Hi all,
I am making a single thread for each and every medical topic, with news and research corresponding to it.
So this thread shall contain all Cardiology research news.
P.S. Please dont post Cardiology research news anywhere else on the forum.
Most importantly : PLEASE POST A DISCLAIMER BEFORE YOU POST THE NEWS AND A RELEVANT FOOTNOTE AT THE END OF THE ARTICLE. THIS IS A NEW RULE THAT APPLIES TO ALL THE POSTS HERE. A FOOTNOTE MAY CONTAIN YOUR OPINION OR VIEWS OR REFERENCE TO OTHER RELATED NEWS ARTICLES.
And please quote the original source and author.
Sample Disclaimer "This research news has been taken from a reputed news website. It has not been modified or recreated in way, as to preserve the authenticity of it. No Copyright Infringement is intended. This information is posted here for read-only basis. No part of this news is to be reproduced elsewhere, unless due credit is given to the original source and author.
Disclaimer :This research news has been taken from a reputed news website. It has not been modified or recreated in way, as to preserve the authenticity of it. No Copyright Infringement is intended. This information is posted here for read-only basis. No part of this news is to be reproduced elsewhere, unless due credit is given to the original source and author.
Blood Test Predicts Heart Attack Risk
Protein Measurement Linked to Risk for Strokes, Heart Attack, and Heart Failure
By Salynn Boyles
WebMD Medical NewsReviewed by Louise Chang, MDJan. 9, 2007 -- A simple blood test may help doctors identify heart patients who are at high risk for having heart attacks, strokes, and heart failure.
The test, which measures blood levels of a protein called NT-proBNP, was found to be highly predictive of such cardiovascular events in a study involving almost 1,000 heart patients thought to have stable coronary heart disease.
Patients with the highest levels of the protein in their blood were eight times as likely as patients with the lowest levels to die or suffer a heart attack, stroke, or heart failure during the study. Even taking into account other risk factors such as sex, age, smoking, and cholesterol levels, there was still an increased rate of such problems.
Pinpointing Patients at Risk
NT-proBNP was found to independently predict cardiovascular risk, suggesting it can be a useful addition to tests already used in heart disease, like echocardiograms (a sonogram of the heart), stress tests, and other protein biomarkers.
The study is published in the Jan. 10 issue of The Journal of the American Medical Association.
"We have known that this marker was predictive, but the question has been, 'Does it really tell us anything that these other tests don't tell us?'" researcher Kirsten Bibbins-Domingo, MD, PhD, tells WebMD. "We found that it does, and the hope is that it can be used with these tests to help physicians pinpoint which patients have the highest risks."
The blood test is already used in hospital emergency departments to help ER doctors identify heart failure in patients who have shortness of breath and other symptoms of the disease. Heart failure occurs when the heart's ability to pump blood is weakened, which can result in a backup of fluid in the lungs and other areas.
Protein Levels vs. Heart Risk
It has not been clear if the test has value for predicting risk in asymptomatic heart patients thought to have stable heart disease.
In an effort to address this issue, Bibbins-Domingo and colleagues from the University of California, San Francisco and the San Francisco VA Medical Center assessed the association between plasma NT-proBNP levels and cardiovascular risk in [snip] patients followed for an average of 3.7 years.
During this time, roughly a quarter of the patients either died or had a hospitalization from a nonfatal heart attack, stroke, or heart failure event.
The annual event rate among patients with the highest NT-proBNP levels at study entry was 19.6%, compared with just 2.6% among patients with the lowest levels.
There were four times as many heart attack cases reported among patients with the highest levels of the protein compared with those with the lowest, and four times as many strokes.
But the strongest association was seen for heart failure. Eighty cases of heart failure were reported among patients with the highest NT-proBNP levels, compared with just three cases among patients with the lowest levels.
"After adjusting for all other risk factors, it's clear that this marker is picking up something that we are otherwise unable to detect with standard tests such as echocardiography," says study researcher Mary Whooley, MD.
