Health-Medical-Fitness-Diet-zk: Heart

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duminică, 5 august 2012

Molecule Discovered That Converts Stem Cells Into Heart Cells

For years, scientists have been looking for a good source of heart cells that can be used to study cardiac function in the lab, or perhaps even to replace diseased or damaged tissue in heart disease patients. To do this, many are looking to stem cells. Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham), the Human BioMolecular Research Institute, and ChemRegen, Inc. have been searching for molecules that convert stem cells to heart cells for about eight years - and now they've found one. Writing in Cell Stem Cell, the team describes how they sifted through a large collection of drug-like chemicals and uncovered ITD-1, a molecule that can be used to generate unlimited numbers of new heart cells from stem cells.

"Heart disease is the leading cause of death in this country. Because we can't replace lost cardiac muscle, the condition irreversibly leads to a decline in heart function and ultimately death. The only way to effectively replace lost heart muscle cells - called cardiomyocytes - is to transplant the entire heart," said Mark Mercola, Ph.D., director of Sanford-Burnham's Muscle Development and Regeneration Program and senior author of the study. "Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation."

Searching for a needle in a haystack

Stem cells are important because they do two unique things - 1) self-renew, producing more stem cells and 2) differentiate, becoming other, more specialized cell types. To obtain a large number of a certain cell type, such as heart cells, the hard part is figuring out the signals that direct them to become the desired cell type.

Mercola's group has been hunting for heart-inducing signals for 15 years - in embryos and in stem cells. To find a synthetic molecule that might one day lead to a drug therapy to regenerate the heart, they joined forces with a team of medicinal chemists at the Human BioMolecular Research Institute led by John Cashman, Ph.D. With funding from the California Institute for Regenerative Medicine, they used sophisticated robotic technology to methodically test a large collection of drug-like chemicals, looking for that needle in a haystack that, when added to stem cells, results in cardiomyocytes. The winning compound was ITD-1.

Therapeutic applications

There's no shortage of therapeutic possibilities for ITD-1. "This particular molecule could be useful to enhance stem cell differentiation in a damaged heart," explained Erik Willems, Ph.D., postdoctoral researcher in Mercola's lab and first author of the study. "At some point, it could become the basis for a new therapeutic drug for cardiovascular disease - one that would likely limit scar spreading in heart failure and promote new muscle formation."

Mercola, Willems, and Cashman are now working with San Diego biotech company ChemRegen, Inc. to further develop ITD-1 into a drug that one day might be used to treat patients.

More scientific detail

The researchers discovered that ITD-1 blocks a cellular process known as TGF? signaling. TGF? (short for transforming growth factor-?) is a protein produced by one cell type to influence others' behaviors, such as proliferation, scarring, and even stem cell differentiation. TGF? works from outside the cell, binding to a receptor on the surface of a responding cell to initiate an intracellular signaling cascade that causes genes to be switched on or off, ultimately altering cellular behavior - in this case making heart muscle.

ITD-1 triggers degradation of the TGF? receptor, thus inhibiting the whole process. With TGF? signaling turned off, stem cells are set on a course toward cardiogenesis. ITD-1 is the first selective inhibitor of TGF?, meaning that it might also have applications in many other processes controlled by TGF?.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our heart disease section for the latest news on this subject. This research was funded by the California Institute for Regenerative Medicine, the National Heart, Lung, and Blood Institute of the U.S. National Institutes of Health, the Human BioMolecular Research Institute, the American Heart Association, the German Research Foundation, and the T Foundation.
The study was co-authored by Erik Willems, Sanford-Burnham and ChemRegen Inc.; Paul J Bushway and Joaquim Cabral-Teixeira, Sanford-Burnham; Dennis Schade, ChemRegen Inc. and Human BioMolecular Research Institute; Wenqing Cai, Sanford-Burnham; Patrick Reeves, Harvard Medical School; Marion Lanier, ChemRegen Inc. and Human BioMolecular Research Institute; Christopher Walsh, Salk Institute for Biological Studies; Tomas Kirchhausen, Harvard Medical School; Juan Carlos Izpisua Belmonte, Salk Institute for Biological Studies and Center for Regenerative Medicine in Barcelona; John Cashman, ChemRegen Inc. and Human BioMolecular Research Institute; Mark Mercola, Sanford-Burnham and ChemRegen Inc.
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marți, 13 decembrie 2011

Risk Of Death And Stroke In Those With Heart Disease Increased By Herbal Amphetamine

Main Category: Alcohol / Addiction / Illegal Drugs
Also Included In: Stroke; Heart Disease
Article Date: 13 Dec 2011 - 2:00 PST

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Chewing the natural stimulant khat increases the risk of death and stroke in patients with heart disease compared to those who are not users, according to new research in Circulation: Journal of the American Heart Association.

