Q10 and why it maybe useful for Heart Failure patients
If you have a look at our previous posts on Q10 we have advocated a look at this interesting supplement. Of course as usual if you are tempted to use it make sure you speak to your clinician and please note that it does have a procoagulant effect therefore if you are on warfarin then consult your warfarin nurse.
Researchers claim that patients who took the supplement, known as Coenzyme Q10, alongside their normal medication during a two-year study had lower levels of mortality than those who did not.
They say that doctors should now consider including the supplement, which costs around 25p per tablet, as part of the treatment of people who have a heart condition.
The supplement known as CoQ10, occurs naturally in the body and plays a role in turning sugar into energy for the cells.
Heart muscle contains large amounts of CoQ10, but previous research has shown that it decreases in patients who have suffered heart failure.
The new study, which involved 420 patients who had suffered heart failure, showed that those who took three 10mg tablets of CoQ10 a day had lower levels of heart failure two years later.
Fewer of the patients who had taken the supplement had died at the end of the study.
Professor Svend Mortensen, from the Heart Centre at Copenhagen University Hospital, who led the study, said: “The CoQ10 treated patients had reduced hospital admission rates for worsening heart failure and lower cardiovascular death, both of which may reflect a significant improvement in cardiac function.
“CoQ10 should be considered as a part of the maintenance therapy of patients with chronic heart failure.”
The results were presented at Heart Failure 2013 – the main annual meeting of the Heart Failure Association of the European Society of Cardiology – in Lisbon, Portugal.
It is also found in foods such as red meat and fish, but at very low levels that deemed to be insufficient to impact on heart failure.
The molecule is known to play an essential role in the mitochondria, the tiny power stations found inside almost every cell of the body that convert sugar into energy.
The new study, known as the Q-SYMBIO trial, followed patients in Denmark, Sweden, Austria, Slovakia, Poland, Hungary, India, Malaysia and Australia.
After two years, 14% of patients taking CoQ10 had suffered problems with their heart compared to 25% of those who had been taking a placebo.
Just 9% of the patients taking CoQ10 had died compared to 17% taking the placebo.
CoQ10 is currently sold over the counter at pharmacists, including Boots, as an energy booster.
Statins, one of the drugs taken by heart failure patients to control cholesterol, is also known to block the synthesis of CoQ10 in the body, causing levels to drop.
It is unclear how many of the patients in the study were taking statins and the CoQ10 could have been compensating for this effect in the study.
But Professor Mortensen said he hoped to conduct a trial to see how taking CoQ10 with statins could improve heart patient mortality rates compared to just taking statins alone.
He added: “Statins reduce CoQ10, and circulating CoQ10 prevents the oxidation of LDL effectively, so I think ischemic patients should supplement statin therapy with CoQ10.
Helen Williams, a consultant pharmacist for cardiovascular disease at NHS Southwark Clinical Commissioning Group and a member of the Royal Pharmaceutical Society, said: “this is a relatively small study for a cardiovascular trial.
“We have often been misled before by small studies that fail to show benefits when extended to larger numbers of patients, so I would great these results with cautious optimism.”
We believe that any positive trial is worth exploring and should not be dismissed in public before a larger clinical trial can take place.
A review shows that pharmacists play a very useful role in managing heart failure. Their involvement reduces the risk of hospitalisation which both improves patient quality of life and reduces the public health burden of heart failure.
Medications for heart failure include angiotensin-converting enzyme (ACE) inhibitors and beta-blockers. The problem is that these are under-used. A multi-disciplinary approach, including input from a pharmacist, could perhaps improve outcomes for the patient with heart failure. Researchers at the University of Alberta, Edmonton, Canada, have looked back at research on heart failure that has involved input from a pharmacist.
The researchers found 12 studies covering over 2,000 patients with heart failure where care given by a pharmacist was compared with usual care. In seven studies, the pharmacist was the key person, helping with medication, education, adherence, and communication with the physician. In other studies, the pharmacist was part of a team looking after the patient with heart failure. The team analyzed whether involvement of the pharmacist reduced mortality and hospitalisation for both all causes and for heart failure.
