Videos uploaded by user “Cardio Debate”
Stress Cardiomyopathy & Takotsubo Syndrome - Prof Abhiram Prasad
Abhiram Prasad, Professor of Interventional Cardiology & Honorary Consultant Cardiologist at St George's Hospital, University of London, UK, speaks to Cardio Debate about stress cardiomyopathy and Takotsubo syndrome. For more interviews please visit www.cardio-debate.com *TRANSCRIPT* Stress cardiomyopathy: What is it? How do you diagnose this and how frequent is it? Stress cardiomyopathy is often considered a relatively new syndrome. It has probably always been around but we’ve just got better at diagnosing it. It probably accounts for about two per cent of all heart attack or myocardial infarction patients, and if you just take women alone it’s probably as high as six per cent of women presenting with myocardial infarction. The diagnosis is a diagnosis of exclusion – so in other words we don’t have a single test that can diagnose this, so different institutions and investigators have put out diagnostic criteria as a result - the Mayo Clinic Criteria is perhaps one of the most commonly used, which has four different criteria in it. And diagnosis is made when all those criteria are met. Essentially you need to exclude conditions that mimic it, for example obviously acute myocardial infarction, but myocarditis, spontaneous coronary artery dissection and so on. These have to be excluded, and then you make the diagnosis of stress cardiomyopathy as a result. Is it benign? When we first recognised the condition we were mostly recognising people presenting with the emotional triggers, and certainly that group of patients seemed to do very well, and long-term outcomes seemed to be quite good. Over time we started recognising patients with all sorts of other triggers, particularly physical triggers in the hospital, sick patients and intensive care units and so on. So some of the more recent data suggest that perhaps the outcomes are not as benign as we thought in the past, and probably very similar to patients with acute myocardial infarction. That said, if you look at patients who survive their initial hospitalisation in many studies the long-term outcomes seem to be very similar to controls and the majority of the deaths seem to be non-cardiac. It’s still a way off ongoing research and we’ll learn a lot more in the years to come. What are the treatments? Again, it’s a condition in which we don’t understand the pathophysiology in detail yet, and until we do so targeted treatments do not exist. So we treat the condition very much like other conditions that present with a reduction in systolic function. So initially it’s very much supportive treatment – treatment of acute heart failure, arrhythmias, and so on, very much like a heart attack – but once the patient has got through that acute period we usually treat them for systolic dysfunction – beta blockers and ACE inhibitors. We don’t know if that helps recovery but we don’t want to miss a patient who has been misdiagnosed, for example, didn’t really have stress cardiomyopathy but say, has a myocardial infarction. I think it’s important not to miss that early window of remodeling so we must treat them with beta-blockers and ACE inhibitors. And then after about 6 to 8 weeks, once repeat imaging has confirmed that the heart function has recovered and indeed the diagnosis was stress cardiomyopathy then the treatment can be tailored a little bit. And at that point we enter the area of the unknown. We don’t really know whether we should continue long-term beta-blockers, or ACE inhibitors for that matter. My personal practice is to stop the ACE inhibitors at that time, at some point after a few months, and then continue long-term beta-blocker therapy with a view of preventing recurrences given that we think the underlying causes is a catecholamine-mediated mechanism.
Views: 4814 Cardio Debate
Microvascular Angina - Prof Juan Carlos Kaski
Juan Carlos Kaski, Professor & Past Director of the Cardiovascular and Cell Sciences research Institute, St George's University of London, UK, speaks to Cardio Debate about microvascular angina. For more interviews like this one please visit www.cardio-debate.com
Views: 1944 Cardio Debate
Sudden death in athletes - Prof Sanjay Sharma
Dr Sanjay Sharma, Professor of Cardiology and Lead for the Inherited Cardiomyopathies and Sports Cardiology Unit, Cardiovascular and Cell Sciences Research Institute. St George's, University of London, UK, speaks with Cardio Debate about sudden death in athletes. Transcript What is the magnitude of the problem of sudden cardiac death in the young in the UK and worldwide? Sudden Cardiac Death is a feared complication of cardiovascular disease in the UK. It affects about 120,000 people in this country, and the vast majority are aged between 50 and 80 years old. Very occasionally a young individual will die suddenly from a heart problem and these deaths clearly cause a lot of concern in the community because they are counter-intuitive and lead to a large number of life years lost. The magnitude of the problem is actually greater than what we once believed, and affects 12 and 16 young individuals per week, and that amounts to between 600 and 1000 deaths (per year). If one imagines that these individuals lose around 50 years of life each, and that these diseases can be detected through simple measures such as ECG, echocardiography, and that there are treatments that actually prevent these deaths, then I think it’s very important that we do try to identify young individuals who might be at risk. How do you identify high-risk patients? The sad thing about this whole thing is that sudden death in young people affects people who are apparently well and look healthy, and have no symptoms at all. In fact 80% of young individuals who die suddenly from heart diseases such as the cardiomyopathies and the ion channel diseases, and congenital accessory pathways of the heart have no symptoms whatsoever and sudden death is the first presentation. It’s important to emphasise that many of these conditions are genetic, therefore it is very important to be aware whether a first-degree relative such as a father, a brother or a sister may also be affected, or may have died prematurely. In individuals who have that sort of family history it’s not very difficult. Those individuals do need comprehensive evaluation for heart muscle diseases and electrical faults. It’s very difficult to identify others because they have no symptoms at all, and some form of screening procedure is required. And probably the most effective screening procedure is the ECG, and this practice is conducted by sporting organisations throughout the UK including the Football Association, the English Institute of Sport, the Rugby Union and the Rugby League. But you can see that it’s confined to the highest echelons of sport, whereas we know that the vast majority of people who die are usually sedentary and recreational, and often of school age – so something a little more elaborate is needed in this country. Who in the UK are carrying our screening programmes to identify patients at high risk of sudden death? In Italy where there is a nationally sponsored screening programme, the ECG has been very useful at detecting young individuals with heart diseases. And since its implication about 30 years ago, sudden death in sport particularly, has gone down from 3.6 per 100,000 to 0.4 per 100,000 and that represents a 90 per cent reduction in sudden cardiac death in sportsmen. There is no nationally sponsored screening programme in the UK, but there are certain charitable organisations such as Cardiac Risk in the Young (CRY) who do promote and perform screening at a cost-effective rate of value of £35 each. And this involves a health questionnaire pertaining to cardiovascular symptoms or a family history, and an ECG. Now the ECG will clearly detect electrical faults such as Wolff-Parkinson-White syndrome, Long QT syndrome and Brugada syndrome, but it will also raise the suspicion of a heart muscle disorder such as hypertrophic cardiomyopathy in which ECG is abnormal in around 95 per cent of cases. In this country, if we do perform the CRY screening programme, which we have done in about 20,000 people here at St George’s, then we find the pick up rate for a very serious condition is 1 in 300. The chance, or the ability to identify a relatively minor congenital abnormality is 1 in 100, at the expense of a false positive rate of less than 4 per cent. Can you give us some clues as to what to look for when trying to characterise individuals who want to engage in sport but may be at a high risk of cardiac events? To read the full transcript for this interview visit www.cardio-debate.com
Views: 1554 Cardio Debate
New insights in the Brugada syndrome - Elijah Behr
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 2800 Cardio Debate
Is early repolarisation a disease? - Andrew Krahn
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 1715 Cardio Debate
High blood pressure: Guidelines for treatment & high pressure goals - Prof Bryan Williams