Value Unknown
While there is some suggestion that the test could prove useful for identifying heart risk in the general public, its most immediate use is for patients with established heart disease.
But even among these patients, its role in disease management is not yet clear, cardiologist Robert Bonow, MD, tells WebMD.
Bonow is chief of cardiology at Northwestern University Medical School and a former president of the American Heart Association.
"We aren't sure at this point what to do with this information once we have it," he says. "We can treat these patients [with elevated NT-proBNP] very aggressively, but we should be doing that anyway."
Bonow adds that while NT-proBNP may prove to be a useful test for asymptomatic patients with heart disease, "we don't really know this yet."
In an editorial accompanying the study, Marvin Konstam, MD, of Tufts University School of Medicine agreed that it remains to be seen if NT-proBNP will prove useful for the management of patients with heart disease.
Konstam tells WebMD that more study is needed to determine the value of such testing.
"The real home run will be when we identify a marker and an intervention to go along with it to lower risk," he says. "The best example of this is LDL, or bad, cholesterol. We not only know that LDL cholesterol is a predictor of heart risk, but we know that we can lower that risk with drugs."
Disclaimer :This research news has been taken from a reputed news website. It has not been modified or recreated in way, as to preserve the authenticity of it. No Copyright Infringement is intended. This information is posted here for read-only basis. No part of this news is to be reproduced elsewhere, unless due credit is given to the original source and author.
Moderate Drinking May Lower Risk for Men With High Blood Pressure
By Daniel J. DeNoon
WebMD Medical NewsReviewed by Louise Chang, MDJan. 2, 2007 -- A drink or two a day isn't bad for men with high blood pressure -- and may lower their risk of heart attack, according to new research.
The finding comes from a long-term study of nearly 12,000 male doctors, dentists, and pharmacists with high blood pressure.
Many doctors now warn men with high blood pressure not to drink alcohol, which is known to raise blood pressure.
That recommendation may have to change, say researchers Joline W.J. Beulens, MSc, of the University Medical Center in Utrecht, Netherlands, and colleagues.
Every four years from 1986 to 2002, the men in the Dutch study filled out questionnaires about alcohol use, diet, and health.
Men who drank moderately -- one or two drinks per day -- had a lower risk of heart attack. However, their risk of heart disease and death from any cause was no lower than that of men who did not drink.
"Men with hypertension who drink moderately and safely may not need to change their drinking habits," Beulens and colleagues conclude.
In an editorial accompanying the study, National Cancer Institute researcher Anne C.M. Thiebaut, PhD, and colleagues warn doctors and patients to take the findings with a grain of salt.
Thiebaut and colleagues note that self-report surveys -- particularly those on nutrition -- are notoriously prone to reporting errors. That is, people who actually consume very little of something often overreport their consumption. And those who actually consume a great deal of something often underreport.
This is particularly true of surveys on alcohol use.
"The uncertainties surrounding measurement error should send a strong message to those who formulate recommendations about nutrition," Thiebaut and colleagues suggest. "The discretion of silence may be preferable to the valor of setting recommendations."
The Beulens study and the Thiebaut editorial appear in the January issue of Annals of Internal Medicine.
Main Category: Psychology / Psychiatry
News
Article Date: 05 Aug 2007 - 0:00 PDT
Men who are hostile and prone to frequent intense feelings of anger and depression could be harming their immune systems and putting themselves at risk for coronary heart disease as well as related disorders like type 2 diabetes and high blood pressure, a new study finds.
Steven Boyle, Ph.D., of Duke University Medical Center and colleagues studied 313 male Vietnam veterans who were part of a larger 20-year study on the effects of Agent Orange.
For the study, which appears in the August issue of the journal Brain, Behavior, and Immunity, the veterans underwent a standard psychological test used to assess hostility, depression and anger.
