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Diabetes drugs increase risk of heart failure, research shows

07-27-2007 · EurekAlert!

A class of drugs commonly used to treat type 2 diabetes may double the risk of heart failure, according to a new analysis by researchers at Wake Forest University School of Medicine and colleagues.

Keywords: diabetes, drugs, risk, heart, failure, research, shows, diabete, drug, show

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Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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Drug's potential adverse side effect explained
09-06-2007 · EurekAlert!
Drugs that are agonists of the receptor PPAR-gamma are used to treat individuals with diabetes. However, it has been suggested that their use is associated with a slightly increased risk of heart failure. A potential explanation for this adverse effect that is observed in a minority of patients is outlined in a new study in the Journal of Clinical Investigation.
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Glycemic control medication appears to have favorable effect regarding risk of cardiovascular events
09-11-2007 · EurekAlert!
A meta-analysis of previous research suggests that use of pioglitazone -- a glycemic control medication for patients with type 2 diabetes -- significantly reduces the risk of heart attack, stroke and death, but increases the risk for serious heart failure, according to an article in the Sept. 12 issue of JAMA.
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Mitochondrial 'bottleneck' cracked
01-27-2008 · EurekAlert!
Scientists have shown for the first time how a particular family of diseases are passed down from mother to child and how this can lead to the severity of the disease differing widely. The research, funded by the Wellcome Trust, offers hope of being able to predict a child's risk of developing a mitochondrial disease which can cause muscle weakness, diabetes, strokes, heart failure and epilepsy.
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Debate Renewed: Diabetes drug ups heart risk
09-15-2007 · Science News Online
A popular diabetes drug significantly increases the risk of heart failure and heart attack in those who take it.
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Use of diabetes medication by older adults linked with increased risk of heart problems, death
12-11-2007 · EurekAlert!
Older patients treated with the diabetes medications known as thiazolidinediones (which include rosiglitazone) had a significantly increased risk of heart attack, congestive heart failure and death, compared with the use of other hypoglycemic drugs, according to a study in the Dec. 12 issue of JAMA. The authors suggest that these results provide further evidence that this class of medication may cause more harm than good.
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New research shows ACTOS is associated with a 38 percent lower risk of heart attack
09-19-2007 · EurekAlert!
New research, including two studies presented this week at the 43rd Annual Meeting of the European Association for the Study of Diabetes, further support the cardiovascular safety of ACTOS (pioglitazone HCI) and its benefits regarding improved blood glucose and blood lipid levels for patients with type 2 diabetes.
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Heart failure: Mayo Clinic reveals abnormality in filling of the heart is frequent culprit
11-07-2006 · EurekAlert!
Difficulties in the heart's ability to fill with blood are common causes of heart failure -- and appear to be as significant in placing a heart patient at risk of death as are deficiencies in the heart's ability to pump blood, new research from Mayo Clinic shows.
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Mechanical 'artificial hearts' can remove need for heart transplant by returning heart to normal
11-01-2006 · EurekAlert!
Mechanical "artificial hearts" can be used to return severely failing hearts to their normal function, potentially removing the need for heart transplantation, according to new research. The mechanical devices, known as Left Ventricular Assist Devices (LVADs), are currently used in patients with very severe heart failure whilst they await transplantation. The new study shows that using an LVAD combined with certain drug therapies can shrink the enlarged heart and enable it to function normally once the LVAD is removed.
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Longer anthracycline therapy reduces heart failure in adult cancer patients
11-22-2006 · EurekAlert!
Stretching out a dose of chemotherapy over six or more hours may reduce the risk of heart problems caused by certain commonly used cancer drugs, according to a new review of recent research.
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