There was no overall reduction in mortality with pharmacist intervention. But there was a significant reduction in hospitalisation rates, by around one third, both overall and for heart failure if the pharmacist was involved.
Heart failure is one of the leading causes of hospitalisation. These hospitalisations are, the researchers say, too often attributed to problems with medication. Therefore, more input from the pharmacist, who is the one who knows most about medication, might be expected to decrease the risk of hospitalisation.
It is also not clear from the current study what kind of pharmacist intervention makes the most difference when it comes to looking after patients with heart failure. But the finding that their work can reduce hospitalizations by one third underlines the key role medication plays in managing heart failure. Therefore, a pharmacist should always be involved in caring for the patient with heart failure.
Gene Therapy for UK Heart Failure Patients
Patients with severe heart failure are to be treated with gene therapy for the first time in Britain.Earlier clinical trials have suggested the treatment could reverse damaging changes inside cardiac cells that weaken the muscle and reduce the ability of the heart to pump blood.
The condition affects up to 1,000,000 people in the UK.
Doctors backed by the British Heart Foundation will give 100 patients an infusion of a harmless virus that has been genetically engineered to carry an extra gene, called SERCA2a.
The virus infects cardiac cells. Once inside, the gene becomes activated and makes a protein crucial to normal beating of the heart.
Dr Alexander Lyon, consultant cardiologist at The Royal Brompton Hospital, is leading the Cupid 2 trial. He said: “When the heart muscle is injured it activates a series of compensatory changes, but over time fatigue sets in which results in the natural version of this gene switching off. ”When the gene is repaired it produces more of the functional protein and the problem is reversed.”
The first patients will be given the treatment in the next three to six weeks at hospitals in London and Glasgow.
They will be tracked and compared to another group of study volunteers who will receive a dummy treatment.
A previous pilot study in the United States found the treatment dramatically reduced emergency hospitalisations and deaths.
The 39 patients given the gene are still in a stable condition after three years.
Professor Sian Harding, head of the British Heart Foundation’s Centre for Regenerative Medicine at Imperial College London, whose team developed the therapy, said: “It’s been a painstaking, 20-year process to find the right gene and make a treatment that works. ”But we’re thrilled to be working with cardiologists to set up human trials that could help people living with heart failure.”
Warfarin in decline, alternatives on the Up?
Pulse magazine is reporting that GPs are increasingly prescribing the newer anticoagulant alternatives to warfarin for the prevention of stroke, although their uptake has been slower than expected due to cost concerns.
An analysis of NHS primary care prescribing data for the past three years shows a fourteen-fold increase in the use of the newer anticoagulants dabigatran, rivaroxaban and apixaban in 2012, compared with 2011.
There was also a 9% increase in the use of warfarin from 2011 to 2012, leading experts to conclude that newer anticoagulants are being reserved for patients who are unsuitable for warfarin.
Pulse reported last year that following the NICE approval of dabigatran in March for certain patients with atrial fibrillation, CCGs put restrictions in place to limit use of the drug, with some warning its use as an alternative to warfarin could ramp up primary care drug budgets by as much as 20%.
This looks to have put a lid on demand, alongside concerns about the safety profile of some of the newer alternatives.
The figures from the NHS Information Centre Prescribing and Primary Care Services show that the total number of NHS prescriptions in 2012 for warfarin rose to 10.2 million prescriptions dispensed last year, compared with 9.4 million in 2011.
The total prescribed items for dabigatran – including those prescribed in patients with atrial fibrillation and venous thromboembolism – went up from around 3,200 in 2011, to 48,300 in 2012. Prescriptions for rivaroxaban and apixaban also rose, but their use remains much lower than that of dabigatran.
To read the full article from Pulse click here
Now we all know how important it is to not get depressed about your condition so certainly to us this is not surprising however this is a strong step in the right direction to demonstrate the importance of being positive.
Depression could make heart failure even more fatal, a new study suggests.
Researchers from the Mayo Clinic in the US found that people with heart failure who are moderately to severely depressed have a 4x higher risk of death, compared with people with heart failure who are not depressed. They also have a 2x higher risk of being hospitalised or having to go to accident and emergency.
