Optical Coherence Tomography: Modest Benefit in PCI

ROME, ITALY — The first randomized trial to investigate the use of optical coherence tomography (OCT) in PCI has suggested that the procedure is safe and may be associated with some benefit[1].

The DOCTORS study was presented today at the European Society of Cardiology (ESC) 2016 Congress and simultaneously published online in Circulation.
The OCT technology visualizes the artery and stent placements, allowing the operator to make alterations on stent expansions and positioning. The intravascular procedure allows improved plaque characterization and can lead to improvements in lesion coverage, stent expansion, or apposition, explained lead investigator Dr Nicolas Meneveau (University Hospital Jean Minjoz, Besançon, France). Downsides of its use include prolonged procedural time and higher exposure to contrast media, as well as the cost issue.
The main result of DOCTORS study showed a modest 2-point improvement in fractional flow reserve (FFR) in NSTEMI patients undergoing PCI guided by OCT compared with those undergoing PCI guided by fluoroscopy alone.
Meneveau said: "This is a small absolute benefit in FFR, but it was statistically significant." Asked whether this would be clinically relevant, he said couldn't comment on that, although it is known that an increase in FFR is associated with a reduction in clinical outcomes. "We obviously need a clinical end-point study to look at clinical benefit," he commented
He added: "But we did show that OCT affected physician decision making, leading to a change in procedural strategy in half of cases, most commonly optimization of stent expansion. The benefit was obtained at the cost of a longer procedure with higher fluoroscopy time and more contrast medium, but without an increase in periprocedural MI or kidney dysfunction."
Meneveau said he also could not comment on whether the benefit shown in this study was worth the additional exposure to contrast media.

"Important Milestone "
In an accompanying editorial in Circulation[2], Dr William Wijns (National University of Ireland, Galway) and Dr Stylianos A Pyxaras (Medizinische Klinik, Coburg, Germany) note that invasive imaging such as OCT or intravascular ultrasound (IVUS) is used extensively in Japan and a little in the US and Asia but is almost nonexistent in Europe. They say that the intracoronary images obtained with these approaches give the physician significant information, but their use is restricted by reimbursement issues, as they have not been shown to affect patient outcomes. They therefore describe the DOCTORS study as an "important milestone" to accumulate global evidence to support the role of OCT guidance during complex PCI and to extend the guidelines supporting its use.

"Safety Encouraging" Senior author of the study, Dr François Schiele (University Hospital Jean Minjoz, Besançon, France), told heartwire from Medscape that he was encouraged by the safety results in the study. "When the DOCTORS study was conceived, I was concerned about possibility of side effects, as this is a very invasive intervention and prolongs the PCI procedure. But we didn't show any harm. The safety side actually looks good. This is valuable information, as OCT is widely used in many centers and we need to know that it is safe." On the benefit, Schiele said: "Although the overall benefit was only two units in FFR, which is a modest amount, it could have an impact. We know that an increase in FFR is linked to reduced outcomes. But for some patients the FFR increase was much higher and would be likely linked to a clinical benefit." He explained that at present OCT is often used before PCI if information is missing on angiography, particularly if it is an important artery such as the left main that is being stented. "But actually we found that it gave us much more useful information after stenting to identify incomplete expansion or malapposition . . . so we can fix those problems."

For the study, 240 NSTEMI patients were randomized to OCT-guided PCI (use of OCT pre- and post-PCI) or to standard fluoroscopy-guided PCI.

Results showed that OCT use led to a change in procedural strategy in 50% of patients. Post-PCI OCT revealed stent underexpansion in 42% of patients, stent malapposition in 32%, incomplete lesion coverage in 20%, and edge dissection in 37.5%. This led to the more frequent use of poststent overdilation in the OCT-guided group vs the angiography-guided group (43% vs 12.5%, P

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Gene discovery points to new treatments for heart disease

The findings could also lead to new treatments for other common diseases.

A gene discovery could pave the way for the development of new treatments for heart disease, after researchers found that it is responsible for blood vessel formation, or angiogenesis. The findings have resulted from an international research collaboration part-funded by the British Heart Foundation (BHF). The paper was published in the journal Nature Communications.

