Paul Heesom's Zambezi Blast for Heart Failure Charity

Paul’s Marvellous Zambezi Blast

Read why Paul Heesom is braving crocodile-infested waters for our heart failure charity this month with a global adventure, the Pumping Marvellous Zambezi Blast

On September 9th, Paul Heesom begins a week-long trip to push his boundaries, on a once-in-a-lifetime adventure in aid of people living with heart failure across the UK, on his epic 200-mile trip along the world’s wildest water run, the Zambezi Blast!


“Losing Dad to heart failure in January 2016 was a devastating blow to my family and myself. He was our cheeky chappy. The life and soul and would light up any room. I miss him terribly.


The Pumping Marvellous website and literature helped Mum and the family try and understand why he had been taken from us at a relatively young 75. Sharing thoughts with others helped immensely.


Giving something back to Pumping Marvellous as way of a thank you was something I felt I wanted to do, and in so doing raising awareness to heart failure.


Two years ago, as part of a 40 strong team, I scaled Mt Kilimanjaro and as a group we set a Guinness World Record for the Highest ever game of Rugby League. Dad was immensely proud of what myself and the team had managed to achieve. So with that feat in mind I set about finding a similar challenge to take me out of my comfort zone yet again. With the help of Global Adventures Ltd I found just that Challenge. On 9th September 2017 I will fly to Zambia in Southern Africa to take on the Mighty Zambezi River. Again as part of a team I will Kayak and raft 200 miles of raging white water rapids in the Batoka gorg.


Dad was a prolific traveller and Africa was one of his favourite destinations. I’m sure he would’ve love the thought of this adventure. Gigantic Grade 5 rapids, camping out under the stars in the African bush. Pods of Hippos and Crocodiles to circumnavigate. Along with all the other wild animals and creepy crawlies that Zambia has to throw at us.


Training for this challenge has been tough and arduous but it’s all gone really well. I’m feeling ultra fit and chomping at the bit to get started at the foot of the great Victoria Falls.


A huge thankyou to The Pumping Marvellous family and all who have donated to my justgiving page so far, you’ve all been a massive help and support in bringing this challenge together. I won’t let you down guys! ❤️”


There is still time to donate to Paul’s epic challenge – Please visit his fundraising page to add your support and add messages of encouragement.

If you feel it might be time to take on your own challenge of a lifetime, please visit Global Adventure Challenges and ask to fundraise for the Pumping Marvellous Foundation, the UK’s heart failur echarity.

Click here to find out more about heart failure.

NIQOR National Heart Failure Audit

More Patients than Ever Surviving Heart Failure, National Audit Finds

More patients than ever surviving heart failure following key improvements, audit finds

Acute heart failure necessitating hospital admission is a life threatening condition. The quality of care including specialist involvement during an admission, determines the immediate and long-term outcomes including likelihood of survival. Yet while the audit reports several improvements, it also found that the quality of care varies from one hospital to another, and within a hospital, between the specialist and other wards.


The audit is commissioned by the Health Quality Improvement Partnership (HQIP) as part of the National Clinical Audit and Patients Outcomes Programme (NCAPOP).


The latest National Heart Failure (HF) Audit is the largest to date and is based on 66,695 admissions to hospitals in England and Wales between April 2015 and March 2016. This represents 82% of HF admissions as the patient’s primary diagnosis in England and 77% in Wales.


The National HF Audit monitors the treatment and care of people with an unscheduled admission to hospital who are discharged with a primary diagnosis of heart failure. This is the 9th National HF Audit report which reports data from 137 NHS Trusts in England and 6 Health Boards in Wales.


  • During hospital admissions more than 90% of patients received an echocardiogram, a key diagnostic test. However, rates are higher for those admitted to cardiology (96%) than general medical (85%) wards. Specialist input irrespective of the place of admission is associated with higher rates (95%) of echocardiography.


  • The prescription of key disease-modifying medicines for patients with HF and a reduced left ventricular ejection fraction (HF-REF) has increased, including beta- blockers (87%) and mineralocorticoid antagonists (53%); treatments that are both life-saving and inexpensive.


  • Prescription rates for all three key disease modifying medications [angiotensin converting enzyme inhibitors (ACEI), beta-blockers (BB) and mineralocorticoid (aldosterone) receptor antagonist (MRA)] for patients with HF-REF has increased from 35% to 53% for those admitted to Cardiology wards over the last six years.