The study shows just how important it is to pay attention to patients’ mental health, as “depression is a key driver of healthcare use in heart failure,” study researcher Alanna M. Chamberlain, Ph.D., M.P.H., an assistant professor of epidemiology at the Mayo Clinic, said in a statement. The new study is published in the journal Circulation: Heart Failure.
The findings are based on 402 people with heart failure, with an average age of 73, who were from three Minnesota counties in the US. The study participants completed a survey with nine questions some time between 2007 and 2010 that analyzed their depression status. Then, the participants were followed for about a year and a half.
Researchers found an association between having depression and risk of being hospitalized or dying in the followup period. The risks went up with severity of depression. For example, according to the survey, people with mild depression were 60% more likely to die, and 35% more likely to have to visit the emergency room than those without depression. They were also 16% more likely to be hospitalised.
However, researchers did note a caveat to the findings. “We measured depression with a one-time questionnaire so we cannot account for changes in depression symptoms over time,” Chamberlain said in the statement. “Further research is warranted to develop more effective clinical approaches for management of depression in heart failure patients.”
Similarly, another new study published in the Journal of the American Heart Association shows that anxiety and depression raise risk of death among people with heart disease. Specifically, anxiety doubles risk of death from any cause among heart disease patients, and patients with both anxiety and depression have a tripled risk of dying. That finding, from Duke University researchers, is based on data from 934 people with an average age of 62.
Eplerenone appears to reduce the risk of cardiovascular mortality and heart failure after a heart attack by more than one-third, according to research presented at the American College of Cardiology‘s 62nd Annual Scientific Session.
The REMINDER (Reduction of heart failure morbidity in patients with acute ST-elevation myocardial infarction) trial was a randomized, double-blind trial of 1,012 patients who had a heart attack caused by a complete blockage of one of the heart’s arteries. Patients had no signs or history of heart failure. They were given either eplerenone or placebo in addition to standard therapy. Overall, patients taking eplerenone were 38% less likely to have poor outcomes than those given a placebo.
Eplerenone counteracts a hormone called aldosterone, which can increase blood pressure.
“This is the first randomized trial to test a mineralocorticoid receptor agonist during the acute phase of heart attack, and the results suggest a clinical benefit,” said Gilles Montalescot, MD, PhD, lead investigator of the study and professor of cardiology and head of the Cardiac Care Unit at Piti–Salp-tri-re Hospital, Paris.
A drug often used to treat chronic heart failure may not ease symptoms in people with one form of the disease, a new study suggests.
Spironolactone failed to improve symptoms or quality of life among 422 patients with diastolic heart failure — a form of the disease that affects about half of all people with heart failure.
The drug did, however, benefit the structure and function of patients’ hearts. And experts said it’s too early to know what to make of the results, which appear in the Feb. 27 issue of the Journal of the American Medical Association.
“It would be premature to say this is not beneficial,” said Dr. Sanjiv Shah, a cardiologist at Northwestern University Feinberg School of Medicine, in Chicago, who was not involved in the study.
Shah is involved in an ongoing study of spironolactone’s effects in people with diastolic heart failure. And that trial is focusing on the big questions: Can the drug prevent or delay hospitalizations, or prolong people’s lives?
Spironolactone is in a class of drugs called aldosterone receptor antagonists. They cause the kidneys to eliminate excess water and sodium from the body, so they can lower blood pressure and get rid of fluid build-up in some people with heart failure.
Studies have shown that spironolactone can extend the lives of some heart failure patients — namely, those with a low “ejection fraction.
The problem is that heart failure is a “syndrome” - or a collection of signs and symptoms – rather than a disease. So a treatment that works for some patients may not work as well for others.
In systolic heart failure, the heart’s left ventricle (the main pumping chamber) cannot contract strongly enough, and many people with this form of heart failure have a reduced ejection fraction.
In the diastolic form, the left ventricle doesn’t relax enough between contractions, which means it cannot fill up with as much blood as it should. But the heart’s ejection fraction is actually normal.
Diastolic heart failure is trickier to diagnose, and doctors know less about how to best treat it, said Dr. John Cleland, a cardiologist at Hull York Medical School in Kingston-upon-Hull who co-wrote an editorial published with the study.
