The £1.40 heart pill lifesaver: 10,000 patients a year could be saved by newly-licensed drug

The disgrace here is that it took so long for the drug to be made available. How many people have died needlessly in the last 5 years?

A pill costing only £1.40 a day could save the lives of thousands of heart failure patients every year. The drug ivabradine, which slows the heart rate and improves its pumping ability, cut deaths by up to 39 per cent in trials.

Professor Martin Cowie, consultant cardiologist and specialist in heart failure at the Royal Brompton Hospital, said that at a conservative estimate it could save between 5,000 and 10,000 lives a year. It could also slash National Health Service costs by cutting hospital admissions by more than a quarter.

Ivabradine, also known as Procoralan, is licensed in the UK for treating angina and has been available on the NHS for around five years with a good safety record. But today it is being licensed by European safety regulators for treating heart failure.

The NHS drug-rationing body, the National Institute for Health and Clinical Excellence, has yet to decide whether it is affordable for treating heart failure, but around 20,000 patients currently take it for angina.

Prof Cowie, who was involved in a trial of 6,500 patients, insisted it would save the NHS money. He said: ‘I hope this gets approved because it’s very good value for money in reducing the number of hospitalisations alone.’

Made by Servier, the drug is relatively cheap, costing the NHS about £500 a year per patient. Around one in five of 900,000 Britons with heart failure – almost 200,000 patients – could benefit from the treatment.

Trial findings showed a 39 per cent reduction in death from heart failure, a 17 per cent drop in the risk of dying from any cause and a 26 per cent cut in the need for hospital stays among patients using the drug.

Prof Cowie said today’s European licensing decision was ‘great news for both doctors and patients, and is a significant step forward in the management of heart failure’. He added ivabradine would make a dramatic difference to many who could not take beta blockers, the standard drugs used to reduce heart rate. He said even some on the maximum beta blocker dose still had a heart rate that was too fast – more than 75 beats a minute.

Ivabradine lowers the rate to around 60 beats a minute without reducing blood pressure, which means the damaged heart pumps more efficiently at a slower rate.

Prof Cowie said: ‘Heart failure is a very common problem. We have trial results showing ivabradine not only improves symptoms and prevents disease progression, but also helps patients return to normal daily activities and increases their enjoyment of life.

'One in five patients could benefit – the key to whether current treatment is working is whether their heart beat is still too high. This is easy to check – a doctor just has to take their pulse, or the patient can do it.’

Around 100,000 people a year are thought to die from heart failure, which occurs when damage to the organ leaves it too weak to pump blood efficiently around the body. About 68,000 new cases are diagnosed each year. Symptoms include fatigue, breathlessness, increased heart rate and swollen ankles.

Treating heart failure soaks up one to two per cent of the total NHS budget, with direct medical costs alone amounting to £625million a year.

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Cannabis-like chemical could help keep couch potatoes slim

A long way from this leading to a drug, however

A natural cannabis-like chemical in the brain may hold the key to keeping couch potatoes slim, early research suggests. Scientists in the US found that blocking the compound allowed mice to gorge on high fat food and take little exercise without putting on weight or becoming unhealthy.

The genetically modified animals produced limited amounts of the endocannabinoid 2-AG, a chemical related to the active ingredient in cannabis. All mammalian brains, including those of humans, contain 2-AG, which is believed to control neural circuits involved in metabolism.

'We discovered that these mice were resistant to obesity because they burned fat calories much more efficiently than normal mice do,' said study leader Professor Daniele Piomelli, from the University of California at Irvine.

'We had known that endocannabinoids play a critical role in cell energy regulation, but this is the first time we found a target where this occurs.' The mice stayed slim because they developed a hyperactive form of 'brown fat' - a special type of fat that generates heat and keeps animals warm.

Not only did they not gain weight when fed a high-fat diet, but they failed to develop any of the expected signs of metabolic syndrome. This is a combination of problems such as obesity and high blood pressure which increase the risk of heart disease and diabetes.

But the scientists, who report their findings in the journal Cell Metabolism, caution that it is too soon for couch potatoes to be celebrating.

'To produce the desired effects, we would need to create a drug that blocks 2-AG production in the brain, something we're not yet able to do,' said Prof Piomelli. 'So don't cancel that gym membership just yet. But as you hit the treadmill, think about the added health benefits if you could train your brain to make fewer endocannabinoids.'

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