The men had a series of blood levels taken on three occasions between 1992 and 2002. Researchers measured two immune system proteins known as C3 and C4. Both are markers of inflammation, which is the body's response to injury or infection. Changes in C3 and C4 are associated with a number of diseases, including some that negatively can affect the arteries around the heart, such as diabetes.
Men whose psychological screening showed the highest level of hostility, depressive symptoms and anger had a 7.1 percent increase in their C3 levels, while men with low levels of these attributes showed no change over the 10-year study period.
The researchers factored in other risk factors for higher C3 levels such as smoking, age, race, alcohol use and body mass index (a measure of obesity). They also could find no known influence of Agent Orange exposure on the increased C3 levels.
"We showed positives associations between psychological attributes and 10-year changes in C3 among initially healthy middle-aged males," the researchers write. Neither group showed significant increases in C4 levels.
"Hostile, depressed and angry people see the world around them in a different way, and sometimes they see it as them against the world," said study co-author Edward Suarez, Ph.D. "That kind of lifestyle often leads to greater stress and possibly changes in the way the body functions that could lead to disease."
Could psychological treatment reduce C3 levels? "At present, we do not know if interventions to reduce hostility and anger would lead to a decrease in C3 or other markers of inflammation," Boyle said. However, he added, "Even if inflammation is not decreased by such interventions, lower levels of anger and hostility will likely lead to better relationships and increased well-being."
Boyle SH, Jackson WG, Suarez EC. Hostility, anger, and depression predict increases in C3 over a 10-year period. Brain, Behavior, and Immunity, 21(6), 2007.
Health Behavior News Service
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Main Category: Stroke / Neuroprotection News
Article Date: 04 Aug 2007 - 0:00 PDT
According to an article published in the British Medical Journal (BMJ), actively screening elderly people in the community improves detection of atrial fibrillation, which is a major risk factor for stroke. Atrial fibrillation is the chaotic beating of the top chambers (atria) of the heart which can cause a rapid irregular pulse.
About 1% of the general population suffers from atrial fibrillation. However, the prevalence leaps to 5% among the over 65s. An electrocardiography can diagnose it rapidly and at fairly low cost. By treating more atrial fibrillation patients earlier, as a result of screening, it would be possible to cut the number of stroke cases significantly.
There are two ways to screen for atrial fibrillation - Opportunistic and Systematic screening
-- Opportunistic screening means a health care professional (HCP) would check the patient's heartbeat (take his/her pulse) during an unrelated consultation. If anything irregular were detected, an electrocardiography would follow.
-- Systematic screening means targeting a whole population, inviting people for screening by electrocardiography.
In this study the researchers wanted to find out whether Systematic Screening was more effective in detecting atrial fibrillation in the community than Opportunistic Screening.
14,802 patients were identified. They were all aged 65 or more, and were selected from 50 general practices throughout England. These were then divided into 25 intervention and 25 control practices.
In the intervention practices patients were randomly allocated to systematic screening and opportunistic screening. Screening happened over 12 months in each practice, spanning the period October 2001 to February 2003.
Screening practices detected significantly more atrial fibrillation cases than the control practices. Opportunistic and Systematic screenings detected more or less the same number of new cases. Both processes were acceptable to patients and did not raise their anxiety.
The authors say that routine electrocardiography within this population group is not necessary for the detection of atrial fibrillation, as long as the patients' pulse is always taken during a routine or unrelated visit.
Systematic screening cannot be justified for detection of atrial fibrillation, concluded the authors. It is more labor intensive and costly and does not have a better detection rate than opportunistic screening.
Screening versus routine practice in detection of atrial fibrillation in patients aged 65 or over: cluster randomised controlled trial
David A Fitzmaurice, F D Richard Hobbs, Sue Jowett, Jonathon Mant, Ellen T Murray, Roger Holder, J P Raftery, S Bryan, Michael Davies, Gregory Y H Lip, T F Allan
Main Category: Cardiovascular / Cardiology News
Article Date: 01 Aug 2007 - 12:00 PDT
A report led by researchers at Beth Israel Deaconess Medical Center (BIDMC) helps explain the origins of cardiac fibrosis, a stiffening of the heart muscle that leads to a variety of cardiac diseases, most notably heart failure.