  • Irrespective of the place of admission, 47% of patients with HF-REF seen by a member of the specialist HF team as an inpatient, were prescribed all three disease modifying drugs, a key performance indicator (KPI). This has increased from 45% in 2014-15, albeit with considerable room for further improvement.


  • The number of patients seen by HF specialists remains high at 80% in 2015-16. In particular, HF nurses saw more HF patients admitted onto general medical wards (33%) than in 2014-15 (24%). This is important as specialist care improves mortality.


  • The mortality of patients hospitalised with heart failure is significantly lower in 2015-16 at 8.9% compared to 9.6% in 2014-15. However, mortality remains high and there are large variations in mortality amongst hospitals.
  • HF mortality rates in hospital are better for those admitted to cardiology wards.


  • If the patients identified within this audit cycle as having HF-REF, who left hospital on none of the three disease modifying drugs had been prescribed all three, then upwards of an additional 212 patients would likely have been alive at the time of census. With more comprehensive prescription and dose optimisation across the audit there is the ability to prevent numerous additional deaths.


Professor Theresa McDonagh, Clinical Lead for Cardiology and Heart Failure at King’s College Hospital, London and the HF Audit Clinical Lead said, “These results from our National Audit, are encouraging but leave room for further improvement. For the first time we have seen a small improvement in mortality in hospital, at 30 days and at one year. Hopefully we are now beginning to see the effects of better management of Heart Failure in hospital. We know how to diagnose it, investigate it and (for the majority of patients with reduced ejection fraction), we have effective treatments.  Specialist care in hospital matters. Getting onto the correct drugs matters and coordinated specialist care post discharge matters. There is still much to do! The audit provides the data to allow health care providers to engineer change to deliver better care.”


Dr Suzanna Hardman, Consultant Cardiologist and Whittington Health HF lead said, “The audit provides a wealth of hospital specific data alongside stark overall messages and has the potential to drive improvements in the quality of care. We have seen this in the most recent cycle with reductions in inpatient and subsequent mortality, attributed to early access to diagnosis with HF specialist care involving cardiologists and HF nurses, the prescription of disease modifying drugs and HF specialist follow up within two weeks of leaving hospital. But this pattern of care, which follows the most recent NICE guidance, and related standards, is still not accessed by all. This failure to implement current guidance continues to contribute to avoidable premature deaths. Variations in care both within a hospital and between hospitals are reported. It is time to ensure that all HF patients have a higher priority and timely access to the specialist unit and all that follows”.


The report authors also recommend all services dealing with heart failure patients (virtually all hospitals), and those commissioning HF services, study these findings and develop robust pathways where all patients are seen by a specialist who supervises their medication, both in hospital and, especially, on discharge and on review. Otherwise these patients will continue to experience excess readmission and mortality, they warn.

The full report will be published on the NICOR website on Thursday 10th August 2017 at

Cardiotrophin – How to trick your heart into thinking you exercise

Cardiotrophin – How to trick your heart into thinking you exercise

Cardiotrophin improves heart health and repairs damage in lab models

Researchers have discovered that a protein called cardiotrophin 1 (CT1) can trick the heart into growing in a healthy way and pumping more blood, just as it does in response to exercise and pregnancy. They show that this good kind of heart growth is very different from the harmful enlargement of the heart that occurs during heart failure. They also show that CT1 can repair heart damage and improve blood flow in animal models of heart failure. The results are published in Cell Research. The research team is from The Ottawa Hospital, the University of Ottawa, the University of Ottawa Heart Institute and Carleton University.

Heart failure is a leading cause of death and disability in high-income countries and a growing problem around the world. It occurs when the heart can’t pump enough blood through the body, often because a heart attack has damaged the heart muscle tissue.

“When part of the heart dies, the remaining muscles try to adapt by getting bigger, but this happens in a dysfunctional way and it doesn’t actually help the heart pump more blood,” said Dr. Lynn Megeney, senior author of the study and a senior scientist at The Ottawa Hospital and professor at the University of Ottawa.

“We found that CT1 causes heart muscles to grow in a more healthy way and it also stimulates blood vessel growth in the heart. This actually increases the heart’s ability to pump blood, just like what you would see with exercise and pregnancy.”