Researchers found that when they turned off the gene, called Wars2, in rats and zebrafish, there was reduced blood vessel growth both in the heart and throughout the rest of the body. This has confirmed the vital role of the Wars2 gene in blood vessel formation.

The Wars2 gene has previously been linked to obesity and cancer in large genetic studies, known as Genome Wide Association Studies (GWAS), which look for versions of genes which are common among people with a disease. Researchers are able to see if a gene is associated with a particular condition.

The heart muscle relies on a constant supply of blood, to keep blood pumping around the body. Coronary heart disease is just one of the diseases where this supply of blood is implicated, and the heart muscle has a reduced blood supply. The discovery of the Wars2 gene will allow scientists to test new molecules to find ways of enhancing the effect of the gene to increase the blood supply to the heart.

In contrast, diseases such as breast cancer, could be targeted with treatments aimed at blocking the function of the gene. Cancerous tumours rely on a blood supply which provides them with nutrients and oxygen in order to grow and proliferate. Blocking Wars2 and reducing blood vessel formation could starve tumour cells from the outside in.

Professor Stuart Cook, who led the study, is head of the Cardiovascular Genetics and Genomics group within Genetics & Imaging at the National Heart and Lung Institute (NHLI). He said:

"Angiogenesis is vital for supporting life and providing nutrients to all parts of the body.

"Finding a way to control angiogenesis not only provides a target for the development of anti-cancer therapies, but may also prove useful in similarly starving abnormal blood vessel growth elsewhere in the body, like in diabetic eye disease."

Dr Rizwan Ahmed, at Royal Brompton & Harefield NHS Foundation Trust, who worked on the study, said: "We are now one step closer to improving heart function in people with an obstructed or reduced blood flow to the heart muscle. Our findings could lead to new treatments to stimulate blood vessel production in the heart. "The next step is to find medications to activate blood vessel production specifically in the heart muscle, using this gene. This research was an important step forward to help us target a gene known to be important in a range of conditions."

Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation, which helped fund the research, said: "This careful genetic study has found a new gene that controls cardiac blood vessel growth, opening up the potential for new therapies to enhance blood supply to the failing heart. "This new insight into the role of Wars2 in blood vessel growth will allow researchers around the world to explore a fresh new target to treat diseases which are characterised by impaired blood vessel formation."

The research was also supported by the Medical Research Council (MRC), Leducq Foundation, Tanoto Foundation Singapore, NMRC Singapore, Goh Foundation Singapore, Ministry of Education, Youth and Sports of the Czech Republic, The Czech Science Foundation, NIHR Cardiovascular Biomedical Research Unit at Royal Brompton & Harefield NHS Foundation Trust, London, UK. European Union EURATRANS award, Helmholtz Alliance ICEMED, Deutsche Forschungsgemeinschaft from Grant Agency of the Ministry of Health of the Czech Republic.
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Virtual heart reveals new clues to heart failure

Scientists have produced a detailed computer model of a heart that shows the electrophysiology of congestive heart failure, according to a study published in PLOS Computational Biology.

Congestive heart failure (CHF) is a leading cause of death in the United States.
According to the Centers for Disease Control and Prevention (CDC), around 5.7 million Americans have heart failure.

About half of the people who are diagnosed with this condition die within 5 years of diagnosis.

Heart failure does not mean that the heart has stopped, or will stop, completely. It refers to a condition in which the heart is not able to pump enough blood for the body to function properly. As a result of heart failure, fluid and blood can back up into the lungs, the person may experience tiredness, breathlessness, and edema, or a buildup of fluid in the legs, ankles, and feet.

Heart failure can happen as a result of coronary artery disease, high blood pressure, and diabetes.
It is more likely to affect people over the age of 65 years, and especially those who are overweight. People who have previously had a heart attack are more at risk. It tends to affect men more than women. However, the mechanisms that cause it, including its electrophysiological (EP) mechanisms, are not well understood. It is hoped that the new "virtual heart" could benefit the development of new drugs to treat the disease.