Since ancient times, people in the Arabian Peninsula and East Africa have chewed the fresh leaves of the Catha edulis plant which has effects similar to amphetamines and cocaine. It causes euphoria, hyperactivity, restlessness, loss of appetite and weight loss.

In Yemen, some people have khat picnics, chewing the leaves for as much as three hours, like tobacco chewing. Its use has spread globally throughout Western Europe and into the United States. Seven metric tons of khat travel through Heathrow Airport in England each week, and fresh and dried khat has been seized and confiscated in the United States where it is illegal, researchers said.

In the 2nd Gulf Registry of Acute Coronary Events (Gulf RACE-2) Study, researchers - comparing 1,408 khat chewers to 5,991 people who didn't use khat - found: In the hospital, khat users had a 7.5 percent death rate from heart disease compared to 3.8 percent in those who were not khat users. At one month, the death rate was 15.5 percent among khat users and 6.4 percent for non-khat users. At one year, the death rate was 18.8 percent among khat users compared to 10.8 percent among non-users. For the study, researchers enrolled men and women from 65 hospitals in Saudi Arabia, Bahrain, Yemen, Qatar, United Arab Emirates and Oman.

About 96 percent of the khat users were from Yemen, where khat is legal and socially acceptable, unlike the other countries in the study.

"Global awareness of the negative impact of khat chewing on health and social life is warranted before it becomes endemic," said Jassim Al Suwaidi, M.B., Ch.B., study co-author and Consultant Cardiologist and Director of Cardiovascular Research in the Department of Cardiology and Cardiovascular Surgery at Hamad General Hospital in Doha, Qatar. "This report underscores the importance of improving education about the cardiovascular risks of khat chewing as well as the need for further studies in the field."

Furthermore, researchers found: Khat chewers were more likely to be men (only 14 percent were women) and had lower cardiovascular risk factors such as diabetes mellitus, hypertension and dyslipidemia. Death rates were consistently higher among khat users up to age 80, but khat chewing occurs across the spectrum of young and old, male and female. Users were more likely to experience adverse health effects, including heart failure, recurrent ischemia, a second heart attack, cardiogenic shock and stroke compared to non-users. Women were as likely as men to experience adverse heart effects. Male khat chewers were more likely to develop stroke, particularly hemorrhagic (bleeding) stroke, compared to non-users. The increased risk of stroke wasn't significant among women using khat. The worse in-hospital outcomes may be related to delays in people getting to the hospital after the onset of symptoms and failing to receive thrombolytic (clot-busting) therapy or treatment with beta blockers, researchers said. Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alcohol / addiction / illegal drugs section for the latest news on this subject. Co-authors are: Waleed M. Ali, M.D.; Al Habib KF, M.D.; Ahmed Al Motarreb, M.D.; Rajvir Singh, Ph.D.; Ahmad Hersi, M.D.; Hassam Al Faleh, M.D.; Nidal Asaad, M.M.B.S.; Shukri Al SaiF, M.D.; Wael Almameed, M.D.; Kadhim Sulaiman, M.D.; Haitham Amin, M.D.; Jawad Al-Lawati, M.D.; Nizar Al Bustani, M.D.; Norah Q. Al-Sagheer, M.D.; and Awad Al-Qahtani, M.B.Ch.B.
Author disclosures and sources of funding are on the manuscript.
American Heart Association Please use one of the following formats to cite this article in your essay, paper or report:

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luni, 12 decembrie 2011

ADHD Drugs Do Not Raise Stroke, Heart Attack Or Sudden Cardiac Death Risk

Editor's Choice
Academic Journal
Main Category: ADHD
Also Included In: Cardiovascular / Cardiology; Psychology / Psychiatry
Article Date: 12 Dec 2011 - 11:00 PST

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Young and middle-aged adults who are prescribed ADHD (attention deficit/hyperactivity disorder) drugs do not have a higher chance of developing serious cardiovascular events, such as sudden cardiac death, heart attack or stroke, researchers from Kaiser Permanente Northern California, Oakland, reported in JAMA (Journal of the American Medical Association).

The authors explained that there had been concerns regarding the cardiovascular consequences of taking ADHD medications. This is because they can raise the patient's heart rate and blood pressure.

However, this latest study, involving 150,359 adults with ADHD, found no higher risk of having a cardiovascular event in people taking ADHD medications compared to those who don't. All the adults were young to middle-aged.