He agreed that it’s too soon to draw conclusions from the current findings, and that doctors will know more when Shah’s study results are in.
Ventricular re-modelling at its most exciting!
Ventrix, Inc. announced today that its VentriGel™cardiac repair scaffold safely and effectively mitigated left ventricular remodeling and improved cardiac function in pigs after myocardial infarction, or a heart attack. The findings, made during pre-clinical studies, were published today in the journal Science Translational Medicine. Based on these and other results, Ventrix will initiate a clinical trial for VentriGel later this year.
“These results give us strong validation that VentriGel has the potential to prevent the development of congestive heart failure in patients who are recovering from heart attack,” said Adam Kinsey, Ph.D., CEO of Ventrix. “We will continue to develop VentriGel for this indication, for which there is a very acute need and large market potential.”
As medical management and surgical tools have advanced, more and more patients are surviving heart attacks. However, damage to the heart during myocardial infarction can lead to a growth of dense scar tissue which cannot contribute to the pumping function of the heart. Over time, the heart wall will thin causing heart failure. Currently, the only successful treatments for end-stage heart failure are heart transplantation or left ventricular assist devices.
In the study, the VentriGel scaffold was injected into pigs two weeks following heart attack via a minimally-invasive catheter. Three months after injection, more cardiac muscle and less scar tissue was found in the VentriGel-treated group compared to controls that did not receive VentriGel. This led to significant improvements in contractility and cardiac function and prevented heart failure in treated animals. Ejection fraction, one measure of cardiac function, was significantly greater after delivery of VentriGel.
VentriGel is a biomaterial scaffold designed specifically for the repair of damaged myocardium (heart muscle). It is injected via catheter in a minimally-invasive procedure that does not require surgery or general anesthesia.
Heart Skips a beat with the new Pumping Marvellous Toolkit
The BHF have got staying alive and now Pumping Marvellous have got “heart skips a beat” by Olly Murs. We would like to thank everybody for their hardwork and dedication in making this video such a success and we really hope it energises people who have been newly diagnosed with heart failure to have some attitude, belief and success in managing their heart failure symptoms. Also remember this video is also good for carers / caregivers and families to learn about how to help.
This video accompanies the Patient Heart Failure toolkit that has been developed by Pumping Marvellous for the NHS in England and Wales to support self management.
Sounds a bit peculiar, interested read on…
Researchers at the University of Minnesota’s and the Lillehei Heart Institute have utilised molecular genetic engineering to optimise heart performance in models of diastolic heart failure by creating an optimized protein that can aid in high-speed relaxation similar to fast twitching muscles.
Within heart cells, calcium plays a major role in helping normal heart pump function. However, in diastolic failure the calcium signaling process is slowed; calcium levels rise to the peak needed for the squeezing action of the heart but don’t then drop quickly enough for an efficient relaxation period – the condition known as diastolic heart failure. University researchers were able to pinpoint a specific protein, parvalbumin – which aids in high-speed relaxation of fast twitching muscles in nature – and optimize it to become a calcium sponge for heart muscle. As a result, the optimized protein, ParvE101Q, soaks up excess calcium at a precise instant, allowing the heart to relax efficiently after contraction. Still with us…
The advance offers a solid conceptual step forward in solving the puzzle of diastolic heart failure. The next step will be determining the best possible delivery mechanism for the protein, which should allow the discovery to be used in clinics.
“In nature, there are unique organisms known to be able to contract and relax muscles quickly,” said Joseph M. Metzger, Ph.D, a University of Minnesota Medical School professor and chair of the Department of Integrative Biology and Physiology. “We hoped research and discovery could help identify what was promoting this highly efficient activity so we could harness it for use in the heart. We’ve discovered that our optimised variation of parvalbumin can fulfill that role by treating diastolic heart failure.”
If they can develop an ideal delivery system for the optimized protein, the researchers believe they may have found a unique clinical application to treat diastolic heart failure.
I suppose we will all have to wait and see. We apologise for the level detail we sometimes go into but it generally cannot be described in any other way.