The animal study, which appears in the Advance Online Publication of Nature Medicine, also demonstrates that a bone morphogenic molecule known as rhBMP7 can reverse the cardiac fibrosis process, offering the possibility of a therapeutic target for this debilitating condition.
"Heart disease is the number-one cause of death in the Western world," explains the study's lead author Elisabeth Zeisberg, MD, a scientist in the Division of Matrix Biology at BIDMC and an Instructor of Medicine at Harvard Medical School (HMS). "And most people who suffer from heart disease have developed scarring of the heart tissue, known as fibrosis."
Fibrosis develops when the body's natural wound-healing process goes awry. Under normal conditions, specialized cells known as fibroblasts deposit layers of collagen protein to form a scar and thereby enable wounds to heal. However, in abnormal circumstances -- and for unknown reasons -- excessive production of matrix proteins, such as collagen, results in pathological scarring, or fibrosis. In the heart, the buildup of matrix leaves the organ stiff and inflexible, unable to properly relax and function.
"Fibrosis can develop in any organ in the body," explains Zeisberg. "While it's known that fibroblast cells are responsible for cardiac fibrosis, the source of these fibroblasts has remained unknown until now."
Zeisberg and senior author Raghu Kalluri, PhD, Chief of the Division of Matrix Biology at BIDMC, speculated that a specialized form of epithelial-mesenchymal transition (EMT) known as endothelial-mesenchymal transition might be the mechanism behind this turn-of-events.
"Our laboratory has had a longstanding interest in the area of organ fibrosis and the origin of fibroblasts in this setting," explains Kalluri, who is also Associate Professor of Medicine at HMS. "We have previously demonstrated that in the kidney, liver and the lung, epithelial cells under stress can convert into fibroblasts via epithelial-mesenchymal transition."
So, using knockout mice in which endothelial cells had been marked genetically, the investigators confirmed that during cardiac fibrosis, these cells were indeed converting into activated fibroblasts, which were
depositing scar material and impeding the proper function and electrical conduction of the heart.
In the second part of the study, the investigators turned to the rhBMP7 protein to determine if it could successfully reverse the EndMT process and thereby reduce the development of fibroblasts and lead to the improvement of heart function.
"The rhBMP-7 protein was quite impressive in its ability to recover the function of damaged hearts," says Kalluri. "These findings provide compelling proof that the process of fibrosis can be reversed in the heart and offers the possibility of new therapies for patients who have developed cardiac fibrosis as the result of myocardial infarction, hypertension, valvular diseases or heart transplantation."
Millions of Americans take statins to lower their cholesterol, but how low should you go?
Medical Studies/Trials
Published: Tuesday, 24-Jul-2007
Many scientific studies support the benefits of lowering low-density lipoprotein (LDL) cholesterol, and achieving low LDL cholesterol levels is one of the most important steps in preventing heart disease. New research, however, provides evidence for an association between low LDL levels and cancer risk.
The authors of the study, published in the July 31, 2007, issue of the Journal of the American College of Cardiology (JACC), set out to understand how and why statins cause side effects, particularly damage to the liver and muscle cells. The study findings support taking multiple medications rather than high-dose statins to minimize those side effects. The researchers did not expect to find the increased cancer risk (one additional incident per 1,000 patients) from low LDL levels, and additional studies have already begun to investigate this potential risk further. A key component in future studies will be to confirm the risk and to identify whether the risk may be a side effect of statins or just low LDL.
"This analysis doesn't implicate the statin in increasing the risk of cancer," said lead author Richard H. Karas, M.D., F.A.C.C., professor of medicine at Tufts University School of Medicine. "The demonstrated benefits of statins in lowering the risk of heart disease remain clear; however, certain aspects of lowering LDL with statins remain controversial and merit further research."