Dr. Megeney and his colleagues conducted a variety of studies in mice, rats and cells growing in the lab. In addition to CT-1, some of the studies involved a drug called phenylephrine (PE), which is known to cause the bad kind of heart growth. They found:

  • Heart muscle cells treated with CT-1 become longer, healthier fibres, while those treated with PE just grow wider.
  • CT-1 causes blood vessels to grow alongside the new heart muscle tissue and increases the heart’s ability to pump blood, while PE does neither.
  • When CT-1 treatment stops, the heart goes back to its original condition, just like it does when exercise or pregnancy end. However, the dysfunctional heart growth caused by PE is irreversible.
  • CT-1 dramatically improves heart function in two animal models of heart failure — one caused by a heart attack (affecting the left side of the heart) and one caused by high blood pressure in the lungs (pulmonary hypertension, affecting the right side of the heart).
  • Both CT-1 and PE stimulate heart muscle growth through a molecular pathway that has traditionally been associated with promoting cell suicide (apoptosis), but CT-1 has a better ability to control this pathway.

“This experimental therapy is very exciting, particularly because it shows promise in treating both left and right heart failure,” said Dr. Duncan Stewart, a cardiologist, senior scientist and co-senior author on the paper who is also Executive Vice-President of Research at The Ottawa Hospital and a professor at the University of Ottawa. “Currently, the only treatment for right heart failure is a transplant. And although we have drugs that can reduce the symptoms of left heart failure, we can’t fix the problem, and left heart failure often leads to right heart failure over time.”

“An intriguing aspect of this research was how human CT1 was able to promote a healthy growth response in multiple animal models,” said co-author Dr. Patrick Burgon, scientist at the University of Ottawa Heart Institute and assistant professor at the University of Ottawa. “This suggests the action of CT1 is universally conserved and puts us much closer to therapy.”

The researchers also note that while exercise could theoretically have the same benefits as CT-1, people with heart failure are usually limited in their ability to exercise.

Dr. Megeney and Dr. Stewart have patents pending for the use of CT-1 to treat heart conditions and they hope to develop partnerships to test this protein in patients. If this testing is successful it will take a number of years for the treatment to become widely available.

Pericytes Potential to Reverse Heart Damage

Pericytes Potential to Reverse Heart Damage

New pericytes discovery could reverse tissue damage caused by heart attacks

A new discovery by University of Bristol scientists helps to explain how cells which surround blood vessels, called pericytes, stimulate new blood vessels to grow with the hormone ‘leptin’ playing a key role. Leptin is produced by fat cells which helps to regulate energy balance in the body by inhibiting the appetite. This study, described in Scientific Reports, may have important implications for the treatment of heart attacks and also for cancer, the two main killers in the UK.

The growth of new blood vessels, called ‘angiogenesis’, is an important process occurring both in health and disease. It is involved in the repair of tissues following injury but also has an essential role in the growth and spread of cancer.

The Heart Research UK-funded project studied how pericytes encourage the growth of new blood vessels and the role of leptin, and provides important new information about the mechanisms involved.

One of the current treatments for heart attack is coronary artery bypass surgery. This uses blood vessels from the leg, or elsewhere in the body, to bypass the blocked artery and improve blood flow to the heart muscle. This is invasive and major surgery, with a long recovery time. In the longer term, these findings may help in the development of an alternative treatment to major surgery for heart attack patients.

Importantly, the team found that pericytes produced 40-times more leptin when exposed to low levels of oxygen and that this continued until oxygen levels returned to normal. This may help tissues to build more blood vessels to increase blood flow and oxygen supply. Together with other findings, the research shows that leptin has several important actions which encourage new blood vessel growth in areas where tissues are deprived of oxygen.

In most cases, a heart attack is when a coronary artery becomes blocked and the resulting lack of blood supply to the heart muscle can lead to a damaged heart.  Professor Madeddu’s team has shown that by stimulating the growth of new blood vessels, pericytes have the potential to restore blood supply to damaged heart muscle after a heart attack.

Paolo Madeddu, Professor of Experimental Cardiovascular Medicine from the School of Clinical Sciences, who leads the project at the Bristol Heart Institute, said:

“This new discovery could have important implications for the treatment of heart attacks, which is when a main coronary artery gets blocked, but also cancer. These results reveal a new signalling mechanism that may have a far-reaching and significant impact on cardiovascular regenerative medicine.

“Increasing leptin in pericytes in a damaged heart might help it to heal faster, whereas blocking the production of leptin in cancerous pericytes might starve the tumour of nutrients and force it to shrink.”

