A pill costing less than £1.50 a day has the potential to save the lives of thousands of heart failure patients, medical trials suggest.
The drug, ivabradine, is already available in the UK to treat angina.
Prof Martin Cowie, who led the UK-based part of the study, said it could save up to 10,000 lives each year.
The trial involved more than 6,500 people in 37 countries who already used standard treatments such as beta-blocker drugs.
Over a typical study period of two years, ivabradine cut the risk of death from heart failure by 26%.
It had a similar impact on the likelihood of patients being admitted to hospital.
The research findings were presented at the European Society of Cardiology (ESC) annual meeting in Stockholm.
More than 700,000 UK adults over the age of 45 have heart failure, which leaves the organ too weak to pump blood around the body efficiently. A further 200,000 are undiagnosed.
But a study published yesterday showed the drug – called ivabradine – cuts the risk of death from heart failure by 26 per cent.
Professor Martin Cowie, consultant cardiologist at the Royal Brompton Hospital in London, who led the UK arm of the study, said the results had convinced him to change his clinical practice.
The drug could save 10,000 lives a year at a conservative estimate, said Prof Cowie.
“The evidence represents a significant clinical breakthrough in the management of heart failure and is incredibly important information for patients with this condition,” he said. “We now know that more lives can be saved and improved simply by adding ivabradine to their current treatment in order to take some of the strain off the heart.
“It is vital that the results of this study are implemented and ivabradine is used as part of standard heart failure treatment as soon as possible.” Heart failure is often triggered by other problems such as a heart attack. Around 68,000 new cases are diagnosed each year and around 40 per cent die after just a year.
Treatment for those who are admitted to hospital costs the NHS £625million a year. Patients are commonly prescribed beta blockers, which lower blood pressure, but many suffer side-effects. Ivabradine, which works by lowering the number of heart beats per minute rather than blood pressure, could be used as an alternative.
The drug is already available in the UK and used for patients with angina, or chest pain, but only 10 per cent are prescribed the drug. Drug regulators said yesterday it would need a separate licence to be used in treatment for heart failure but GPs may use their discretion to prescribe the pill “off-label” before the licence is approved.
Ivabradine (INN) (pronounced /??væbr?di?n/) is a novel medication used for the symptomatic management of stable angina pectoris. It is marketed under the trade name Procoralan (Servier), Coralan in India (Servier), Australia or such as in Italy Corlentor (Servier), and was also known as S-16257 during its development. Ivabradine acts by reducing the heart rate in a mechanism different from beta blockers and calcium channel blockers, two commonly prescribed antianginal drugs. It is classified as a cardiotonic agent.
Ivabradine acts on the If (f is for “funny”, so called because it had unusual properties compared with other current systems known at the time of its discovery) ion current, which is highly expressed in the sinoatrial node. If is a mixed Na+–K+ inward current activated by hyperpolarization and modulated by the autonomic nervous system. It is one of the most important ionic currents for regulating pacemaker activity in the sinoatrial (SA) node. Ivabradine selectively inhibits the pacemaker If current in a dose-dependent manner. Blocking this channel reduces cardiac pacemaker activity, slowing the heart rate and allowing more time for blood to flow to the myocardium.
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October 7th, 2010 at 6:05 pm
Brit scientists have discovered a mechanism in the body that causes high blood pressure—a feat that could lead to new treatments for the condition.
Researchers have found for the first time a key step in how the body controls blood pressure and so how the process sometimes goes wrong.
And now they can target the mechanism to stop it from malfunctioning and thus prevent the condition, known as hypertension, which is the leading cause of heart disease and stroke.
The researchers at Cambridge University and Nottingham University discovered the mechanism while studying pre-eclampsia, a potentially deadly form of high blood pressure which occurs in women during pregnancy.
Blood pressure is controlled by hormones called angiotensins which in too high a dose forces blood vessels to contrict, increasing blood pressure.
The scientists, who have spent 20 years researching the hormones, have discovered the very first stage in their development.
They now believe they could develop a way of inhibiting the “switch” that allows the hormones to overproduce and prevent the onset of high blood pressure.
“We have found the first step in the main process that controls blood pressure,” the Telegraph quoted Professor Robin Carrell at the University of Cambridge, as saying.
“We are excited by what we have found because of the potential insights it provides us. Knowledge of what causes a disease is the number one factor needed for its eventual management and treatment.
“By getting a step earlier and looking at an earlier change we are opening up new strategies and coming closer to the reason why some people develop hypertension,” he added.
“Although we primarily focused on pre-eclampsia, the research also opens new leads for future research into the causes of hypertension in general,” said Dr Aiwu Zhou, a British Heart Foundation (BHF) Fellow at the University of Cambridge.
Drugs currently used to treat high blood pressure – such as ACE inhibitors – focus on the later stages of the mechanism that controls blood pressure.
The new study hopes to lead to new inhibitors that nip the condition in the bud before it has caused any damage.
The study was published in Nature.
October 16th, 2010 at 1:10 pm
A breakthrough study has revealed that majority of heart patients are not receiving drugs known as beta blockers, which increase their survival prospects, in required quantity.
For nearly 40 years, these drugs have been proven to increase patients’ survival prospects following a heart attack by decreasing the cardiac workload and oxygen demand on the heart.
“Only 46pc of patients studied were taking 50pc or more of the target dose of beta blockers shown to be beneficial in clinical trials. Furthermore, 76pc of patients were still being treated with the same amount of medication given at discharge. This means that for the vast majority of patients, there wasn’t even an attempt to increase their dose,” said Jeffrey J. Goldberger, a professor of medicine at Northwestern University Feinberg School of Medicine.
“Beta blockers work to keep patients alive after a heart attack, so proper dosing of beta blockers can save many lives,” he added.
Study participants were prescribed very low doses at discharge, in part to assess how their bodies were likely to react to the drug. Researchers then followed up with patients three weeks later to determine if their personal physicians had adjusted the dosage amount.
“One of the reasons for the low dosage at discharge from the hospital can be attributed to patients’ shorter length of hospital stay. Better communication between patients and their personal physicians would help ensure patients are receiving the appropriate dose of beta blockers more quickly, ” the professor further explained.
The study has been published in the American Heart Journal.