Bryan Williams, Professor and Chair of Medicine, University College London, UK, talks to Cardio Debate about the guidelines of high blood pressure treatment, how they compare in different countries, and the recent debate about high pressure goals. For more interviews please visit www.cardio-debate.com *TRANSCRIPT* Guidelines and goal blood pressure in patients with cardiovascular disease: What is your recommendation regarding goals to achieve? There has been a lot of debate about how low we should lower blood pressure. I think the thing that’s clear is the conventional target across most guidelines in the world is less than 140/90 mm Hg. So we try and get everyone’s blood pressure on treatment below 140/90 mm Hg. The only caveat to that is people who are over the age of 80 years, who have recently started treatment and in whom it might be difficult to get it down to those levels. And the best evidence we have is that we should target those to be below 150 systolic. So 150 systolic, get below that over the age of 80 years. Less than 140 systolic over 90 for everybody else. Now recently there was a publication, a big study from the United States called SPRINT, which targeted half the population in the study to a blood pressure below 120. And they showed a very significant reduction in mortality associated with cardiovascular disease, and even total mortality. So this has really fuelled the debate over whether we should be thinking about going even lower than 140 as our target for the treatment of hypertension. Now before we jump to that conclusion we have to look at the SPRINT trial, and the kind of patients that went into that trial, and whether or not the result is generally applicable to the entire population or whether it really reflects a recommendation for a sub-population. So the people in SPRINT had a high risk, they either had cardiovascular disease or chronic kidney disease, or they were over the age of 75 years. They did exclude people with diabetes and patients with a previous stroke, so that’s the first thing. And secondly, many of the patients who went into the trial didn’t have particularly high blood pressure, so it wasn’t particularly difficult to get down to those targets. So you can imagine if you see a patient in your typical clinical with a blood pressure of around 170, the idea, if they were 70 years old, trying to get them to below 120 – we all know that practically that would be quite challenging and technically quite difficult. The other thing in SPRINT is that there was a significant increased risk of developing some side effects, hypotension, dizziness, renal impairment associated with the lower targets. So it didn’t come free – there was an offset in this trial. So I think the data has stimulated debate, I don’t think it’s a definitive outcome. How do I interpret it in my practice? What I tend to do is I get everyone below 140. Then if I’m dealing with a patient who is quite high risk for cardiovascular disease – previously had a stroke, previously had a myocardial infarction, I will say to that patient ‘If you’re feeling okay at 135, we could try and go a bit lower. And it’s possible, if you tolerate that treatment, that you’ll get some added value from that.” So I think what SPRINT has done is given justification to doctors to think about being more aggressive in patients who tolerate lower blood pressures than the conventional target, but we need to monitor them closely to make sure that they are tolerating this, and they are not running into any problems. Should there be the same target blood pressure for everybody? To read the rest of the transcript please go to www.cardio-debate.com/cardio-interviews
Views: 1675 Cardio Debate
Treatment of Atrial Fibrillation - Dr Mark Gallagher
Dr Mark Gallagher, Consultant Electrophysiologist at St George's NHS Foundation Trust in London, UK, speaks with Cardio Debate & Radcliffe Cardiology about Treatment of Atrial Fibrillation during the "Advances in the Pathogenesis and Management of Cardiovascular Disease" 2015 meeting, organised by the Cardiovascular Sciences Research Centre of St George's University and held at the Royal College of Surgeons of England in London, UK. TRANSCRIPT My name is Mark Gallagher, I’m a cardiologist and interventional electrophysiologist at St George’s University Hospital, London, UK. How effective is ablation for treatment of AF? Ablation is the most effective treatment we have for atrial fibrillation. It is particularly effective in paroxysmal atrial fibrillation, and particularly when paroxysmal atrial fibrillation is of relatively recent onset. Easier in structurally normal hearts, more effective in structurally normal hearts, and more effective in younger patients. However, even in older patients, even in patients in their seventies, even in persistent atrial fibrillation that has been present for a year or two – it is quite effective, and is more effective than any of the alternative treatments such as antiarrythmic drugs or just repeated cardioversion. Now when I speak of ablation I speak of catheter ablation or surgical ablation. There are strengths and weaknesses of either of those approaches, but ablation overall is far more effective than any of the alternative treatments to normalize the rhythm in atrial fibrillation. When is it indicated? Well it is indicated for the treatment of symptomatic atrial fibrillation. So in the asymptomatic patient it is still not really clear. There is some evidence to suggest that AF ablation may improve prognosis, but it’s not really clear-cut – not enough to offer it for that indication alone. It is effective in removing atrial fibrillation and therefore removing the symptoms associated with atrial fibrillation, and so it is for the symptoms that we use it. What are the current and future challenges? Well the challenge is to deliver the therapy that is required to enough patients – to do so very safely, and effectively – to cure people on their first procedure. At present we have to do repeat procedures in a substantial proportion of the patients who come for treatment of persistent atrial fibrillation. For paroxysmal atrial fibrillation we’re already pretty good at curing at the first procedure, but for persistent atrial fibrillation it often takes two or more. So the big challenge is to cure those patients on first procedure, to cure a large proportion of them on the first procedure. And to do so with a minimal risk of complications, to keep the risk of all complications below one per cent, to keep the mortality of these procedures down to, say, less than one in 10,000. I think that would be a realistic objective. For more interviews please visit www.cardio-debate.com
Views: 1363 Cardio Debate
ESC 2015: MV Angina treatment: improving vascular function, preventing coronary artery spasm
Microvascular angina is associated with a reduction in blood flow caused by constriction of the small arteries or the inability of the arteries to dilate. Here, at the ESC 2015, Professor Juan Carlos Kaski, Director of the Cardiovascular and Cell Sciences Research Institute at St George’s University of London, UK, talks about how improving the function of the arteries will prevent coronary artery spasm. For more in-depth insight and analysis on issues in cardiology visit the Cardio Debate website: www.cardio-debate.com TRANSCRIPT Microvascular angina is a condition which affects a fairly large amount of people. This condition is essentially based on the presence of reduction in blood flow, caused by either constriction of the arteries of a lack of an ability for these arteries to dilate. And this happens in the presence of completely normal coronary arteries, which is something that has puzzled physicians throughout the years. For many years the condition was not believed to be a real one, and only a few aficionados would actually be keen to propose this diagnosis. But nowadays we have obtained a fairly good deal of evidence that actually allows us to say categorically that microvascular dysfunction leading to microvascular angina is a condition that needs to be treated. Identifying the condition is number one in terms of treating the patient. The second is to find out why the patient has microvascular angina. And there are many tests that we can use in clinical practice to detect that. But once we have identified that the patient is normal, they have angina and there are objective evidences for the presence of myocardial ischemia then we really need to treat these patients accordingly. Many cardiologists still dismiss the idea that the individual has chest pain due to coronary problem, mainly because the arteries are normal. But we now know that there are specific conditions and that is basically improving the function of the arteries and preventing coronary artery spasm.
Views: 1125 Cardio Debate
Catheter ablation in Atrial Fibrillation - CardioEd - Dr Riccardo Cappato
In this free-access CardioEd resource from the recent Cardiology Update 2016 meeting organised by St George's University of London, UK, Dr Riccardo Cappato, Head of Research Institute Electrophysiology and Clinical Arrhythmology at Humanitas Hospital in Milan, Italy, talks about catheter ablation in atrial fibrillation. The Cardiology Update 2016 meeting focused on heart failure management and stroke prevention in patients with atrial fibrillation. For more free-access OnlineMedEd resources visit www.cardio-debate.com *TRANSCRIPT* What are the two most important developments in the management of atrial fibrillation from the viewpoint of an electrophysiologist in the past two years? I would not dichotomise this into two separate fields because the two most relevant fields belong to the same specific field – the first was the introduction of catheter ablation of atrial fibrillation, and the second was its cautious development over the last few years. It was first introduced in 2000, and it addressed for the first time the option of a curative treatment of atrial fibrillation. A century-long lasting recognised arrhythmia for humankind that was always untreatable before. So this was an enormous paradigm shift in our capacity for approaching atrial fibrillation. However, the first outcomes were not as optimal as we might expect at a time when we first recognised that we were able to do it. When we first recognised this, we thought ‘its fixed’ and our expectation was enormously high – say 85 to 90% success rate for every person who would approach atrial fibrillation with catheter ablation. But we soon recognised that success rates were much lower, and recurrence would occur at a later stage, in 70 to 80% of the population. So it was only 20 to 30% of the initial population undergoing catheter ablation in atrial fibrillation that was really fixed by that procedure – which was still an enormously relevant outcome, but less so than expected based on the original findings. When we recognised that more was required in order to improve and increase the number of patients who would be fixed with catheter ablation, we soon developed mapping and ablation strategies that would increase the original findings. And we can now say that catheter ablation of paroxysmal atrial fibrillation can be fixed in 70 to 80 % of the patients presenting with this arrhythmia, and that persistent atrial fibrillation can be fixed in about 50% of the patients - and this by the first ablation procedure. I think these are the two most relevant findings. And now many patients who previously were resigned to living with AF their entire life can enjoy a life of normal sinus rhythm after catheter ablation.