Barbara Harpham, Chief Executive of Heart Research UK, added: “This translational research project is a good example of research that aims to benefit patients as soon as possible. Professor Madeddu and the team have made some important new discoveries. Understanding more about the processes involved may help pave the way for the development of new treatments for heart attacks which could replace coronary bypass operations.”

Paper: The adipokine leptin modulates adventitial pericyte functions by autocrine and paracrine signalling’ by Paolo Madeddu et al in Scientific Reports [open access]

Marketing Authorisation Granted for Veltessa® (Patiromer) To Treat Patients With Hyperkalaemia

Marketing Authorisation Granted for Veltessa® (Patiromer) To Treat Hyperkalaemia


Patiromer is a sodium-free potassium binder licensed for the treatment of hyperkalaemia in adult patients. Hyperkalaemia is a potentially life-threatening condition which can cause fatal cardiac arrest and muscle paralysis. This therapy can also be made available to patients who develop hyperkalaemia while being treated with Renin-Angiotensin-Aldosterone-System (RAAS) inhibitor therapy – typically used in heart failure (HF) and chronic kidney disease (CKD).

The European licensing of patiromer, which applies to the UK, marks the first new drug developed specifically for the treatment of hyperkalaemia in nearly 60 years. Patiromer is a potassium binder that helps to enable optimal dosing of life-preserving therapies in heart failure and chronic kidney disease, and will be available for use in the UK later this year.

Hyperkalaemia presents a challenge for both cardiologists and nephrologists when managing existing RAAS inhibitor therapy which can lead to elevated potassium. Previously, treatment options that manage potassium overload have been limited to therapies first developed nearly 60 years ago. Dr Robert Lewis, Consultant Nephrologist and Chief of Service of the Wessex Kidney Centre in Portsmouth Hospital adds, “The licensing of patiromer is an important advance for clinicians treating the estimated one million people living with chronic kidney disease and hyperkalaemia. With this drug, nephrologists will be able to optimise the management CKD using agents which are of proven value, but which have until now been limited by their tendency to elevate potassium levels”.

In the UK, around 2.6 million people suffer with late stage CKD, around half of which have hyperkalaemia. There are also nearly one million HF patients, of which 2-3% are thought to have hyperkalaemia. Current guidelines recommend treating HF and CKD patients with RAAS inhibitors, but despite their proven benefit, they can also lead to elevated potassium levels which can potentially lead to organ failure. Patiromer has been found to optimise treatment of cardiovascular and renal conditions by safely reducing potassium and addressing challenges clinicians face with current treatment regimens.

“For nearly 60 years there have been no new treatments specifically developed and indicated for persistent elevated potassium, available in Europe,” says Marco Windisch, General Manager, Vifor Fresenius Medical Care Renal Pharma UK Ltd. “The European Commission licencing of patiromer in hyperkalaemia will help many patients better manage elevated potassium and get the maximum benefit from their life preserving renin angiotensin aldosterone system inhibitor therapy.”

Patiromer has been indicated to treat hyperkalaemia, a potentially life-threatening condition in which there is an abnormally high concentration of potassium ions in the blood (with serum potassium levels >5 mmol/l or >5.5 mmol/l) which is associated with increased risk of mortality. HF and CKD patients are at highest risk of developing hyperkalaemia as a result of RAAS inhibitors.

However, RAAS inhibitor treatments inhibit renal potassium excretion, improve CKD patient outcomes and when combined with beta blockers to form ‘triple therapy’, can reduce mortality by 30% in HF patients.

  • The EC licensing of patiromer is based on a comprehensive clinical development programme that included the following studies:
    Pivotal Phase III OPAL-HK study, which evaluated patiromer treatment in patients with hyperkalaemia and CKD who were taking RAAS inhibitors.
  • Phase II AMETHYST-DN trial, which evaluated the use of patiromer over 52 weeks in patients with hyperkalaemia, CKD and type 2 diabetes who were taking RAAS inhibitors.
  • An open-label, Phase I study that evaluated the onset-of-action of patiromer in CKD patients with hyperkalaemia.
microneedle patches with influenza vaccine

Microneedle Patches for Flu Immunisation Phase I Trial

Microneedle patches provide an alternative to conventional needle-and-syringe immunisation, and potentially offer improved immunogenicity, simplicity, cost-effectiveness, acceptability, and safety. In a recent Phase I trial, safety, immunogenicity, and acceptability of the first-in-man study on single, dissolvable microneedle patch vaccination against influenza was evaluated. The influenza vaccine can offer the best available protection against the flu virus, from which some people (including heart failure patients) can find recovery particularly difficult, and in some cases it can lead to serious complications. [See NHS Choices website]

Lead researcher Prof Mark Prausnitz, who is also part of a company that wants to license the technology, said: “If you zoom in under the microscope what you’ll see are microscopically small needles. They puncture painlessly into the skin.”