Tweaking an existing model gives insight into heart's workings The researchers, from the University of California-San Diego, CA, modified an existing model of a healthy rabbit heart to create their simulation.

The model is able to simulate small changes in the heart, from the cellular and tissue levels, up to the whole heart.

An electrocardiogram (ECG) is a tool commonly used by doctors use to diagnose heart abnormalities.

The team hopes to use the numerical model they have created to link changes that occur at the cellular and tissue level when a heart fails to a numerically computed ECG. This, they hope, will help to pinpoint what it is that triggers ventricular fibrillation (VF), and to identify the risk of VF.

At the cellular and tissue levels, the model can replicate the heart's reactions to changes in the levels and flow of calcium, sodium, and potassium. It also can take into account the speed at which the ion channels - which take in those ions - function. At the whole-heart level, it can also show what happens in a healthy, working heart as a result of variations in the different critical chemicals and electrophysiologic components.

New insight into VF VF is a common cause of sudden death. During VF, the electrical waves that occur in the heart break up chaotically. When this happens, it affects the timing of the heart's pumping action. The heart can no longer contract and pump blood to the rest of the body.

Using the new model, researchers in the current study found that this fragmentation and loss of coordination can be caused by a slowdown in cellular processes at the top of the heart. This can lead to heart failure. To learn more about the causes of VF in a person with heart failure, the team set up a test that would simulate a person with heart failure performing physical exercise.
The results suggest that a patient with heart failure who experiences a fast heart rate and variable pacing will be more susceptible to VF. This, they say, is because of a newly identified mechanism that blocks conduction.

The researchers have shown that the model can be used to plan a new drug strategy to prevent the type of fibrillation that is associated with heart failure.
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Death risk higher than heart attack but care lags 30 years behind.

Death risk higher than heart attack but care lags 30 years behind.
The first European advice on emergency care for patients with acute heart failure is published in European Heart Journal: Acute Cardiovascular Care. Acute heart failure carries a higher risk of death than heart attack but care lags 30 years behind.

"Only half of patients discharged with acute heart failure are alive in three years."

"Mortality from acute heart failure is even higher than from a heart attack so it is an urgent situation," said Professor Christian Mueller, chair of the Acute Heart Failure Study Group of the Acute Cardiovascular Care Association (ACCA) of the European Society of Cardiology (ESC).

"Only half of patients discharged from hospital with acute heart failure are alive in three years, even though they felt fine," he continued. "Despite the severity of the condition there are no standard treatment pathways, whereas these were agreed across Europe for heart attack 30 years ago. The paper published today is the first step towards catching up with heart attack care and establishing similar standards for acute heart failure."

Acute heart failure is a chronic disorder that flares up and leads to emergency visits. The vast majority of patients present to an emergency department with sudden and severe shortness of breath (called acute dyspnoea) at rest. In 50% of patients the underlying condition is chronic heart failure. The other 50% could have had a heart attack ten years ago, or their underlying heart condition is undiagnosed.

"Most patients with acute heart failure cannot be cured," said Professor Mueller. "We can effectively treat the acute flare ups of dyspnoea with vasodilators or diuretics that remove the extra fluid on the lungs. But the underlying progressive disease remains and patients need long term follow up to make sure they are on the correct medication at the right dosages."

The paper published today focuses on the pivotal decision of whether to discharge patients with acute heart failure from the emergency department and see them as outpatients, or to admit them to hospital. Until now there was no guidance on this issue. The result is that emergency physicians have tended to act conservatively and admit patients to hospital.

"The hospital is not always the best place to care for acutely ill patients," said Professor Mueller. "While in hospital, patients with acute heart failure - who are 78 years old on average - are at risk of developing infections and they have problems sleeping. There is also pressure on hospitals to avoid expensive admissions when possible. But patients do benefit from more intense follow up while in hospital."

The paper outlines criteria to help clinicians select patients that can be safely discharged from the emergency department. A novel algorithm shows the order of decisions to be made and what to consider at each step.

Professor Mueller said: "The paper aims to kick start the process of emergency medicine physicians and cardiologists joining forces to apply or adjust the algorithm so that it works locally. The patient pathway and decisions on place of treatment will vary depending on reimbursement policies and logistics."