Views: 464 Cardio Debate
ESC 2015: Dose lowering inflammation lower vascular risk? Paul Ridker M.D
Paul M. Ridker, M.D., talks to Cardio Debate about his presentation at the ESC 2015 that examines whether lowering inflammation lowers vascular risk. “We know that lowering cholesterol profoundly lowers event rates. The question is, is the residual risk our patients have driven by cholesterol, or is it also driven by this inflammatory response?” For more in-depth insight and analysis on issues in cardiology visit the Cardio Debate website: www.cardio-debate.com TRANSCRIPT For the past 25 years we’ve been trying to figure out a way, clinically, to address whether lowing inflammation par se will lower cardiac event rates. We showed many years ago that markers of inflammation predict risk, and then we showed that statin drugs lower both inflammation and cholesterol. Then we did our very large-scale JUPITER trial – 18,000 patients around the world showing that if you select people because they have a high inflammatory burden and then give them a cholesterol-lowering drug, they have far fewer event rates. But that trial looked at a lipid-lowering drug that has anti-inflammatory effects. So the next stage has been, can we focus down to agents that have pure anti-inflammatory effects that do not affect cholesterol at all? So we have two trials that are ongoing, one – funded by the United States National Heart, Lung and Blood Institute – is looking at a very commonly used drug, methotrexate, that millions of people take to treat their rheumatoid arthritis. It’s the standard of treatment for rheumatoid arthritis around the world. That drug happens to lower event rates people with in rheumatoid arthritis. So the question now becomes can we in people who don’t have obvious inflammation do that? So that’s the Cardiovascular Inflammation Reduction Trial. It takes post-myocardial infarction patients and randomly allocates them to aggressive care plus placebo, or aggressive care plus this upstream anti-inflammatory drug. Now while that’s an exciting trial, it is using a diffuse broad-spectrum anti-inflammatory agent. So we also wanted a second swing of the bat, to look at a narrowly targeted piece of the puzzle. And this is to do with interleukin-1 Beta. Interleukin-1 is the primary cytokine, it sits upstream from IL-6. IL-6 of course triggers the liver to put out CRP. So we think this is a very focused way of looking at the question. And that drug is Canakinumab which is manufactured by Novartis. It is in use for some very rare genetic disorders. What we are doing with colleagues around the world, we already have more than 10,000 patients randomized to this drug or a placebo, who have already had a heart attack, or who are on high dose statins. It’s an exciting time for this field. Cardio Debate: What are the main challenges? Some of the challenges we face are intellectual. As internists, as cardiologists we have grown up with the lipid hypothesis – and this is not about the lipid hypothesis directly. We know that lowering cholesterol profoundly lowers event rates. The question is, is the residual risk our patients have driven only by cholesterol, or is it also driven by this inflammatory response? Now we have published, and many people have corroborated for many years, that once you’re on a statin the on-treatment level of CRP is just as important as the on-treatment level of LDL-cholesterol. And driving them both down further benefits our patients. But right now we don’t have agents that have proven to do that for the inflammation part, but we do on the lipid part. So one of the biggest challenges we have is educating our physicians. And how do we express to people that this residual inflammatory piece maybe just as important as the cholesterol part? So that’s been the biggest challenge, really. Cardio Debate: How close are we to implementing this in clinical practice? The first of these trials that will complete is the Canakinumab trial, CANTOS. It is an event-driven trial, it needs 1400 events and at that point it will have the power to stop. So we’re about two-thirds of the way there already. So I would think within about two years or so we’ll have a read-out from the first of these. It will be a very exciting time and we’ll learn does lowering inflammation lower vascular risk?
Views: 301 Cardio Debate
Marfan Syndrome - Dr Anne Child
Dr Anne Child is an Honorary Consultant in Genetics and Cardiology at St George's, University of London, and is also involved in the service and research programme for Marfan Syndrome. During this interview Dr Child speaks with Cardio Debate about this inherited disorder of the cardiovascular system. Transcript What is the magnitude of the problem in the UK and worldwide regarding prevalence and cardiac events? I run the Marfan Syndrome Service and Research Programme, and we’re mainly interested in diagnosis and management of this inherited condition. It’s directly transmitted from parent-to-child with a 50 per cent risk. It affects one in 3300 patients worldwide, and here in England we have 18,000 whom we know are affected, but there should be many more. And it contributes to sudden cardiac death, seven per cent of sudden cardiac death is due to ruptured aneurysms. Clinical clues to diagnosis Well the diagnosis is often suggested by the involvement of the eyes, the heart, or the skeleton. These patients, in 40 per cent of them, had dislocated lenses, so ophthalmologists should be aware. Often they are very tall and thin, with long, thin arms and legs, or fingers. Often a dip in the chest or curve in the back – so the skeletal features can also be a clue. And of course from a cardiac point of view, chest pain or a family history of aneurysm or rupture is very important. Where should GPs refer their patients with suspected Marfan? The usual route of referral to make a diagnosis is through the Regional Genetics Unit. And these are available all over the UK. Indeed special Marfan clinics have been set up, manned by a cardiologist and a geneticist in 21 centres. But the Regional Genetics Unit is the best place to start for a diagnosis. There is a genetic test for the gene that causes Marfan syndrome, namely Fibrillin-1. And in 99 per cent of classical cases of Marfan syndrome we find an error that confirms the diagnosis, and can also be used to screen family members, and even to plan an unaffected pregnancy. Available treatments and ongoing trials Here at St George’s University of London, we have a very comprehensive management programme which ensures an almost normal lifespan. So if this is diagnosed early in life it certainly can be managed. There are medications available – atenolol or beta-blocker is the basis of treatment, usually. This drops the blood pressure and slows the rate of the aortic expansion. That’s the main life-threatening event in Marfan syndrome – if the thin aortic wall ruptures and no-one knows it’s going to happen. We can predict this with echocardiography once a year, we can treat with medication, and when the time comes for surgery – when the aortic route is over 4.5 cm – then we can offer open-heart corrective surgery with only a one per cent risk. And most of our patients do lead a normal lifespan. We have a drug trial underway which is funded by the British Heart Foundation, called the AIMS trial. And our aim is to try and prove that losartan, irbesartan, this newer category of drugs is actually better than the old category of beta-blocker. We’re fully recruited, we have 200 patients nationwide. And the results are due in 2018 and will be made available as soon as we have them. But this promises either a supplementary treatment, or an even better life-saving treatment.
Views: 445 Cardio Debate
CV disease in young women: are we winning the "war"? - Prof Noel Bairey Merz
Noel Bairey Merz, Professor of Medicine & Director of the Barbra Streisand Women's Heart Center, Cedars-Sinai Heart Institute, Los Angeles, USA, speaks to Cardio Debate about cardiovascular disease in young women and whether we are winning the "war". For more interviews like this one please visit www.cardio-debate.com TRANSCRIPT What are the main issues you discussed in your lecture regarding Heart Disease prevention in young women? We are not winning the war. In relatively young women under the age of 50, and particularly 35 to 45, women’s heart disease mortality is actually on the rise compared to declines in older women, older men and younger men. Then we talked about reasons for this, and it is quite evident that both in secondary prevention of heart disease as well as primary prevention women are often not recognised, not evaluated and even when they are evaluated and identified as being at risk and eligible for treatment, they are often not treated. We talked about issues of gender in society, gender in medicine where women are viewed more as objects, women are more likely to be told to lose weight if they are diabetic than actually be prescribed a statin, which is in the guidelines. Women with acute coronary syndromes, up to 40% do not have obstructive coronary disease and they are not treated despite guidelines stating that they should be treated and evidence base strongly suggesting that the treatment as effective. So we can conclude that all healthcare providers should look at their own practice. If they question whether or not they live in a gendered society they should take the implicit biased test from Harvard University, it’s available on Google free of charge. https://implicit.harvard.edu/implicit/takeatest.html Basically, what we find is everyone has some gender biases, including healthcare providers and cardiologists, and that we need to go back to clinic and do a better job. And risk assess and treat women when they should be treated.
