finding could save thousands of lives by making it easier for more people to have access to preventive treatment.
The new study compared screening using age alone with screening using age and multiple risk factors, measured via blood tests and medical examination. The authors used existing data to estimate the effects of the two screening approaches on a modelled population of 500,000 people.
Age screening alone using a cut off of 55 years had an 84 per cent detection rate and a 24 per cent false-positive rate. This is equivalent to correctly identifying 84 per cent of all the people in a population who will have a stroke or heart attack, while incorrectly identifying 24 per cent who will not. Current screening methods can achieve the same 84 per cent detection rate with a false-positive rate that is only slightly less -- 21 per cent.
Professor Sir Nicholas Wald is lead author and Director of the Wolfson Institute at Barts and The London School of Medicine and Dentistry, part of Queen Mary, University of London. He said: "This study shows that age screening for future cardiovascular disease is simpler than current assessments, with a similar screening performance and cost effectiveness. It also avoids the need for blood tests and medical examinations.
With age screening all individuals above a specified age would be offered preventive treatment. Everyone would benefit because, for blood pressure and cholesterol, the lower the better. The policy of selecting people above a certain age is, in effect, selecting people at high risk. It recognises that age is by far the most important determinant of that risk with other factors adding little extra prognostic information.
"Prevention is better than measurement," Professor Wald added. "Identifying people at high risk of cardiovascular disease needs to be greatly simplified, enabling people to obtain easy access to preventive treatment from nurses and pharmacists as well as from doctors.
"Offering appropriate preventive treatment to everyone aged 55 and over in England and Wales could prevent over 100,000 heart attacks and strokes every year."
Story Source:
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
Existing screening methods which include measuring cholesterol and blood pressure are expensive and time consuming. The authors of the new study from Barts and The London Medical School say that this finding could save thousands of lives by making it easier for more people to have access to preventive treatment.
The new study compared screening using age alone with screening using age and multiple risk factors, measured via blood tests and medical examination. The authors used existing data to estimate the effects of the two screening approaches on a modelled population of 500,000 people.
Age screening alone using a cut off of 55 years had an 84 per cent detection rate and a 24 per cent false-positive rate. This is equivalent to correctly identifying 84 per cent of all the people in a population who will have a stroke or heart attack, while incorrectly identifying 24 per cent who will not. Current screening methods can achieve the same 84 per cent detection rate with a false-positive rate that is only slightly less -- 21 per cent.
Professor Sir Nicholas Wald is lead author and Director of the Wolfson Institute at Barts and The London School of Medicine and Dentistry, part of Queen Mary, University of London. He said: "This study shows that age screening for future cardiovascular disease is simpler than current assessments, with a similar screening performance and cost effectiveness. It also avoids the need for blood tests and medical examinations.
With age screening all individuals above a specified age would be offered preventive treatment. Everyone would benefit because, for blood pressure and cholesterol, the lower the better. The policy of selecting people above a certain age is, in effect, selecting people at high risk. It recognises that age is by far the most important determinant of that risk with other factors adding little extra prognostic information.
"Prevention is better than measurement," Professor Wald added. "Identifying people at high risk of cardiovascular disease needs to be greatly simplified, enabling people to obtain easy access to preventive treatment from nurses and pharmacists as well as from doctors.
"Offering appropriate preventive treatment to everyone aged 55 and over in England and Wales could prevent over 100,000 heart attacks and strokes every year."
Story Source:
The above story is reprinted (with editorial adaptations by Heart Smart Advice staff) from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
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