His team tested the microneedle patches alongside flu injections. Some of the 100 volunteers got the regular shot in the arm, while others applied the microneedle patch to their wrist for 20 minutes.

It offers the same protection as a regular vaccine, but without pain, according to its developers from Emory University and the Georgia Institute of Technology.

Hear Nadine Rouphael and Mark Prausnitz discussing the findings from their phase 1 trial that uses a dissolvable microneedle patch to deliver an influenza vaccine to patients on The Lancet’s podcast.



Read the full study as published in The Lancet > The safety, immunogenicity, and acceptability of inactivated influenza vaccine delivered by microneedle patch (TIV-MNP 2015): a randomised, partly blinded, placebo-controlled, phase 1 trial

Read more via BBC Health > Painless flu jab patch for people scared of injections

Canakinumab Drug Phase III Study Reducing Heart Attacks

Canakinumab Drug Phase III Study Reducing Heart Attacks

Novartis Phase III study shows ACZ885 (canakinumab) reduces cardiovascular risk in people who survived a heart attack

  • Phase III CANTOS study met the primary endpoint, a composite of heart attack, stroke and cardiovascular death, showing that ACZ885 (canakinumab) in combination with standard of care therapy reduces cardiovascular risk in people with a prior heart attack and inflammatory atherosclerosis
  • Despite current treatments about 40% of heart attack survivors remain at increased risk of  recurrent heart attack, stroke or cardiovascular death because of high-risk inflammatory atherosclerosis[1]; 25% experience another event within five years[2]


Basel, June 22, 2017 – Novartis today announced topline results from the global Phase III CANTOS study investigating the efficacy, safety and tolerability of ACZ885 (canakinumab) in combination with standard of care in people with a prior heart attack and inflammatory atherosclerosis. With more than 10,000 patients enrolled in the study over the last six years, CANTOS is one of the largest and longest-running clinical trials in Novartis’ history.

The CANTOS study met the primary endpoint, demonstrating that when used in combination with standard of care ACZ885 reduces the risk of major adverse cardiovascular events (MACE), a composite of cardiovascular death, non-fatal myocardial infarction and non-fatal stroke, in patients with a prior heart attack and inflammatory atherosclerosis. The full data from the study will be submitted for presentation at a medical congress and for peer reviewed publication later this year.

“Despite current treatment, about 25 percent of heart attack survivors will have another cardiovascular event within five years, making the outcome of the CANTOS study a promising new development for patients,” said Vas Narasimhan, Global Head, Drug Development and Chief Medical Officer, Novartis. “ACZ885 is the first and only investigational agent which has shown that selectively targeting inflammation reduces cardiovascular risk. Our priority now is to thoroughly analyze these important data and discuss them with regulatory agencies.”

Heart attack occurs in about 580,000 people every year in EU5 and 750,000 people in the United States alone[3],[4]. In 2015 there were an estimated 7.29 million heart attacks globally[5]. Despite standard treatment, people with a prior heart attack live with a higher ongoing risk of having another event or dying, and it has been shown that in about four in 10 people, this risk is directly related to increased inflammation associated with atherosclerosis[1]. The recurrent MACE in patients with inflammatory atherosclerosis are associated with increased morbidity, mortality and reduced quality of life and currently represent a major economic burden on patients and healthcare systems around the world.

The Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) (NCT01327846) is a randomized, double-blind, placebo-controlled, event-driven Phase III study designed to evaluate the efficacy, safety and tolerability of quarterly subcutaneous injections of ACZ885 (also known as canakinumab) in combination with standard of care in the prevention of recurrent cardiovascular (CV) events among 10,061 people with a prior myocardial infarction (MI) and with a high-sensitivity C-reactive protein (hsCRP) level of >=2mg/L. The study evaluated three different doses of ACZ885 vs placebo. The primary endpoint of the study was time to first occurrence of major adverse CV event (MACE), a composite of CV death, non-fatal MI, and non-fatal stroke. Secondary endpoints included time to first occurrence of the composite CV endpoint consisting of CV death, non-fatal MI, non-fatal stroke and hospitalization for unstable angina requiring unplanned revascularization; time to new onset type 2 diabetes among people with pre-diabetes at randomization; time to occurrence of non-fatal MI, non-fatal stroke or all-cause mortality; and time to all-cause mortality. The median follow-up time was 3.8 years. The study ran for approximately six years.