Views: 511 Cardio Debate
ESC 2015: Cardiovascular risk and sudden death syndrome in South Asia - Dr Rajay Narain
Despite the recent rise in the number of Indians and South Asians in India and the UK dying from sudden cardiac death syndrome, there is currently no risk profile for these groups. Dr Rajay Narain, Clinical and Research Cardiologist, St George’s University of London, and his team, aim to address this issue. Here he talks to Cardio Debate about his research into cardiovascular risk and sudden death syndrome in South Asians in the UK and in India. For more in-depth insight and analysis on issues in cardiology visit the Cardio Debate website: www.cardio-debate.com Transcript My name is Dr Rajay Narain and I am a research cardiologist at St George’s University Hospital in London, which is one of the biggest research centers in Europe. I work alongside Professor Sanjay Sharma and Professor Juan Carlos Kaski and we are doing a big study on South Asians at the moment in the department, and that is the study I am leading in the department. How are you recruiting patients in India? So basically the study involves recruiting South Asians and Indians in the UK and Indians in India. So it is very easy for us to encourage people in the community centers here in the UK to get involved in the study. So we have our team, we put notice in advance in these community centers and we go with our team and screen for blood pressure, diabetes, cholesterol and do the ECG, and they are seen at the end by a cardiologist. So it’s basically a full MOT, getting everything checked, and then getting information from a cardiologist about the risk profile. We are looking at the incidence of cardiovascular risk profile in the young Indians and young South Asians below 40, so we are trying to recruit people who are less than 40 years of age. Because there are a lot of South Asians who present with heart attack and stroke at a very early age. And to date there is no study looking at the risk profile of South Asians in the UK and doing a comparative study with South Asians in India. So we are trying to do a similar thing to recruiting Indians here, we are recruiting Indians in India, and doing a comparative study looking at all the risk profiles. Why did you choose this particular project? So as I said, in the last few years there has been a rise in the number of South Asians and Indians coming with stroke, heart attack, and obviously we don’t have any data, any information about the risk of having sudden death. Sudden death in young people in the UK, between 14 and 35 years, about 12 to 15 people die each week die from sudden inherited heart diseases, sudden cardiac death. But there is no data on South Asians, so we don’t know anything about what happens in South Asians. So that is why we started this study to make sure we have some data, we can do some study and obviously try to help these people who have this risk profile. What do you expect to achieve? Hopefully over the next three to six months we should be able to complete our study. We should have the risk profile of Indians in India and Indians in the UK, and we can come up with the answer as to what the risk profile is like in these two groups – why this risk profile is high or low in these people. Within the next three to six months we should have some answers. For more interviews please visit www.cardio-debate.com
Views: 276 Cardio Debate
Inflammation and Ischaemic Heart Disease - Prof Robin Choudhury
Prof Robin Choudhury, Professor of Cardiovascular Medicine at University of Oxford and Consultant Cardiologist at John Radcliffe Hospital, Oxford, UK, speaks with Cardio Debate & Radcliffe Cardiology about Inflammation and Ischaemic Heart Disease during the "Advances in the Pathogenesis and Management of Cardiovascular Disease" 2015 meeting, organised by the Cardiovascular Sciences Research Centre of St George's University and held at the Royal College of Surgeons of England in London, UK. Trascript How important is inflammation in the pathogenesis of coronary heart disease? The role of inflammation both in the initiation and the propagation of atherosclerotic cardiovascular disease, it’s a very complex area, it spans both adaptive and innate immunity and we can see evidence from multiple strands – be it from animal models, from human epidemiology, from the studies of human tissue to some extent, from large-scale genetic studies – that inflammation seems to have a clear and mechanistic role in atherogenesis. The real question is whether or not treating inflammation will affect patient outcomes. How will detection of plaque inflammation help patient management? So if we take as a starting point that inflammation is important in the pathogenesis of this disease, then clearly in terms of diagnosis, in grading severity, stratifying patients to receive specific treatments, the ability to image and characterise the inflammation using other tools – for instance circulating biomarkers – potentially contributes a lot. And I think where this field will go is to develop ways of characterising individual patients that will allow us to pair up, to match the diagnostics with specific treatments. Because if we don’t get to that stage then we really have no hope of delivering patients the type of specificity of therapy that they need. For more interviews please visit www.cardio-debate.com
Views: 499 Cardio Debate
Iron deficiency in patients with heart failure - Prof Ewa Jankowska
Ewa Jankowska, Professor and Head of laboratory of applied research on cardiovascular system, Wroclaw Medical University, Poland, talked to Cardio Debate about experiences in iron deficiency in patients with heart failure. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* Why is iron deficiency important in patients with heart failure? Iron deficiency is very common in patients with heart failure. We thought at the beginning that iron deficiency was just because of anaemia in this group of patients. However, later we discovered that iron deficiency itself is much more common than anaemia, and that iron deficiency beyond abnormal haemoglobin levels is related to poor exercise capacity and increased mortality in patients with heart failure. At a later stage we came to the idea of supplementing iron in patients with heart failure. Are there studies supporting the treatment of iron deficiency in heart failure? As we know, iron deficiency has such significant effects on patients with heart failure, we decided to test if intravenous (IV) iron works in patients with heart failure. Until now there have been several small clinical studies that assess the effect of intravenous iron in patients with heart failure, and among these studies two of them merit special attention. One is Fair-HF trial, and the other is the CONFIRM-HF trial. Both the studies have been performed with intravenous ferric carobxymaltose in patients who were iron deficient, and patients who had heart failure with impaired systolic ejection fraction. Importantly, in the Fair-HF trial it was shown that patients with heart failure benefit from IV iron, regarding clinical symptoms and mainly quality of life, regardless of haemoglobin levels. I mean both anaemic and non-anaemic patients benefit from this kind of treatment. In CONFIRM-HF trial, which was published just two years ago, it was shown that IV iron improves exercise capacity in patients with heart failure, increasing the six-minute walking test distance. But what I think was extremely important to demonstrate in the study was one of the secondary end points, it has been shown that intravenous iron can reduce the rate of heart failure hospitalisations in patients with heart failure, which we consider as a very important clinical benefit. What are the key points to highlight about iron deficiency, especially in patients with heart failure? It’s really important to emphasise that iron deficiency works not only in patients with anaemia, but patients who are not anaemic. And why could iron work in these patients? Maybe because iron deficiency is needed for functioning of skeletal muscles. We have more and more evidence showing that iron is needed for the optimal energy metabolism of exercising skeletal muscles, of working myocardium, before we believe that we should supplement iron. Also in patients with normal haemoglobin levels, but who remain iron deficient. What other important aspects are worth mentioning? It’s really important to also realize that the pathophysiology of iron deficiency is different to the iron deficiency in patients with chronic kidney disease. Although many people think that iron deficiency in heart failure is due to augmented inflammation lag in patients with chronic kidney disease, there is no evidence supporting this concept. We know that patients with heart failure who are iron deficient have very low ferritin, have extremely low hepcidin and do not have increased pro-inflammatory molecules in the circulation. Therefore iron deficiency in heart failure is an example of absolute iron deficiency, where in fact body iron stores are almost completely depleted in these patients. Therefore, there is really an urgent need to supplement iron, and the intravenous route is the only one which can quickly and sufficiently supplement the iron stores in these patients.
Views: 706 Cardio Debate
"WISE" & the problem of ischaemic heart disease in women - Prof Carl Pepine
Carl Pepine, Professor of Medicine, UF Health Shands Hospital, Gainesville Florida, USA, talks to Cardio Debate about the problem of ischaemic heart disease in women, and the "WISE" programme (Women's Ischaemic Syndrome Evaluation) For more interviews please visit www.cardio-debate.com *TRANSCRIPT* WISE in an acronym for the Women’s Ischemic Syndrome Evaluation, which grew out of an initiative in our country to address the problem that more women have ischaemic heart disease, more women die of ischeamic heart disease and more women have what’s called ‘normal coronary angiograms’ than men, yet there were no reasonable explanations for those findings. So in 1996 we were funded to begin a series of projects called the WISE programme. This was a consecutive case cohort of almost 1000 women recruited from four different sites in the United States. These women all had symptoms and signs of stable ischameic heart disease, and then had to be referred for a coronary angiogram. We then did various testing routines at the centres and followed the patients, initially for five years, and the more recently we did a 10-year follow up. And what we found was that among the women who had signs and symptoms of ischaemia, two thirds of the women had no obstructive coronary artery disease, which is in distinct contrast to what you would expect in a comparable cohort of men, where 80-90 per cent of the men would have severe obstructive disease. Furthermore, we learned that these women had adverse outcomes, and it clearly was not a benign syndrome. The adverse outcomes consisted of an increase in hospitalisation. Most of those hospitalisations were for heart failure, they of course also had myocardial infarctions and strokes in follow-up. But we were surprised at the increase in hospitalisation for heart failure because these women had normal systolic left ventricular function at their baseline coronary angiography. So when we retrospectively looked at their left ventricular and diastolic blood pressure we found that it was elevated, it was 16. And we also found that in a sample of patients who were hospitalised for these heart failure admissions, that the left ventricular ejection faction was presumed. So this we believe then is a harbinger of heart failure with preserved ejection fraction, which we’re seeing now with increased frequencies, particularly in older women. So those findings were reported initially, and then as I said extended to a 10-year follow-up. And we basically saw again increasing frequencies of those adverse outcomes. Multiple studies, much larger and also extending to men, have replicated those findings. Additionally we found that the women who had testing for endothelial dysfunction and testing for coronary microvascular dysfunction had an alarming increase in the adverse outcomes. So it turned out that those two findings were predictors of those two outcomes. What are the key points? It’s important to evaluate these women. The evaluation shouldn’t stop with the finding of the so-called ‘normal’ angiogram – that’s because the outcome is clearly not benign. And the additional evaluation should consist of additional testing for coronary vascular problems such as endothelial dysfunction and microvascular dysfunction.
Views: 654 Cardio Debate
ESC 2015: Diagnosing angina: Key differences between men and women-Bairey-Merz
Dr Noel Bairey-Merz speaks with Cardio Debate and Radcliffe Cardiology about diagnosing angina and the key differences between men and women.