The findings of this study are being published ahead of schedule because of their public health importance.

The authors explained:

"Between 2001 and 2010, use of medications labeled for treatment of ADHD increased even more rapidly in adults than in children. According to a 2006 U.S. Food and Drug Administration (FDA) advisory committee briefing on the safety of ADHD medications, more than 1.5 million U.S. adults were taking stimulants in 2005, and adults received approximately 32 percent of all issued prescriptions.
Placebo-controlled studies in children and adults indicate that stimulants and atomoxetine [a medication used to treat ADHD] elevate systolic blood pressure levels by approximately 2 to 5 mm Hg and diastolic blood pressure levels by 1 to 3 mm Hg and also lead to increases in heart rate. Although these effects would be expected to slightly increase risk for myocardial infarction [MI; heart attack], sudden cardiac death (SCD), and stroke, clinical trials have not been large enough to assess risk of these events."

Laurel A. Habel, Ph.D., and team set out to determine whether taking ADHD medications during adulthood might be linked to a higher risk of stroke, heart attack or sudden cardiac death (SCD). They gathered data from four computerized health records at four different sites - the earliest site started in 1986, they all ended in 2005. They also used data from a 2007 survey.

All the study participants were aged from 25 to 64 years, who had been taking various ADHD medications which included amphetamine, atomoxetine, or methylphenidate. They matched each ADHD medication user to two non-users in each study site, by sex, birth date, and calendar year. In total, including users and non-users, the study looked at 443,198 individuals.

They reported a total of 1,357 heart attacks, 296 sudden cardiac deaths, and 575 strokes during follow-up.

After examining the data and analyzing them, they found no statistically significant difference in risk between the users and non-users of ADHD medications for the three serious cardiovascular events.

The researchers wrote:

"We also found little support for an increased risk for any specific medication or with longer duration of current use. Results were similar when users were restricted to new users. Rate ratios did not appear to be influenced by prior cardiovascular disease or by prior non-ADHD psychiatric conditions. They also were similar across age groups.
As expected, event rates were substantially higher in the Medicaid population; however, the rate ratio for current use was similar to that in other sites."

Risk of cardiovascular events were no different for one-off, medium and short term users, during their period of taking their medications and for periods over 12 months after discontinuing. There was a similar or very slightly increased risk in new users compared to non-users.

The authors emphasized that they could not rule out a modest rise in serious cardiovascular events, because of some limitations in the study, which did not have full information on a number of factors which could have influenced the results, as well as other factors associated with ADHD drug usage.

Philip Shaw, M.D., Ph.D., who used to work at the NIMH (National Institute of Mental Health) and is now with the Human Genome Research Institute, said the study's findings have raised a number of clinically important issues:

"First, the findings support the final decision by the FDA in 2006 not to place a black box warning of serious cardiovascular events on ADHD medications for all children and adults but to pursue further research. The findings, however, do not directly inform the current black box warning for psychostimulants, which is confined to patients with structural heart lesions.
The study focused on very rare events, which prevented examination of specific subgroups such as individuals with cardiac disease. Joint care by cardiologists and other physicians remains necessary for these individuals.
In addition, the study provides no evidence to support routine obtaining of electrocardiograms before starting treatment, certainly insofar as this recommendation was driven by concerns about serious cardiovascular events."

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our adhd section for the latest news on this subject. "ADHD Medications and Risk of Serious Cardiovascular Events in Young and Middle-aged Adults"
Laurel A. Habel et al
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duminică, 11 decembrie 2011

Similar Blood Pressure Drugs Could Have Different Impacts On Dialysis Patients' Heart Health

Main Category: Blood / Hematology
Also Included In: Cardiovascular / Cardiology; Hypertension; Urology / Nephrology
Article Date: 11 Dec 2011 - 0:00 PST

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Two seemingly similar blood pressure - lowering drugs have different effects on the heart health of dialysis patients, according to a study appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). The results indicate that certain dialysis patients may benefit more from one drug while some should opt for the other.

About 20% of kidney disease patients die within one year after they start dialysis and more than half die after five years - mostly from heart disease. Two classes of drugs, called angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs), act in a similar way to prevent and treat heart disease in the general population. Studies of the drugs in dialysis patients are scarce.

ACE inhibitors and ARBs primarily lower blood pressure, but they also decrease inflammation and can produce other beneficial effects for patients. T. Alp Ikizler, MD (Vanderbilt University Medical Center) and his colleagues looked to see if there is a difference between ACE inhibitor and ARB treatments on dialysis patients' heart health.