The researchers found one additional incident of cancer per 1,000 patients with low LDL levels when compared to patients with higher LDL levels. In their evaluation of randomized controlled statin trials published before November 2005, the researchers looked at 13 treatment arms consisting of 41,173 patients.
Researchers assessed absolute change and percentage of change in LDL reduction and the resulting achieved LDL levels in relation to rates of newly diagnosed cancer in each treatment arm. They also looked at the relationship between low, intermediate and high doses of statins and rates of newly diagnosed cancer. Although they did not find a relationship between percent of change and absolute change in LDL levels, they observed higher rates of newly diagnosed cancer among patients with lower achieved LDL levels. In addition, the new cancers were not of any specific type or location.
Recent data from large-scale statin trials have shown that more intensive LDL lowering can provide significant cardiovascular benefits to higher-risk patients. In response to these findings, recent national guidelines have advocated for lower LDL goals and higher doses of statins to reach them. However, informal observations linking intensive LDL lowering and higher incidence of reported health problems, including liver and muscle toxicity and cancer, has introduced some concern over the safety of such treatments.
These concerns in part prompted the current study. However, the current findings are not definitive, as limitations of the study show. Researchers performed their analysis from summary data taken directly from published manuscripts of each trial. An analysis based on data for each individual patient would have yielded more specific and potentially more compelling results, said Dr. Karas.
"These current findings provide insufficient evidence that there is any problem with LDL lowering that outweighs its significant benefits on vascular disease," said John C. La Rosa, M.D., who wrote an accompanying editorial in the July 31 issue of JACC. However, "we must continue to be vigilant in ensuring that its benefit clearly outweighs its risk."
Although the cancer risk was surprising, the researchers primarily sought to determine how and why statins cause side effects, particularly damage to the liver and muscle cells. For this portion of the study, researchers analyzed 23 statin treatment arms that included 75,317 patients with a combined 309,506 years of follow up. A link between LDL lowering and liver or muscle irritation was not found. However, liver toxicity levels increased with higher statin dosage. Based on their findings, the researchers concluded that moderate-dose therapy with multiple medications including statins may prove to be preferable to high-dose therapy with statins alone. Dr. Karas emphasized that patients are advised to continue their statin treatments and, as always, consult their doctor before discontinuing use of any medication.
"While these results raise important new questions about statin use, they do not demonstrate a causal relationship between statins and cancer," said James Dove, M.D., F.A.C.C., president of the American College of Cardiology. "This study is hypothesis-generating, not hypothesis-proving."
The American College of Cardiology is leading the way to optimal cardiovascular care and disease prevention. The College is a 34,000-member nonprofit medical society and bestows the credential Fellow of the American College of Cardiology upon physicians who meet its stringent qualifications. The College is a leader in the formulation of health policy, standards and guidelines, and is a staunch supporter of cardiovascular research. The ACC provides professional education and operates national registries for the measurement and improvement of quality care
Researchers now demonstrate in rats that a sponge-like patch, soaked in a compound called periostin and placed over the injury, can not only get heart cells to begin dividing and making copies of themselves again, but also improves heart function.
Their findings appear in the July 15 online edition of Nature Medicine.
Periostin is a component of the material that surrounds cells and is derived from the skin around bone. Though the mature heart only has tiny amounts, it's abundant during fetal heart development, and increased amounts are also made after skeletal-muscle injury, bone fracture and blood vessel injury, stimulating mature, specialized cells to begin dividing again. Led by Bernhard Kuhn, MD, in the Department of Cardiology at Children's Hospital Boston, the researchers theorized that placing periostin near the site of a myocardial infarction could help restore this growth-friendly environment and get heart tissue to regenerate.
Kuhn and colleagues at Massachusetts General Hospital and the Mount Sinai School of Medicine first stimulated mature, rod-shaped heart muscle cells (known as cardiomyocytes) with periostin in a Petri dish. About 1 percent of the cells entered the mitotic cell cycle - namely, they began dividing and replicating. (One percent seems like a small proportion, but normally the percentage is close to zero.)