Views: 331 Cardio Debate
Resistant hypertension & treating patients with uncontrolled blood pressure - Prof Thomas Kahan
Thomas Kahan, Professor of Medicine & Cardiologist, Danderyd University Hospital, Stockholm, Sweden, talks to Cardio Debate about resistant hypertension and treating patients with uncontrolled blood pressure. For more interviews please visit www.cardio-debate.com *TRANSCRIPT* What is pseudo-resistant hypertension? Resistant hypertension is a term you use when blood pressure is not controlled. And pseudo-resistant hypertension, or rather apparent hypertension, is what you usually use to describe patients who have three or maybe four drugs, but still have their blood pressure uncontrolled. The difference between true resistant hypertension and pseudo-resistant hypertension is that there are many unrecognized reasons for hypertension that you can actually treat if you do a proper workup. Does it exist? If you look into survey, perhaps half or even two-thirds of all patients treated for hypertension are uncontrolled. And they are then often called ‘pseudo-resistant’ but that is not true because there are few patients with true resistant hypertension – perhaps one our of 10. So it’s a big group in between. But those with true resistant hypertension are a medical challenge because they are difficult to treat, they have a poor prognosis, they have very high risk of cardiovascular events. Is renal denervation the answer to resistant hypertension? If you have true resistant hypertension, we are at the dead end. We have used several drugs, we cannot control the blood pressure. Then there are several device therapies – renal denervation is one of them – that may be the solution. It’s promising, it should work. The physiology is there. But we are not really there in the clinical setting to know how to do it the best way and how to choose the proper patients. But I am quite sure that we will reach it within a few years.
Views: 918 Cardio Debate
Prevention of Sudden Cardiac Death - Dr Elijah Behr
Dr Elijah Behr speaks with Cardio Debate & Radcliffe Cardiology about Prevention of Sudden Cardiac Death during the ‘Advances in the Pathogenesis and Management of Cardiovascular Disease’ 2015 meeting organised by the Cardiovascular Sciences Research Centre of St George's University, held at the Royal College of Surgeons of England in London, UK. Transcript What is the role of implantable devices in inherited arrhythmogenic diseases? The role for implantable devices really depends on the condition. There are some general principles though. The arrhythmia syndromes tend to affect young people, and therefore we need a very high threshold for which to implant young people with electronic devices because of the potential for long-term list of complications. So the first thing to say is only a small minority of arrhythmia syndromes require these devices and implants. Secondly, the approach to risk stratification is very much dependent on the condition and so, for example, if we look at a condition called the Long QT syndrome, which we know very well and we have a lot of data on, we can actually do a certain amount of risk stratification that seems to be effective at determining which patients are at risk. So, for example, we know that young boys are most at risk of the condition in the younger age groups. And if they’re having blackouts or if they’re having a very prolonged QT interval, or both, then they are more likely to benefit from an ICD implant. And then conversely, in adults, young women seem to be at the greatest risk, there seems to be a hormonal shift, during puberty. But not all women with that condition require that sort of protection. Usually it’s if they have serious symptoms and if they’ve had a very prolonged QT interval on the ECG, or they are failing therapy already – so they’ve gone onto therapy and they’ve not succeeded. And in the Long QT syndrome there are other therapies that may hold off the need for an ICD implant, for example sympathetic innervation of the heart. We then move onto a different condition, the Brugada syndrome, where we have a lot less data on risk. And the stratification of risk with Brugada syndrome comes down to whether you have symptoms or whether you have no symptoms. And unfortunately most people with the Brugada syndrome who die from the condition don’t have warning symptoms. So there is a large unmet gap there in terms of the patients who might need an ICD implant to protect them but we can’t predict them so well. So the role for ICD implantation in Brugada syndrome is very clear in someone who has already had symptoms, but unlike in Long QT where you may be able to predict that somebody is going to be at greater risk in the long term, we have a lot of problems with that in Brugada syndrome. So the role for ICD implants there is very difficult at the moment, other than in the patients where it is very obvious to begin with. What are the most recent advances in risk stratification of BRUGADA syndrome? To read the full transcript for this interview visit www.cardio-debate.com
Views: 934 Cardio Debate
HFpEF - Mechanisms and management - Dr Alexander Lyon
Cardiology Update 2016 Meeting organised by St George's, University of London - 2nd December 2016, Royal Society of Art, London UK Management of Heart Failure - Dissecting the new guidelines HFpEF - Mechanisms and management TRANSCRIPT My name is Dr Alexander Lyon, I’m a senior lecturer at Imperial College, London, UK, and a honorary consultant cardiologist at the Royal Brompton Hospital in London. I’m also a member of the Heart Failure Association Board with specialist interest in cardio-oncology and heart failure caused by cancer drugs, and also Takotsubo syndrome and stress and the interaction of heart failure. Which were the most salient aspects of your talk? I had the privilege and challenge of discussing heart failure with preserved ejection fraction (HFpEF) which is a growing clinical problem for our health care services, but we’re limited in terms of our understanding of this condition and therefore how we can treat it. I reviewed some of the information about some of the mechanisms. I personally believe there are many different subtypes of this condition. So whereas with heart failure with reduced ejection fraction patients we’ve had success using some common treatments across them all irrespective of etiology, when we move into HFpEF we haven’t been successful with the ‘one size fits all’ common pathways. So therefore we need to do more research to understand particular types of patients, not least related to their comorbidities. So I discussed how comorbidities are and the different ‘flavours’ of HFpEF, and from that then we can start to understand the biology of each one, and personalise treatment approaches. And I finished by giving some real world advice on what we can do with the patients today whilst we still need further research on how to manage the patient of tomorrow better.
Views: 708 Cardio Debate
Endothelial Dysfunction - Dr Luigi Gnudi
Dr Luigi Gnudi talks to Cardio-Debate.com about causes and consequences of endothelial dysfunction and the basics for rational management of this condition.
Views: 1523 Cardio Debate
ESC 2015: MINOCA diagnosis and finding underlying cause-Prof Beltrame
Professor John Beltrame speaks to Cardio Debate and Radcliffe Cardiology about MINOCA diagnosis and if this should prompt further investigation to find the underlying cause. TRANSCRIPT What is MINOCA? MINOCA stands for Myocardial Infarction with Non-Obstructive Coronary Arteries. So to fulfill the criteria for this condition you have to have the universal criteria for acute myocardial infarction, so that’s a troponin rise associated with clinical features of a myocardial infarction, as well as having evidence of non-obstructive coronary arteries on angiography – so that’s having no stenosis that are 50 per cent or more. And that’s the definition of MINOCA. When is it important to diagnose this condition? The condition is diagnosed shortly after angiography. So when a patient presents with what’s thought to be an acute myocardial infarction undergoes coronary angiography and no significant stenosis are recognized, that’s when the diagnosis is made. So it’s not a diagnosis where these is a clear cause for the myocardial infarction with the raised troponin. For example, if you have a young patients who presents with a viral-like illness associated with pleuritic chest pain, the diagnosis of myocarditis is the likely cause and you are merely taking angiography to exclude significant coronary artery disease. Then that diagnosis should be myocarditis and not MINOCA. Whereas the reason for establishing the diagnosis of MINOCA is where the cause is not quite clear, and it is to prompt the clinician for further investigation. So for example, in some cases because there is no significant coronary artery disease some clinicians would suspect that perhaps the patient hasn’t had a myocardial infarction. However it is important to understand what the cause is. So similar to heart failure, you can diagnose heart failure and then you have to diagnose the cause. You diagnose MINOCA and you have to find the underlying cause. And probably the most common cause is myocarditis, but there are certainly other causes that need to be considered. So the first investigation that really should be considered is a cardiac MRI, because when you undertake a cardiac MRI it will give you the diagnosis of myocarditis, you can also see if there is a typical myocardial infarct on the MRI, and may also give you clues to other unusual causes such as a cardiomyopathy. Why is MINOCA important? It’s important because in contemporary cardiology the underlying is not identified. So one of the important causes coronary artery spasm, the cause of the myocardial infarction. So if that’s the case, and our research shows that somewhere between 20 to 25% of cases coronary artery spasm is responsible, this can be treated effectively with calcium channel blockers. And so if a diagnosis of MINOCA is not made and therefore it prompts further investigation, such as looking for coronary artery spasm, then effective treatment may not be implemented. Another causes to consider in about 10% of cases is that there may be an underlying thrombotic disorder, and so screening should be undertaken for that. But as we said the most common cause is myocarditis, and a cardiac MRI will help you identify that cause. So again, the reason for making the diagnosis of myocarditis, is similar to heart failure, is to find the underlying cause of MINOCA. For more interviews please visit www.cardio-debate.com
Views: 348 Cardio Debate
Endothelial dysfunction in coronary artery disease - Prof Julian Halcox
Prof Julian Halcox, Professor of Cardiology at the Cardiff University, UK, talks to Cardio-Debate.com about endothelial dysfunction in coronary artery disease.