The researchers randomized 15 dialysis patients to receive an ACE inhibitor, an ARB, or a placebo for one week. Then patients received no treatment for three weeks, after which they were again randomized to receive an ACE inhibitor, an ARB, or a placebo for one week. This wash-out/treatment cycle was then conducted once more. Tests were conducted after each treatment cycle.

The investigators found that ARBs were more effective at fighting inflammation while ACE inhibitors were better at preventing blood vessel damage. Both of these properties could help prevent heart disease. The results suggest that ACE inhibitors and ARBs have different effects on dialysis patients' heart health that go beyond their similar blood pressure - lowering capabilities.

"The implication is that the choice of each of the drugs in dialysis patients could depend on the profile of each individual considered for treatment, which would be a more personalized approach to therapy," said Dr. Ikizler. This implies that different dialysis patients might respond to each drug differently and that some would get the most benefit from ACE inhibitors while others would benefit more from ARBs. The findings emphasize the need for a long-term randomized clinical trial to compare the effects of ARBs and ACE inhibitors on different aspects of heart health in dialysis patients.

Study co-authors include Jorge Gamboa MD, Mias Pretorius MD, Deanna Todd-Tzanetos MD, James M. Luther MD, Chang Yu, PhD, and Nancy J. Brown MD (Vanderbilt University Medical Center).

Disclosures: Dr. Ikizler is a consultant to Abbott Renal, Abbott Nutrition, Renal Advantage, Inc., AMGEN, Novartis, Bristol Myers Squibb, and Baxter Renal. Dr. Brown is a consultant for Novartis, Merck, and Boehringer-Ingelheim.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our blood / hematology section for the latest news on this subject. "Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis" online at http://jasn.asnjournals.org/ December 8, 2011, doi: 10.1681/ASN.2011030287.

The content of this article does not reflect the views or opinions of The American Society of Nephrology (ASN). Responsibility for the information and views expressed therein lies entirely with the author(s). ASN does not offer medical advice. All content in ASN publications is for informational purposes only, and is not intended to cover all possible uses, directions, precautions, drug interactions, or adverse effects. This content should not be used during a medical emergency or for the diagnosis or treatment of any medical condition. Please consult your doctor or other qualified health care provider if you have any questions about a medical condition, or before taking any drug, changing your diet or commencing or discontinuing any course of treatment. Do not ignore or delay obtaining professional medical advice because of information accessed through ASN. Call 911 or your doctor for all medical emergencies.

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vineri, 9 decembrie 2011

Similar Blood Pressure Drugs Could Have Different Impacts On Dialysis Patients' Heart Health

Main Category: Heart Disease
Also Included In: Urology / Nephrology
Article Date: 09 Dec 2011 - 2:00 PST

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Two seemingly similar blood pressure lowering drugs have different effects on the heart health of dialysis patients, according to a study appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). The results indicate that certain dialysis patients may benefit more from one drug while some should opt for the other.

About 20% of kidney disease patients die within one year after they start dialysis and more than half die after five years mostly from heart disease. Two classes of drugs, called angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs), act in a similar way to prevent and treat heart disease in the general population. Studies of the drugs in dialysis patients are scarce.

Article adapted by Medical News Today from original press release. Source: American Society of Nephrology
Visit our heart disease section for the latest news on this subject. American Society of Nephrology Please use one of the following formats to cite this article in your essay, paper or report:

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joi, 8 decembrie 2011

Endurance Exercise Linked To Damage In The Right Ventricle Of The Heart

Main Category: Sports Medicine / Fitness
Also Included In: Cardiovascular / Cardiology
Article Date: 08 Dec 2011 - 1:00 PST

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Researchers have found the first evidence that some athletes who take part in extreme endurance exercise such as marathons, endurance triathlons, alpine cycling or ultra triathlons may incur damage to the right ventricles of their hearts - one of the four chambers in the heart involved in pumping blood around the body.

The research, published online in the European Heart Journal [1], found that although the damage was reversed within a week of a competitive event in most of the 40 athletes studied, five of them (13%) showed evidence of more permanent damage, with magnetic resonance imaging (MRI) showing scarring of the heart muscle (known as fibrosis). These five had been competing in endurance sports for longer than those who did not show the same damage.

Dr André La Gerche (MD, PhD), a postdoctoral research fellow at St Vincent's Hospital, University of Melbourne, Australia, but who is currently based at the University Hospitals Leuven, Belgium, said: "It is most important that our findings are not over-extrapolated to infer that endurance exercise is unhealthy. Our data do not support this premise."