"We found a small subpopulation of cells that could, with proper stimulation, re-enter the cell cycle," says Kuhn, who was awarded the Young Investigator's Award for this research by the American College of Cardiology in March. "This finding supports the idea that differentiated cardiomyocytes can proliferate."
Using a small patch fashioned from a sponge-like material called Gelfoam, they then moved to experiments in rats with induced heart attacks. In half the rats, a patch that had been incubated with periostin was placed over the infarct site; the others received Gelfoam only.
Twelve weeks later, the treated patches were still releasing biologically-active periostin. The periostin-treated rats had improved cardiac pumping ability, as indicated by increased ejection fraction and improved ventricular remodeling on echocardiograms, and decreased left-ventricular wall stress on catheterization. They also had less scarring of heart tissue, a reduction in infarct size and a denser network of blood vessels feeding the area. In contrast, the rats receiving Gelfoam alone showed little if any improvement.
At the cellular level, the periostin-treated group had a 100-fold increase in the number of cardiomyocytes entering the cell cycle, and grew, on average, 6 million more cardiomyocytes, far exceeding the number of dying cells. (For perspective, the average rat heart has about 20 million cardiomyocytes overall.)
Kuhn, a pediatric cardiologist, envisions using a sustained-delivery periostin patch not only to treat adults with heart attack, but also to encourage cardiomyocyte proliferation in children with congenital heart disease.
"Many patients with severe congenital heart disease eventually hit a place where the heart isn't pumping adequately," Kuhn says. He envisions inserting the patch via a catheter, directly through the skin or during heart surgery performed for other reasons.
"The most elegant approach would be systemic therapy - finding the most relevant parts of the periostin molecule and giving it by infusion," he says.
Mark Keating, MD, then in Children's Department of Cardiology and now at the Novartis Institute for BioMedical Research, was senior investigator on the study. Last fall, a separate study from Keating's laboratory at Children's showed that a combination of two agents - FGF1 and an inhibitor of the enzyme p38 MAP kinase - also rescued heart function in a rat model.
However, both of these agents have the potential for side effects, whereas periostin appears safe and practical to administer.
The research was funded in part by grants from the National Institutes of Health.
Children's Hospital Boston is home to the world's largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 500 scientists, including eight members of the National Academy of Sciences, 11 members of the Institute of Medicine and 10 members of the Howard Hughes Medical Institute comprise Children's research community. Founded as a 20-bed hospital for children, Children's Hospital Boston today is a 347-bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children's also is the primary pediatric teaching affiliate of Harvard Medical School.
Medical Research News
Published: Thursday, 5-Jul-2007
We've all wondered how a seemingly healthy person can actually be at high risk for heart disease or a heart attack
Now researchers have uncovered a new clue to this mystery. The culprit: myeloperoxidase (MPO), a protein secreted by white blood cells that both signals inflammation and releases a bleach-like substance that damages the cardiovascular system.
Although MPO is intended to kill harmful bacteria, it may instead inflame the body's arteries and cripple protective substances in the blood, according to a study published in the July 10, 2007, issue of the Journal of the American College of Cardiology (JACC). As a result, long before conventional risk factors set off alarms, elevated MPO levels signal that harmful plaque has been building up.
"We were surprised to find that many years before a cardiovascular event actually occurs, MPO is increased," said Matthijs Boekholdt, M.D., Ph.D., a resident in cardiology at Academic Medical Center in Amsterdam, the Netherlands. "This could open up completely new areas of research and diagnosis. As we learn more about these processes, we hope to be able to identify 'vulnerable blood' as a reliable tool for detecting vulnerable patients."
Not only does MPO change low-density-lipoprotein (LDL) cholesterol into a harmful oxidized form that can cause atherosclerosis, the "bleach" produced by MPO damages the arteries directly, causing cell death and erosion of the arterial lining, a process that can create unstable plaques. MPO also hampers the protective effects of high-density-lipoprotein (HDL) cholesterol and reduces the availability of nitric oxide, a natural chemical that relaxes the blood vessels.