Views: 509 Cardio Debate
Postmenopausal women and microvascular angina - Prof Peter Collins
Peter Collins, Professor of Clinical Cardiology at Imperial College of London, UK, speaks with Cardio Debate about microvascular angina in postmenopausal women. For more interviews like this please visit www.cardio-debate.com TRANSCRIPT I’m Professor Peter Collins, Professor of Clinical Cardiology at Imperial College and the Royal Brompton and Harefield NHS Trust. And I’ve been speaking on post-menopausal women and microvascular angina. What are the main challenges in HRT? What are the indications? The main challenges in HRT are really to identify patients who you feel will benefit from it, and the majority of patients that we treat in our clinic have menopausal symptoms. We know that post-menopausal symptoms like hot flushes, tiredness, irritability and vaginal dryness are all improved significantly with hormone therapy. And basically if patients have cardiovascular disease or angina with those symptoms, then those are the patients who we feel may benefit from the addition of hormone therapy. And the key with treating these patients is really to identify the lowest dose that will control the symptoms and then, if needed, to up-titrate the dose of the hormone. Now one of the issues with hormone therapy is that there are different oestrogens, there are different progestins, there are different routes of administration and there are different doses. I’m not suggesting that cardiologists should treat women with hormone therapy for these post-menopausal symptoms. But it may be that if these women are identified as having symptoms then a gynecologist can be asked for help, and an opinion as to what forms of hormones may be applicable to those women, and in what doses and routes of administration. In our clinic we favour the naturally occurring oestrogen which is 17-beta estradiol, and transdermal therapy will then avoid first liver pass, and that, we think, is more cardiovascularly favourable than giving oral HRT. There is a slight increase of deep venous thrombosis risk in women who take hormonal therapy, and that’s about an increase of three women per 10,000 women treated in a year. So that’s a very small increase in risk, but that is the only established risk in younger women with regard to HRT. Who should initiate and monitor HRT in women with microvascular angina? It very much depends on the skills of the cardiovascular physician. If the cardiovascular physician is confident and knows enough about the area to be able to prescribe then that would be acceptable. But we really recommend that if that’s not the case then they get the help of an endocrinologist or a gynecologist, and we promote a team effort, so that these patients can be dually managed by the gynecologist, the endocrinologist and the cardiovascular physician. What are the risks of treatment? The risks of treatment, as I’ve already explained, are a slight increase in deep venous thrombosis risk, and again that’s about three per 10,000 women treated for a year. So it’s a very small risk, but it’s a real risk. And women are often accepting of that risk because of the beneficial effects of the menopausal symptoms. Menopausal symptoms can be very bad, and affect the general well being of the woman quite badly, and therefore that sort of morbidity is addressed by the HRT and they often say “Well, if there is a small risk, I’m prepared to accept that risk for the benefit that I’m getting with regard to the management of the symptoms.”
Views: 745 Cardio Debate
HF-pEF Syndrome & Coronary Artery Spasm - Prof Filippo Crea
Filippo Crea, Professor of Cardiology in the Catholic University of Rome, Italy, talks to Cardio Debate about coronary artery spasm. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* What is HF-PEF? HF-pEF is Heart Failure with Preserved Ejection Fraction. This is an interesting syndrome because for many years we thought heart failure is when you have reduced ejection fraction, or a severe valve disease. In the past few years we have been learning that about 50 per cent of patients with heart failure, they do not have reduced ejection fraction – which was supposed to be the hallmark of heart failure – nor valve disease. In these patients ejection fraction is normal, yet these patients have the same symptoms as the patients with heart failure with reduced ejection fraction. And what we have been learning is that the outcome of these patients is a bit better than that of patients with reduced ejection fraction but definitely much worse than that in subjects without heart failure. What are the mechanisms? The mechanisms are mainly related to the fact that the amount of fibrosis in the heart increases. This makes the heart stiffer and this is the cause of symptoms and the cause of the alterations we can pick up on echocardiography. Echocardiography in these patients is characterized by LVH (left ventricular hypertrophy) or impaired diastolic function, or atrial enlargement. And the diagnosis of HF-pEF is based on these situations – firstly symptoms and signs of heart failure, and then changes on echocardiography characterized again by LVH, dilated atria or impaired diastolic function. When these things come together we have the diagnosis of heart failure with preserved ejection fraction where the main issue is a sort of “stiff” heart. What are the treatments? Definitely this is an unmet need because so far no treatment has been found to improve the outcome of patients with HF-pEF. And also we don’t have a validated treatment able to improve symptoms in these patients with HF-pEF. Of course we have a wide array of drugs that can be used, but no treatment has been found to systematically improve symptoms. So the treatment, the symptomatic treatment of these patients, is very empirical. We have to start with drugs that are likely to work, and if they don’t work we have to try other drugs. And, eventually, in the vast majority of these patients we get some improvement of symptoms. As for the outcome, many drugs have been tested in order to improve the outcome for these patients. But, really, we so far don’t have a success story.
Views: 757 Cardio Debate
Young Onset Dementia - Prof Peter Garrard
Peter Garrard, Associate Professor in Neurology, St George's, University of London, talks to Cardio Debate about young onset dementia. Transcript Definition and how to diagnose – any diagnostic markers available in everyday practice? It’s somewhat arbitrary but we think of young onset dementia as dementia that occurs within working age, so under the age of 65 years. It’s a somewhat arbitrary definition and actually the statistics show demographically is that the instance and prevalence on dementia is very low in this working-age age group – so less than one per cent of the population. And then as people age the incidence increases by five per cent per year, so that over the age of 90 it’s estimated that around a quarter or even one third of people meet the criteria for dementia. But the significance of this is that it is a disease of aging, for which ageing is one of the major risk factors. So when we see a patient in general practice with symptoms that are suggestive of cognitive failure – so memory impairment, language loss, behavior change, inability to navigate or use visual apparatus to perform the tasks of daily life – its always regarded as a low probability that they’re going to have anything seriously wrong with them. Whereas in an older person, because the prior probability is so high, a diagnosis of dementia will be suspected much more often – so there’s often a delay. I think the most important biomarkers to look out for at a clinical level, the characteristic symptom complex, characteristic symptom areas – is to realize that dementia doesn’t always present with memory loss or forgetfulness. It can present with difficulty in navigation, difficulty with using visual information – difficulty with reading, with driving, with navigating around the house. And this is quite frequently is dismissed as being a symptom of visual impairment, which it isn’t – it’s visual processing impairment. That must always be taken seriously. And then there are language symptoms – changes in word finding ability, changes in ability to understand more complex words. And there are these rather unusual behavioural symptoms, where people’s personalities change from being compatible with leading a normal life in social work environments, with beginning to exhibit bizarre behaviours. Mechanisms of young onset dementia – is there a genetic background involved? With regard to the underlying mechanism of these conditions, there are – we think of them in terms of underlying pathology – and overall the commonest the underlying pathology causing dementia is going to be Alzheimer’s disease. But overall, and in a younger onset population, those patients with the underlying pathology of Alzheimer’s disease would account for maybe one third of the population, and of the remainder a large percentage will probably be caused by premature vascular disease, and then perhaps an equally large percentage with non-Alzheimer neurodegenerative conditions. There are also groups of patients with non-neurodegenerative conditions, inflammatory conditions, toxic conditions, alcoholism, all presenting in that age group with cognitive decline. But the non-Alzheimer neurodegenerative conditions fall into two distinct subtypes, and they are defined according to the protein that accumulates in the brain. So with Alzheimer’s disease as everyone knows it’s Amyloid-Tau clots and tangles, and in the non-Alzheimer neurodegenerative cases there’s one group where Tau alone without Amyloid accumulates, and we call them tauopathies. And there’s another group where the accumulating abnormal protein is something known as TDP43. And Tau and TDP43 both accumulate principally in frontal and temporal regions, so they’re front-of-brain neurodegenerative syndromes, whereas Alzheimer’s is more posterior. So with Alzheimer’s we see more visual and memory problems, but with the anterior ones wee see more language and behavior problems. Now, the mechanisms in the vast majority of all these underlying pathologies are unknown. But a proportion of them will be accounted for by having inherited a faulty gene, which are normally autosomally dominantly transmitted. So those ones will be easily recognized as they will give a very reliable and good family history, both of their own generation and their parents generation, possibly further back too. But those only account for about 5 to 10 per cent, probably, of all the young onset dementias. Perhaps slightly more in the non-Alzheimer group. But by far the majority are sporadic, and the causes of sporadic neurodegenerative syndromes are totally unknown, and they are a source of intensive research across the world. And the first person who finds out a mechanism for sporadic Alzheimer’s or tauopathy or TDP43 will become very famous indeed, very quickly. To read the full transcript visit www.cardio-debate.com
Views: 543 Cardio Debate
Ventricular Tachycardia - Dr Magdi M Saba
