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High blood pressure, low energy -- a recipe for heart failure

Many people with long-standing high blood pressure develop heart failure. But some don't. Daniel P. Kelly, M.D., and colleagues at Washington University School of Medicine in St. Louis and other institutions are trying to figure out what could explain that difference.

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Keywords: blood, pressure, low, energy, recipe, heart, failure

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1. Systolic blood pressure level for patients with heart failure may help predict risk of death
   11-07-2006 · EurekAlert!
   Patients with heart failure and low systolic blood pressure at hospital admission are more likely to have poor outcomes including higher mortality rates and increased rates of rehospitalization, despite medical treatment, according to a study in the Nov. 8 issue of JAMA.
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2. Preventing or reducing enlarged heart decreases risk of heart failure
   09-12-2007 · EurekAlert!
   For high-blood-pressure patients, preventing or reducing enlarged heart reduces risk of heart failure. The study is published in the Sept. 4 Annals of Internal Medicine and led by physician-scientists at NewYork-Presbyterian Hospital/Weill Cornell Medical Center in New York City.
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3. Systolic blood pressure predicts mortality in heart failure patients
   11-07-2006 · EurekAlert!
   A team of academic researchers report that systolic blood pressure taken at hospital admission may be a key factor in predicting mortality risk and revealing important disease characteristics for heart failure patients.
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4. Women with high or increasing blood pressure are up to three times more likely to develop diabetes
   10-09-2007 · EurekAlert!
   One of the largest studies to investigate the relationship between blood pressure and type 2 diabetes has found that women who have high blood pressure levels are three times more likely to develop diabetes than women with low blood pressure levels. This effect was independent of body mass index and other conditions that are known to predispose people to cardiovascular disease and diabetes, researchers report in the European Heart Journal.
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5. Metabolic syndrome -- don't blame the belly fat
   07-16-2007 · EurekAlert!
   Abdominal fat, the spare tire that many of us carry, has long been implicated as a primary suspect in causing the metabolic syndrome, a cluster of conditions that includes the most dangerous heart attack risk factors: prediabetes, diabetes, high blood pressure, and changes in cholesterol. But researchers have found that insulin resistance in skeletal muscle leads to alterations in energy storage that set the stage for the metabolic syndrome.
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6. New study: Pycnogenol reduces heart failure
   05-16-2007 · EurekAlert!
   A study to be published in an upcoming edition of the journal of Cardiovascular Toxicology reveals Pycnogenol natural pine bark extract from the French maritime pine tree, helps prevent damage that high blood pressure causes to the heart. The study demonstrates Pycnogenol counteracts the "wearing out" of the heart, which may aid the five million Americans living with heart failure. Previous studies have shown Pycnogenol supplementation to be associated with improved cardiovascular health, such as cholesterol reduction, blood pressure control and prevention of thrombosis.
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7. Drug does not reduce risk of death for heart attack patients with refractory shock
   03-26-2007 · EurekAlert!
   The medication tilarginine, a drug that was believed could be beneficial for patients who develop cardiogenic shock (low blood pressure due to impaired cardiac function) after a heart attack, did not reduce the risk of death up to six months after a heart attack, according to a JAMA study published online March 26. The study is being released early to coincide with its presentation at the American College of Cardiology's annual conference.
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8. Energy drinks may pose risks for people with high blood pressure, heart disease
   11-06-2007 · EurekAlert!
   Downing an 'energy drink' may boost blood pressure as well as energy, researchers said in a small study presented at the American Heart Association's Scientific Sessions 2007.
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9. 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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10. Lungs' pressure needn't threaten heart transplant survival
    11-06-2007 · EurekAlert!
    Heart surgeons at Johns Hopkins say people who need heart transplants can largely avoid transplant failure due to elevated blood pressure in their lungs with the help of proper drug treatment.
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