The importance of long term follow up is emphasised, regardless of whether patients are discharged directly from the emergency department or spend a period in hospital before being sent home. Follow up planning should be done by the emergency team in collaboration with the general practitioner (GP), cardiologist, and others involved in the patient's long term care.

"It's never ever possible to treat acute heart failure sufficiently in 24 hours in the emergency department," said Professor Mueller. "Intense follow up will always be needed. It's the task of the emergency department physician to either make the first follow up appointment or to ensure that this will occur. Patients should be seen by their GP within 48 hours to fine tune the number of drugs and their doses, and assess vital signs, blood pressure, electrolytes and kidney function."

He concluded: "Ultimately we hope this guidance will improve the management of patients with acute heart failure and make some inroads towards giving them a better outlook."



Researchers show simple test could predict what happens after a heart attack

Research presented at the British Cardiovascular Society (BCS) Conference has proven that a wire inserted into an artery which supplies blood to the heart, called a coronary artery, after someone has a heart attack can predict if they will go on to develop heart failure.

The study, from the University of Glasgow and funded by the British Heart Foundation (BHF) uses a pressure- and temperature-sensitive wire which can be used to accurately work out the extent of injury in a blood vessel supplying blood to the heart. They discovered that this test - known as the index of microvascular resistance or IMR - can be used to predict if someone is likely to go on to develop heart failure or even die.

There are around 175,000 heart attacks in the UK each year1 - one every three minutes. For those who survive a heart attack there is a risk that the heart will have been damaged and this can lead to heart failure. Heart failure can have a huge impact on a person's life, leaving them tired, short of breath and unable to do simple tasks like walk or take a shower by themselves. Early treatment following a heart attack can reduce the chance of heart failure and improve a person's wellbeing and chances of survival.

After a suspected heart attack, a patient is routinely given a coronary angiogram to identify any narrowed blood vessels. An angiogram visualises the affected blood vessels using a catheter threaded towards the heart from a distant blood vessel in the arm or leg. Currently, cardiologists make treatment decisions based on this standard assessment technique but it can only identify narrowed vessels and cannot tell the doctor if, or how much, heart blood vessel damage has occurred.

The wire technique can be used to work out the level of damage to the arteries in a matter of minutes. This allows doctors to quickly and accurately identify patients who are at a high risk of heart failure after their heart attack based on the damage to their arteries.

The patients who took part in this new research were enrolled in the Golden Jubilee National Hospital. All heart attack patients were eligible to take part to allow the findings to be applied to all heart attack patients in the future. Patients who took part in the project will have life-long follow-up to see if the IMR result predicts survival in the long term. The BHF also funded this follow-up so that the patients' long-term health can be assessed.

Professor Colin Berry, lead researcher and cardiologist from the University of Glasgow and Golden Jubilee National Hospital, said:
"Heart attacks lead to heart failure which is a big problem in the UK, and has a huge impact not only on the individual, but on the families and carers of those suffering - affecting whole communities.

"Thanks in large part to the work of the British Heart Foundation, 70 per cent of people who have a heart attack now survive, but this means we now see an increased number of people surviving but left with damaged hearts and heart failure.

"We want to improve the outlook for people after they have a heart attack and develop new treatments to limit heart damage, reducing the burden of heart failure."

The pressure wires used in this study were supported by funding from the Golden Jubilee National Hospital and the Chief Scientist Office of the Scottish Government.

Professor Jeremy Pearson, Associate Medical Director at the BHF, which funded the study, said:
"More and more people are surviving heart attacks due to the huge advances we've made in cardiology, but that isn't the end of the story. A heart attack causes damage which can leave a person facing a horrendous daily struggle.

"If we can identify the people at greatest risk of developing heart failure following a heart attack, and treat them more quickly, we could reduce the effects that these terrible events can have on individuals and communities. What we need now is for the public to help us fund more research to find possible new treatments for people with heart failure."