About heart attack and inflammatory atherosclerosis
Heart attack occurs in about 580,000 people every year in EU5 and 750,000 people in the United States alone[3],[4]. In 2015 there were an estimated 7.29 million heart attacks globally[5]. Despite standard treatment, patients who have had a prior heart attack live with a higher ongoing risk of secondary major adverse cardiovascular events (MACE), a composite of cardiovascular (CV) death, non-fatal MI, and non-fatal stroke. It has been shown that in about four in 10 people, this risk is directly related to the increased inflammation associated with inflammatory atherosclerosis as measured by a high-sensitivity C-reactive protein (hsCRP) biomarker level of >= 2mg/L[1]. The recurrent MACE in people with inflammatory atherosclerosis are associated with increased morbidity, mortality and reduced quality of life and currently represent a major economic burden on patients and healthcare systems around the world.

About ACZ885
ACZ885 (canakinumab) is a selective, high-affinity, fully human monoclonal antibody that inhibits IL-1ß, a key cytokine in the inflammatory pathway known to drive the continued progression of inflammatory atherosclerosis[6]-[10]. ACZ885 works by blocking the action of IL-1ß for a sustained period of time, therefore inhibiting inflammation that is caused by its over-production[11],[12]. ACZ885 is the first and only agent which has shown that selectively targeting inflammation significantly reduces cardiovascular risk in patients who have had a prior heart attack and have an increased cardiovascular inflammatory burden.



[1] Ridker P. How Common Is Residual Inflammatory Risk? Circ Res. 2017;120:617-619
[2] Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association. Circulation. 2017;135:e146-e603
[3] EU5 MI trend. Based on Eurostat discharge data. Novartis data on file.
[4] Mozaffarian D, et al. Heart Disease and Stroke Statistics – 2016 Update: A Report From the American Heart Association. Circulation. 2017; 135(23):e1-324.
[5] Roth G, et al. Global, Regional, and National Burden of Cardiovascular Diseases for 10 Causes, 1990 to 2015. JACC. Available online May 17, 2017.
[6] Fearon WF, Fearon DT. Inflammation and cardiovascular disease: role of the interleukin-1 receptor antagonist. Circulation. 2008;117:2577-2579.
[7] Duewell P, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464(7293):1357-61.
[8] Rajamaki K, et al. Cholesterol Crystals Activate the NLRP3 Inflammasome in Human Macrophages: A Novel Link between Cholesterol Metabolism and Inflammation. PLoS One. 2010; 5(7):e11765.
[9] Ridker PM, Luscher TF. Anti-inflammatory therapies for cardiovascular disease. Eur Heart J. 2014; 35(27):1782-91.
[10] Ridker PM. From C-Reactive Protein to Interleukin-6 to Interleukin-1. Circ Res. 2016; 118:145-156.
[11] Ridker PM, et al. Effects of Interleukin-1ß Inhibition with Canakinumab on Hemoglobin A1c, C-Reactive Protein, Interleukin-6 and Fibrinogen. Circulation. 2012; 126(23):2739-48.
[12] Ridker PM, et al. Interleukin-1ß inhibition and the prevention of recurrent cardiovascular events: rationale and design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS). Am Heart J. 2011; 162(4):597-605.


Beetroot Juice May Provide Benefits to Heart Disease Patients

Beetroot Juice May Provide Benefits to Heart Disease Patients

Nitrate supplementation [Beetroot Juice] decreases sympathetic nerve responses that contribute to heart disease risk

Bethesda, Md. (May 10, 2017)—A new study finds that dietary nitrate—a compound that dilates blood vessels to decrease blood pressure—may reduce overstimulation of the sympathetic nervous system that occurs with heart disease. The research team looked specifically at beetroot juice, a source of dietary nitrate, to explore its use as a future targeted treatment option for people with cardiovascular disease. The study, published ahead of print in the American Journal of Physiology—Heart and Circulatory Physiology, is the first to study the effects of nitrate supplementation on sympathetic nerve activity.