However, he said that the findings did suggest that there might be some athletes who might have been born with a susceptibility to develop damage as a result of long-term endurance exercise.

"Virtually all of the changes in the athletes' hearts had resolved one week after having taken part in a competitive event. In most athletes, a combination of sensible training and adequate recovery should cause an improvement in heart muscle function; that is, the heart rebuilds in a manner such that it is more capable of sustaining a similar exercise stimulus in the future. This positive training response can be over months rather than weeks," he explained. "The question from our research is whether there are some athletes in whom extreme exercise may cause injury from which the heart does not recover completely. If this occurs, affected athletes may be at risk of reduced performance - a cardiac 'over-training' syndrome - or it may cause arrhythmias. If this occurs, it is likely to affect only a minority of athletes, particularly those in whom more intense training fails to result in further improvements in their performance."

Dr La Gerche and his colleagues in Australia and Belgium recruited 40 elite athletes in Australia who were planning to compete in one of the four endurance events [2]. The athletes were already well trained (training intensely for more than 10 hours a week), performing well (having finished within the first 25% of the field in a recent event), and had no known heart problems.

The researchers studied the athletes, using echocardiography, MRI, and blood tests, at three time points: two to three weeks prior to the race, immediately after the race (within one hour), and 6-11 days after the race.

Results showed that immediately after the race the athletes' hearts had changed shape, with the volume increasing, while the function of the ventricle decreased. Levels of a chemical called B-type natriuretic peptide (BNP), which is secreted by the ventricles in response to excessive stretching of heart muscle cells, increased. Right ventricle function recovered in most athletes after one week, but in the five who had been training and competing for longer than the others, MRI detected signs of scarring (fibrosis). The researchers also found that the post-race changes to the function of the right ventricle increased with the duration of the race.

In contrast, the left ventricle, which, up to now has been the most studied in athletes, showed no changes.

Dr La Gerche said: "Our study identifies the right ventricle as being most susceptible to exercise-induced injury and suggest that the right ventricle should be a focus of attention as we try to determine the clinical significance of these results. Large, prospective, multi-centre trials are required to elucidate whether extreme exercise may promote arrhythmias in some athletes. To draw an analogy, some tennis players develop tennis elbow. This does not mean that tennis is bad for you; rather it identifies an area of susceptibility on which to focus treatment and preventative measures."

He concluded: "It is important to note that this is one component of an evolving understanding of how the right ventricle is the 'Achilles heel' of heart function during exercise. We previously studied heart function during intense exercise and demonstrated that the load on the right ventricle (stress, work and oxygen demand) increases to a greater extent than in any of the other heart chambers. Professor Hein Heidbuchel, who I work with, has shown that the source of ventricular arrhythmias in affected athletes is almost always the right ventricle. Finally, it has been shown that intense exercise in rats causes inflammation, fibrosis and arrhythmias in the right but not the left ventricle. Hence, there are consistent messages, all implicating the right ventricle and yet it has been neglected in the vast majority of studies regarding cardiac changes in athletes. Now there is sufficient evidence to invest in the long-term prospective studies that are required."

In an accompanying editorial [3], Professor Sanjay Sharma, of St George's University London (UK), who is medical director of the London Marathon, writes that although the study is small, "the results provide food for thought and the data should be embraced to galvanise more detailed and longitudinal assessment of large groups of endurance athletes. The potential for such projects is enormous considering the colossal increase in participation rates in endurance events such as the marathon. The long-term conclusions of the authors may appear preposterous to some, but could prove to be the retrospective 'elephant in the room'."

In a statement for this press release, Prof Sharma said: "My personal feeling is that extreme endurance exercise probably does cause damage to the heart in some athletes. I don't believe that the human body is designed to exercise at full stretch for as long as 11 hours a day, so damage to the heart is not implausible. It is too early to say that taking part in endurance sports causes long-term damage to the right ventricle, but this study is an indication that it might cause a problem in some endurance athletes with a predisposition and, therefore, it should be studied further."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our sports medicine / fitness section for the latest news on this subject. [1] "Exercise induced right ventricular dysfunction and structural remodelling in endurance athletes". European Heart Journal. doi:10.1093/eurheartj/ehr397
[2] The distances for each event are as follows: marathon = 42.2 kms; endurance triathlon = 1.9km swim, 90 kms cycle, 21.1 kms run; alpine cycling = 207 kms; ultra triathlon = 3.8 kms swim, 180 kms cycle, 42.2 kms run.
[3] "Exercise-induced arrhythmogenic right ventricular cardiomyopathy: fact or fallacy?". European Heart Journal. doi:10.1093/eurheartj/ehr436
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