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Cardiovascular disease (CVD) kills 51% of women in Europe and breast cancer kills 3%

Cardiovascular disease (CVD) kills 51% of women in Europe and breast cancer kills 3%, bucking the misperception that CVD is a man's disease. CVD is the top killer in women and is largely preventable. The call for women to reduce their risk comes from the European Society of Cardiology (ESC) on International Women's Day.

Dr Susanna Price, ESC spokesperson and consultant cardiologist at the Royal Brompton Hospital in London, UK, said: "CVD is still largely considered a man's problem with breast cancer commonly perceived as the greater issue for women. However, CVD is the top killer of women in Europe, resulting in 51% of deaths compared to 3% caused by breast cancer." 1

She added: "Women's risk of heart disease tends to be underestimated by both the public and the medical profession because of the perception that oestrogen protects them. In reality this just delays the onset of CVD by 10 years.2 The result is that women's risk factors are left untreated, leaving them more vulnerable to heart attack, heart failure and sudden cardiac death when the protection fades after menopause."

Despite these misconceptions, the facts are that:

CVD is the main cause of death in women in all countries of Europe3 CVD causes 51% of deaths in women and 42% of deaths in men in Europe1 CVD kills 51% of women in Europe and breast cancer causes 3% of deaths1 The risks of smoking are higher in women because women metabolise nicotine faster, especially those taking oral contraceptives2 Type 2 diabetes doubles CVD risk in men but more than triples the risk in women4 Women are more likely to be severely disabled after a stroke than men5. "Another reason CVD is under-recognised and under-treated in women is that they can have different or atypical symptoms," said Dr Price. "Instead of chest pain, women having a heart attack may experience nausea/vomiting, shortness of breath, jaw pain, fatigue, palpitations, syncope (fainting) or cardiac arrest6, 7. They need to call the emergency number urgently as soon as the symptoms of a heart attack or stroke start."

Stroke symptoms include sudden numbness or weakness of the face, arm and/or leg, especially on one side of the body, sudden confusion, trouble seeing, dizziness or sudden severe headache with no known cause.

The effects of CVD are often worse in women than in men. Women are more likely to be severely disabled after a stroke than men, and although they receive greater benefit from clot busting drugs (thrombolysis), fewer receive them.5 This could be because the drugs are most effective 3-6 hours after symptoms begin and women are less likely than men to reach the hospital within this time period.

Compared to men, women less often know the risk factors and take part in screening. Worryingly, the risks of smoking are higher in women because they metabolise nicotine faster, especially those taking oral contraceptives.2 Dr Price said: "In common with men, women can reduce their risk of CVD by not smoking, being active, having a healthy body weight, getting their blood pressure and cholesterol checked and taking treatment if levels are high."

However, women are less likely to receive proven therapies than men, including aspirin, statins, coronary revascularization after an acute coronary event8 and oral anticoagulants to prevent stroke when they have atrial fibrillation, despite their higher risk.5

Women may respond differently to therapy because they have different hormone levels, lower body weight and a higher percentage of body fat. For example aspirin reduces the risk of stroke but does not affect the occurrence of myocardial infarction in women, while in men aspirin reduces the risk of myocardial infarction with a non-significant increase in the risk of stroke.5 But Dr Price said: "In many cases the safety and effectiveness of treatments in women are unknown because they have been tested mainly in men. Clinical trials are needed that include only women and/or more equal proportions of both sexes."

She concluded: "CVD is by far the biggest cause of death in women but is still underestimated as a health problem for them. Greater awareness is needed by women and the medical profession to ensure that women reduce their risk factors and decrease their chances of having a heart attack and stroke."