Activation of the sympathetic nervous system—caused by increased sympathetic nerve activity—results in elevated heart rate and blood pressure and blood vessel constriction. Sympathetic nerve activity (sympathetic outflow) also increases with some forms of cardiovascular disease, including high blood pressure and heart failure. The aim of the study was to show that “acute nitrate supplementation using beetroot juice can decrease muscle sympathetic outflow at rest and during exercise,” the Canadian research team wrote.

Twenty young adult volunteers (average age: 27) participated in two separate testing visits in which they blindly received either a nitrate supplement or a placebo. On both visits, the research team recorded the blood pressure, heart rate and muscle sympathetic nerve activity (MSNA) and measured muscle activity at rest and during handgrip exercise with the participants’ non-dominant hand. Measurements were recorded at the beginning of the visit and then again after the volunteers drank nitrate-rich beetroot juice or a placebo and had rested on their backs for three hours.

MSNA burst rate, denoting the frequency of nerve activity, was lower when the volunteers drank beetroot juice compared to when they drank the placebo. Sympathetic nerve activity also decreased during exercise. “Surprisingly, no differences in blood pressure were detected at rest or during exercise,” the research team noted. “These results provide proof-of-concept that dietary nitrate supplementation can modulate central sympathetic outflow and suggest that the established cardiovascular benefits [of dietary nitrate] are likely to involve a neural contribution.”

The article, “Acute beetroot juice supplementation on sympathetic nerve activity: A randomized, double-blind, placebo-controlled proof-of-concept study,” is published ahead of print in the American Journal of Physiology—Heart and Circulatory Physiology.


Pumping Marvellous Note: Remember that Beetroot is incredibly easy to grow at home in the UK, and needs little maintenance beyond the initial sow and thinning. Choose a hardy variety like Boltardy or one of the may other delicious varieties. Give it a grow!

Click here for more heart news >

Favourable Effects of Vitamin D in Chronic Heart Failure - VINDICATE Study Dr Klaus Witte

Favourable Effects of Vitamin D in Chronic Heart Failure – VINDICATE

Favourable effects of vitamin D on cardiac function in patients with chronic heart failure secondary to left ventricular systolic dysfunction – the results of the MRC-funded VINDICATE Study

A daily dose of vitamin D3 improves heart function in people with chronic heart failure, a five-year University of Leeds research project has found. Dr Klaus Witte, from the Leeds University School of Medicine and Leeds Teaching Hospitals NHS Trust, led the study, known as VINDICATE, and here share his thoughts with us and our heart failure community.

“This is a significant breakthrough for patients. It is the first evidence that vitamin D3 can improve heart function of people with heart muscle weakness – known as heart failure. These findings could make a significant difference to the care of heart failure patients,” said Dr Witte.


Chronic heart failure is due to reduced pumping function of the heart and affects about 900,000 people in the UK and more than 23 million worldwide. The condition can affect people of all ages, but it is more common in older people – more than half of all people globally with heart failure are over the age of 75.


The most frequent cause of heart failure is heart muscle damage following a heart attack although high blood pressure, heart valve problems and infections can also lead to heart failure. The weakness is reflected by symptoms of shortness of breath and fatigue. Despite very good therapies including tablets and in some patients special pacemakers, many people with heart failure have persistent symptoms, and the heart muscle weakness remains.


“We found that almost all patients with heart failure in Leeds were deficient in vitamin D and that the degree of deficiency related to markers of severity. Vitamin D3 levels are largely dependent upon exposure to sunlight, yet levels are low throughout the year because heart failure patients are often older, spend less time in the sun, and also make less vitamin D3 in response to sunlight than younger people. Vitamin D3 production in the skin is also reduced by sunscreen.”


Vitamin D is known to have bone strengthening effects by improving calcium deposition in the skeleton, yet the substance is involved in many other systems, including muscle contraction, immune function, and insulin release, all of which may be abnormal in patients with heart failure. Up until now, there were no data suggesting that replacing vitamin D has any benefit in patients with heart problems.


The study, which was funded by the Medical Research Council, involved more than 160 patients from Leeds who were already being treated for their heart failure using proven treatments including beta-blockers, ACE-inhibitors and pacemakers.

Participants were asked to take 4,000 IU [100 μg] vitamin D3 or a dummy (placebo) tablet daily for one year. Those patients who took vitamin D3 experienced an improvement in heart function which was not seen in those who took a placebo.