Dr Magdi M. Saba, Consultant in Cardiac Electrophysiology and Senior Lecturer at St George's University of London, UK, talks to Cardio Debate about Ventricular Tachycardia. Transcript What are the criteria that define high risk VT? The criteria that define high risk ventricular tachyarrhythmias are multiple, but if we come to think about ventricular tachycardia and its main cause it’s probably ischaemic heart disease and scar. So scar-related ventricular tachycardia is probably the most serious thing we’re looking for. So I would suggest when we see a patient with ventricular tachycardia the first thing we want to know is what their ejection fraction looks like, if they have a history of coronary disease, myocardial infarction – so an echocardiogram, would show us some areas of hypokinesia, akinesia, or even an ECG that shows you where the Q-waves are. Prior history of ischaemic heart disease is very telling – and that’s a typical high-risk patient with ventricular tachycardia. And other causes of ventricular tachycardia such as cardiomyopathies, non-ischaemic cardiomyopathies such as, for example arrhythmogenic cardiomyopathy, which affects mainly the right ventricle but could also involve the left ventricle, are high risk features. The way to diagnose is a little bit more tricky. There’s ECG criteria, major and minor criteria on cardiac imaging, so cardiac MRI in that instance would probably be helpful. And depending on the type of ventricular tachycardia we see, we can look at the ECG and say whether it is left ventricular or right ventricular. And the age of the patient, and their history – we can typically define the patient who needs further imaging. There are less risky forms of VT – a VT that involves normal hearts, or ostensibly normal hearts on echo, typically from the outflow tracts. The right ventricular outflow tract, occasionally from the papillary muscles, and these are labeled as ‘normal heart VTs’. Of course there is something abnormal about them, but normal in terms of structure and no evidence of scar or infiltrative disease. Is the R/T phenomenon a marker of risk? So the R/T phenomenon is something that we see very occasionally. It’s a premature ventricular complex that happens on the T-wave, somewhere in the vulnerable window around the peak of the T-wave – just before or after the peak. And it can lead to a fast ventricular arrhythmia, typically ventricular fibrillation. Not monomorphic VT, it’s usually related to triggered activity, not automaticity, and it can frequently occur with drug-related issues. We don’t see it clinically that often. It’s not something that we tend to worry about in terms of the coupling interval of the ectopic beat, they typically occur after the T-wave. But when we see it happen, or if we see brief runs of non-sustained VT after that phenomenon we tend to worry about them a little bit more – but fortunately it’s not that common. And the way to risk stratify these patients would be with a treadmill test, for example, also an ECG to see if there is anything we can predict. If on an exercise treadmill test, for example, there is more ectopy, triggered activity and more disorganised ventricular arrhythmia then these would be high risk features. But again this is not something we see that often. Current therapeutic approaches for high risk VT The methods we have at our disposal to treat ventricular arrhythmias are multiple. Fortunately we are in a technologically-advanced state compared to 20 years ago. So let’s take a patient with VT. A middle-aged person with a prior history or myocardial infarction, the typical scenario. We get an echocardiogram, we confirm, let’s say, there’s an anterior wall scar. We confirm this with an MRI to really define the topography of the scar, how deep it is, “transmural”, the patient will ultimately get a defibrillator because that’s indicated for secondary prevention. So that’s probably the mainstay, is to have the back-up of a defibrillator, an ICD implantable cardioverter defibrillator to protect them from sudden death. That’s number one. To read the full transcript for this interview visit www.cardio-debate.com
Views: 1404 Cardio Debate
New drugs for the management of heart failure - Prof Martinez - ESC2016
Professor Felipe Martinez from Universidad Nacional de Córdoba, Argentina, speaks to Cardio Debate & Radcliffe Cardiology about the new drugs and treatments for the management of heart failure during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* Could you describe the main advances in chronic HF pharmacology? Yes, I would say that we have now two main groups of new drugs. The first one is an old intervention that has changed its name from “anti-aldosteronic” (agents) to “mineralocorticoid receptor antagonists”. This group has shown solid evidence in preventing heart failure mortality, heart failure hospitalization, etc. The other group is the really new one, which is already on the market, which they call ARNI – angiotensin receptor neprilysin inhibitors – which (represents) a dual inhibition of the renin-angiotensin-aldosterone system. And the trademark is the real advance in improving the outcomes, mainly mortality and heart failure hospitalization in patients with chronic heart failure. How do these advances translate into clinical practice? I could say that most cardiologists around the world have been using ACE inhibitors and angiotensin antagonists in the past 30 years or so. Now we have to change our mind to this new class of intervention, because the scientific evidence showed by results of clinical trials by these two groups of drugs has a real impact on clinical practice. So that is the real issue to reconsider. Cardiologists might take into account these new drugs, which are really, really improving the prognosis of chronic heart failure. What are the new drugs in the pipeline we should look out for? I would say that there are many. I would point out one group which is called the SGLT-2 inhibitors that surprisingly have been produced as anti-diabetic drugs, but an initial trial has demonstrated a clear benefit in improving the cardiovascular outcomes – mainly mortality, heart failure hospitalization, myocardial infarction, etc. Now do to this striking result most of the sponsors are planning new mega-trials using this drug only in patients with heart failure. So the million-dollar question is, are they going to demonstrate a great benefit in heart failure despite the patients being diabetic or not – we don’t know yet. And we’re going to have the answer in a couple more of years.
Views: 157 Cardio Debate
Inflammation in Atherogenesis and Plaque Disruption - Prof Göran Hansson
Prof Göran Hansson, Head of the Cardiovascular Research Laboratory at the Centre for Molecular Medicine Karolinska University Hospital, Stockholm, Sweden, speaks with Cardio Debate & Radcliffe Cardiology about Inflammation in Atherogenesis and Plaque Disruption during the "Advances in the Pathogenesis and Management of Cardiovascular Disease" 2015 meeting, organised by the Cardiovascular Sciences Research Centre of St George's University and held at the Royal College of Surgeons of England in London, UK. Transcript What makes inflammation such an appealing hypothesis in atherogenesis? Inflammation is present in the atherosclerotic lesion, together with cholesterol derived from lipoproteins and components from the vessel wall itself. Cholesterol is a great risk factor, very important as is high blood pressure. But they cannot, alone, explain the disease process that we see. The disease is not only an accumulation of cholesterol, but a response of the tissue that includes inflammatory cells, immune cells. And therefore inflammation is a crucial component of this disease. But we don’t understand enough about how it operates, but it’s there. It’s a fact. What is the role of macrophages in plaque distribution? Macrophages, activated macrophages, are found at sites of plaque disruption, and they make molecules – enzymes – that can chop up components of the fibrous plaque. So therefore the macrophage is unlikely to illicit plaque disruption by weakening the plaque by chopping up the collagen components so that the plaque is fragile and vulnerable and therefore cracks when it is hit by the force of the blood pressure. What roles do lymphocytes play in this context? The T-lymphocytes, which are the main type of lymphocytes present at these sites in the plaque – they are really the conductors of the orchestra of inflammation. The T-cell can tell the monocyte or macrophage to become activated. Other types of T-cells can inhibit macrophage activation. So the T-cell can really control the whole process. And we do find activated T-cells as well as activated macrophages, at the site of plaque rupture. Furthermore, the T-cell makes cytokines that inhibit collagen formation and smooth muscle accumulation and therefore they reduce cap formations. They both act on the vascular components – the cap and the macrophage, and they really control the disease process in that way. For more interviews please visit www.cardio-debate.com
Views: 377 Cardio Debate
Pathophysiology and management of reperfusion injury | ESC2016 | Cardio Debate
Professor Bernard Gersh from Mayo Clinic in Rochester, USA, speaks to Cardio Debate & Radcliffe Cardiology about pathophysiology and management of reperfusion injury, during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* Why, despite so much research and promising animal trial data, have we seen no major breakthroughs regarding the management of perfusion injury? It’s a good question, and I’m not sure I can think of an area where there has been such a huge gap between the experimental evidence and the clinical evidence. Reperfusion injury is complex. It’s a very complex pathophysiology, there are a lot of processes and there are lot of potential targets. There are a lot of people who have disputed whether reperfusion injury is actually clinically relevant. I think it is. And after a wealth of animal studies that are all positive, basically none of the clinical trials have reached their primary end point. It’s been a big agenda with disappointing results, and I think the big question is why. The most correct answer is we don’t really know. But I think there are a number of explanations. I think we have to accept that dogs and cats are not the same as humans. The species differences are very different. Differences in collaterals in-between species may have a effect. The other reason why there is a big difference is, in the animal experimental model you create an infarction by putting a ligature on a virgin artery and then you release it. Myocardial infarction in the patient is very different because it is an atherosclerotic coronary artery, there is thrombus there, thrombus dissolves, reforms – it’s a very different model, a different process. I think differences in collaterals play a role, I think species differences are a major factor, and I think it’s a different pathological process so we probably need a better animal model that we don’t have at the moment. And that would be an animal model of an atherosclerotic artery that is subject to myocardial infarction. The bottom line is big agenda, unimpressive results. Is there anything new on the horizon that has potential? Yes there are a number of ongoing trials and a number of different compounds. The one I still think carries a great deal of promise is the phenomenon of ischaemic preconditioning –and particularly remote ischaemic preconditioning. Now, there have been some trials of ischaemic conditioning that turned out to be neutral. But I think there are some technical explanations in the design of the trials that account for the fact that they are neutral. So I think that’s an area that is alive. I won’t say it’s alive and well, but it is alive and interesting and needs to be developed further. And personally I think is probably the most interesting approach to modifying reperfusion injury. If we really could modify it, it could have a big impact – on the size of the infarction and the prognosis.