Earlier studies in patients with chest pain and heart disease have shown that elevated levels of MPO identify those at highest risk for a heart attack. "The novelty of the present study is that it is the first large-scale study to examine the relationship of MPO to cardiovascular risk in apparently healthy individuals," Dr. Boekholdt said.
For the study Dr. Boekholdt and colleagues recruited healthy people living in Norfolk, United Kingdom, between 1993 and 1997, as part of a larger community-based research program known as the European Prospective Investigation Into Cancer and Nutrition (EPIC). They took baseline blood samples from each participant and froze the samples for future analysis.
After an average of eight years, 1,138 EPIC-Norfolk participants had been admitted to the hospital or died from the effects of coronary artery disease (CAD), including heart attack. The researchers matched these patients with study participants who remained healthy throughout the follow-up period, selecting those of the same gender and similar ages and enrollment times.
The average blood levels of MPO were significantly higher in those who developed heart disease than in those who remained healthy. In fact, when MPO levels were divided into four groups, patients in the highest fourth were 1.49 times as likely as those in the lowest fourth to develop CAD or have a heart attack. When traditional risk factors-blood pressure, LDL and HDL cholesterol levels, body mass index, smoking and diabetes-were taken into account, an MPO level in the highest fourth increased the risk of heart disease by 1.36 times.
Equally important, elevated MPO levels signaled increased risk even in those with acceptable levels of LDL cholesterol, HDL cholesterol or C-reactive protein, a widely acknowledged marker of inflammation.
"MPO levels help to identify individuals at increased risk for CAD when traditional risk screening fails," Dr. Boekholdt said.
The search for blood tests to help identify patients at risk for heart attack is a very important one, said Christopher Cannon, M.D., F.A.C.C., who did not participate in the study and is an associate professor of medicine at Harvard Medical School, Boston, MA. "One fascinating aspect of this study is that this marker of inflammation precedes by nearly a decade the development of clinical coronary disease," he said. "This suggests MPO could be used to catch the disease in a very early stage and help in true prevention of CAD.
"Another interesting aspect of MPO is that it may be a marker for unstable plaque. Even more than the number or severity of coronary plaques, we want to know the risk of plaque rupture, and this evolving new marker may help in that regard. More study is needed, but among the hundreds of markers tested to date, MPO looks like a "keeper" that will one day become part of clinical care," Dr. Cannon said.
Researchers are continuing to assess the value of MPO in different patient groups as well as in relation to other biomarkers, Dr. Boekholdt said. Key questions include whether, and under what circumstances, MPO should be added to the laboratory tests used to screen for cardiovascular disease, and whether blocking MPO could prevent cardiovascular disease.
The EPIC-Norfolk study is supported by program grants from the Medical Research Council UK and Cancer Research UK, with additional support from the European Union, Stroke Association, British Heart Foundation, and the Wellcome Trust. Some of the measurements in this study were supported by Wyeth. One of the study's authors, Stanley L. Hazen, M.D., Ph.D., is named as a co-inventor on pending patents filed by the Cleveland Clinic Foundation relating to the use of myeloperoxidase as a biomarker for cardiovascular disease.
The American College of Cardiology is leading the way to optimal cardiovascular care and disease prevention. The College is a 34,000-member nonprofit medical society and bestows the credential Fellow of the American College of Cardiology upon physicians who meet its stringent qualifications. The College is a leader in the formulation of health policy, standards and guidelines, and is a staunch supporter of cardiovascular research. The ACC provides professional education and operates national registries for the measurement and improvement of quality care. More information about the association is available online at
The American College of Cardiology (ACC) provides these news reports of clinical studies published in the Journal of the American College of Cardiology as a service to physicians, the media, the public and other interested parties. However, statements or opinions expressed in these reports reflect the view of the author(s) and do not represent official policy of the ACC unless stated so.
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