Dr Klaus Witte and team, from the Leeds University School of Medicine and Leeds Teaching Hospitals NHS Trust


Changes in heart function were measured by cardiac ultrasound (known as an echocardiogram). This allows us to measure how much blood pumps from the heart with each heartbeat, known as ejection fraction. The ejection fraction of a healthy person is usually between 60% and 70%. In heart failure patients, the ejection fraction is often significantly lower – in the patients enrolled into the VINDICATE study the average ejection fraction was 26%. In the 80 patients who took Vitamin D3, the heart’s pumping function improved from 26% to 34%. In the others, who took placebo, there was no change in cardiac function.


“One key aspect of this study is that we avoided using a calcium-based supplement, as calcium can cause further problems for heart failure patients. Crucially, the tablets were well tolerated by our patients and we saw no important side effects on kidney function.”


The findings from the VINDICATE study were presented at the American College of Cardiology 65th Annual Scientific Session & Expo in Chicago on April 4, 2016.


“In conclusion, we have shown for the first time that a high dose of vitamin D taken daily is safe and improves heart function in patients with heart failure. The next step is to use the information from this study to find out if improving the heart function reduces hospital admissions and extends the life of patients with heart failure. To this aim we have submitted an application to the National Institute of Health Research in the UK for VINDICATE 2 which will involve 1278 people with heart failure across the country for 4 years. The team at Pumping Marvellous have provided valuable advice in the development of VINDICATE 2 so please check back here to hear about the status of our application and, if funded, the status of the trial,” said Dr Klaus Witte.



Dr Klaus Witte MD, FRCP, FESC, FACC Associate Professor and Consultant Cardiologist
Dr Klaus Witte MD, FRCP, FESC, FACC

Dr Klaus Witte MD, FRCP, FESC, FACC Associate Professor and Consultant Cardiologist

NIHR Clinician Scientist

University of Leeds and Leeds Teaching Hospitals NHS Trust





One year of 4000 IU 25(OH)-Vitamin D3daily in heart failure with impaired cardiac function
One year of 4000 IU 25(OH)-Vitamin D3daily in heart failure with impaired cardiac function
TYRX™ Absorbable Antibacterial Envelope

Infections Down With Antibacterial Envelope for ICD/CRT

Clinical use of antibacterial envelope mesh cuts infection rate for ICD/CRT implants

The TYRX Absorbable Antibacterial Envelope and the TYRXNeuro Absorbable Antibacterial Envelope are the first commercially available implantable medical devices designed to stabilize Cardiac Implantable Devices  [CRTs and ICDs] and Implantable Neurostimulators [INSs] and to help reduce their infection.

Medtronic PLC has signed up more than 140 U.S. hospitals and clinics in a program that aims to cut infection rates in heart devices using its innovative dissolvable surgical antibacterial envelopes and rebates. Medtronic are confident in the Tyrx envelope’s ability to reduce infection rates and are signing “risk sharing” agreements with health care providers [in the US] that say the company will pay a substantial rebate toward the high cost of removing an infected Medtronic device and implanting a new one, if a Tyrx envelope was used in the original surgery and an infection sets in anyway.

Infection rates for pacemakers, implantable defibrillators and cardiac resynchronization therapy (CRT) devices vary. But in general, it is purported that more complex devices like CRTs are more prone to infections, and so are replacement devices, which are placed in the fibrous “capsule” of scarlike tissue that formed around the original device, where it is more difficult to fight infection.

A contemporary absorbable version is currently under evaluation in the prospective World-Wide Randomized Antibiotic Envelope Infection Prevention Trial (WRAP-IT) randomized trial [enrolling now by invitation], with a projected enrollment of more than 7700 patients receiving ICD or CRT upgrades or replacements.

Source: Antibacterial Envelope Is Associated With Low Infection Rates After Implantable Cardioverter-Defibrillator and Cardiac Resynchronization Therapy Device Replacement
Charles A. Henrikson, M. Rizwan Sohail, Helbert Acosta, Eric E. Johnson, Lawrence Rosenthal, Roman Pachulski, Dan Dan, Walter Paladino, Farhat S. Khairallah, Kent Gleed, Ibrahim Hanna, Alan Cheng, Daniel R. Lexcen, Grant R. Simons
JACC: Clinical Electrophysiology May 2017, 388; DOI: 10.1016/j.jacep.2017.02.016