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Efficacy of a Device to Narrow the Coronary Sinus in Refractory Angina

ORIGINAL ARTICLE Efficacy of a Device to Narrow the Coronary Sinus in Refractory Angina Stefan Verheye, M.D., Ph.D., E. Marc Jolicœur, M.D., Miles W. Behan, M.D., Thomas Pettersson, M.D., Paul Sainsbury, M.D., Jonathan Hill, M.D., Mathias Vrolix, M.D., Pierfrancesco Agostoni, M.D., Thomas Engstrom, M.D., Marino Labinaz, M.D., Ranil de Silva, M.D., Marc Schwartz, R.C.I.S., Nathalie Meyten, M.D., Neal G. Uren, M.D., Serge Doucet, M.D., Jean-François Tanguay, M.D., Steven Lindsay, M.D., Timothy D. Henry, M.D., Christopher J. White, M.D., Elazer R. Edelman, M.D., Ph.D., and Shmuel Banai, M.D. N Engl J Med 2015; 372:519-527February 5, 2015DOI: 10.1056/NEJMoa1402556

BACKGROUND Many patients with coronary artery disease who are not candidates for revascularization have refractory angina despite standard medical therapy. The balloon-expandable, stainless steel, hourglass-shaped, coronary-sinus reducing device creates a focal narrowing and increases pressure in the coronary sinus, thus redistributing blood into ischemic myocardium.

METHODS We randomly assigned 104 patients with Canadian Cardiovascular Society (CCS) class III or IV angina (on a scale from I to IV, with higher classes indicating greater limitations on physical activity owing to angina) and myocardial ischemia, who were not candidates for revascularization, to implantation of the device (treatment group) or to a sham procedure (control group). The primary end point was the proportion of patients with an improvement of at least two CCS angina classes at 6 months.

RESULTS A total of 35% of the patients in the treatment group (18 of 52 patients), as compared with 15% of those in the control group (8 of 52), had an improvement of at least two CCS angina classes at 6 months (P=0.02). The device was also associated with improvement of at least one CCS angina class in 71% of the patients in the treatment group (37 of 52 patients), as compared with 42% of those in the control group (22 of 52) (P=0.003). Quality of life as assessed with the use of the Seattle Angina Questionnaire was significantly improved in the treatment group, as compared with the control group (improvement on a 100-point scale, 17.6 vs. 7.6 points; P=0.03). There were no significant between-group differences in improvement in exercise time or in the mean change in the wall-motion index as assessed by means of dobutamine echocardiography. At 6 months, 1 patient in the treatment group had had a myocardial infarction; in the control group, 1 patient had died and 3 had had a myocardial infarction.

CONCLUSIONS In this small clinical trial, implantation of the coronary-sinus reducing device was associated with significant improvement in symptoms and quality of life in patients with refractory angina who were not candidates for revascularization. (Funded by Neovasc; COSIRA ClinicalTrials.gov number, NCT01205893.) Supported by Neovasc.

Disclosure forms provided by the authors are available with the full text of the article at NEJM.org. SOURCE INFORMATION From Antwerp Cardiovascular Center, Ziekenhuis Netwerk Antwerpen Middelheim, Antwerp (S.V., N.M.), and Ziekenhuis Oost–Limburg Hospital, Genk (M.V.) — both in Belgium; Montreal Heart Institute, Montreal (E.M.J., S.D., J.-F.T.), Ottawa Heart Institute, Ottawa (M.L.), and Neovasc, Richmond, BC (M.S.) — all in Canada; Royal Infirmary of Edinburgh, Edinburgh (M.W.B., N.G.U.), Bradford Royal Infirmary, Bradford (P.S., S.L.), and Kings College Hospital (J.H.) and the National Heart and Lung Institute, Imperial College London, and National Institute for Health Research Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Foundation Trust (R.S.), London — all in the United Kingdom; Kristianstad Central Hospital, Kristianstad, Sweden (T.P.); University Medical Center Utrecht, Utrecht, the Netherlands (P.A.); Rigshospitalet, Copenhagen (T.E.); Cedars–Sinai Medical Center, Los Angeles (T.D.H.); John Ochsner Heart and Vascular Institute, University of Queensland–Ochsner Clinical School, New Orleans (C.J.W.); the Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, and the Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston — both in Massachusetts (E.R.E.); and Tel Aviv Medical Center, Tel Aviv University Medical School, Tel Aviv, Israel (S.B.). Address reprint requests to Dr. Banai at the Tel Aviv Medical Center, 6 Weizman St., Tel Aviv 64239, Israel, or at banais@netvision.net.il.Share/Bookmark
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