Views: 184 Cardio Debate
Platelets in Atherogenesis & Acute Coronary Syndrome - Prof Albert Ferro
Professor Albert Ferro speaks with Cardio Debate & Radcliffe Cardiology about Platelets in Atherogenesis & Acute Coronary Syndrome, during the 2015 Cardiovascular Sciences Research Centre Annual Meeting held at the Royal College of Surgeons of England in London, UK. TRANSCRIPT My name is Albert Ferro, I’m a Professor of Cardiovascular Clinical Pharmacology at King’s College London, and I work as a Consultant at Guy’s and St Thomas’ Hospital in London running a hypertension clinic. What is the importance of platelet monocyte interactions in atherogensis and acute coronary syndrome? So what we’ve been looking at over the past few years is the role that interaction between platelets and monocytes has in the generation of atherosclerosis. And what we found is there is a very close correlation between the formation of monocyte platelet aggregates and the degree of atherosclerosis that is present. And there is a linear relationship between MPA formation and things like hypertension, and also there is a relationship between cholesterol levels as well. So we think that the binding of platelets to monocytes is likely to be causal in atherogenesis, because what seems to happen – and we’ve shown this in our experiments – is that that binding causes the monocytes to become more pro-inflammatory and more pro-atherogenic. They are more likely to stick to the vascular endothelium, and from there migrate into the subintima and cause atherosclerosis. As yet we don’t have any direct evidence of that in humans. We have some evidence in animal models and what we’re hoping to do in the future is to translate that into humans, and hopefully show that there is a direct causal relationship. In terms of acute coronary syndrome, we don’t know what the answer is yet. But by inference, if we – as we believe that platelet binding to monocytes causes monocytes to become more pro-inflammatory, and we know that acute coronary syndrome itself has an underlying inflammatory basis – it is likely that MPA formation is involved in acute coronary syndrome as well. But those are questions that we need to do further research on. What are the clinical challenges regarding dual antiplatelet treatment in patients with atherosclerosis? So dual antiplatelet therapy is well-established now in the treatment of patients with acute coronary syndrome, myocardial infarction and in those having intracoronary stents placed. There is a long-standing debate as to whether dual antiplatelet therapy really is superior to P2Y12 inhibition alone. And so we, and others, have some in vitro evidence that adding aspirin on top of a P2Y12 inhibitor may not add very much, if anything, to the antiplatelet effects of the P2Y12 inhibitor. So that’s a long-standing debate and I don’t think we really know the answer to that. All we can say is all the clinical trials have been done with a P2Y12 inhibitor on top of aspirin, and have shown added benefit. But what we don’t know is the other way round – if the patient is already established on the P2Y12 and you add in aspirin, do you have any added benefit from that? And that is highly questionable. What we do also know is that dual antiplatelet therapy gives you an increased risk of bleeding. And so it comes down to risk benefits. At least for coronary syndrome the benefits outweigh the risk. If we’re talking about patients outside of that situation – so patients with stable atherosclerotic disease, or indeed patients who you are treating for primary prevention – I think it becomes much more problematic because there is a much smaller benefit to be gained, and the risk of bleeding is still there. So there is not a clear signal that benefits over risk in that situation. So I think at the present state of knowledge, I think dual therapy is well-established and is indicated in patients with acute coronary syndrome and in those post-PCI. But outside of that situation in the stable patients I think there is no evidence to support its use at the moment. For more interviews please visit www.cardio-debate.com
Views: 278 Cardio Debate
Link between Endothelial Dysfunction and Systemic Hypertension - Prof Albert Ferro
Prof Albert Ferro talks to Cardio-Debate.com about the link between Endothelial Dysfunction and Systemic Hypertension.
Views: 664 Cardio Debate
Sudden death in sports: diagnosis and prevention - Sanjay Sharma
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 357 Cardio Debate
Antianginal agents: Beneficial effects of Ranolazine - Prof John Camm & Prof JC Kaski
Antianginal agents: Beneficial effects of ranolazine
Views: 3021 Cardio Debate
Latest risk prediction in cardiomyopathy - Constantinos O’Mahony
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 193 Cardio Debate
Advances in the Management of Dyslipidaemia (Part 1 of 3) - Prof Julian Halcox
Prof Julian Halcox Professor of Cardiology, Swansea University College of Medicine, speaks with Cardio Debate & Radcliffe Cardiology about the Advances in the Management of Dyslipidaemia, during the 2015 Cardiovascular Sciences Research Centre Annual Meeting, held at the Royal College of Surgeons of England in London, UK. TRANSCRIPT I’m Julian Halcox, I’m Professor of Cardiology at Swansea Medical School. I’m a clinical cardiologist with an interest in cardiac disease prevention. Can you describe the anti-inflammatory effects of HDLs? So HDL is a complex lipoprotein. Epidemiologically there is a very strong relationship between levels of HDL cholesterol and cardiovascular events, with high levels appear to be conferring protection. Certainly associated with a reduced risk of cardiovascular events. Now that’s rather complex because often we see the individuals with the high levels of HDL with better functioning HDL, and conversely people who have lower levels of HDL cholesterol have impaired HDL function. And that’s because HDL is a rather pleotropic lipoprotein. It has a number of effects with many proteins associated with the lipoprotein with a range of effects on the vasculature, and these include anti-inflammatory effects, anti-oxidative effects. It also confers protective effects on the endothelium, it helps with endothelial repair, and perhaps even endothelial-dependent vasodilatation. So when it comes to understanding the relationship between changing HDL cholesterol levels and outcome, things may not be quite so straightforward. As we’ve seen in clinical trials with agents that have quite profound effects on HDL cholesterol levels, treatment with these agents hasn’t necessarily translated into impact on outcome. And that’s because if we think of HDL cholesterol as a marker of function that’s probably incorrect. So having higher levels of HDL doesn’t necessarily mean the HDL is working any better. And in fact it’s highly likely, given what we found out from the clinical trials, that the anti-inflammatory effects and the anti-oxidant effects are very, very important in conferring the protective effect that we seem to see in epidemiological studies. So the challenge really is to be able to identify agents that influence the function of HDL cholesterol, particularly anti-inflammatory and anti-oxidant effects, but also importantly the reverse-cholesterol transport effects. And think of how we’re able to do that. So just further to the idea of HDL cholesterol and it’s protective effects on atherosclerosis, it’s important to consider the case of the Apo-A Milano variation of Apo-A. And this is a type of Apo-A that was identified in a family from Italy, and possession of this type of Apo-A was associated with HDL that appeared to have extremely good reverse-cholesterol transport capability. So interestingly these individuals appeared to have very low levels of HDL cholesterol, but despite that they had very low incidences of myocardial infarction and atherosclerotic cardiovascular disease. And this appeared to be related to the ability of their HDL to translocate lipid from the periphery back to the liver for recycling very rapidly. And indeed, when this Apo-A was reconstituted and put into animal models, and even in a small clinical trial, it seemed to be associated with reduced progression of atherosclerotic disease and indeed regression. This suggests that it’s not just the HDL cholesterol, it’s how the HDL cholesterol is working, which is very, very important. And the challenge will clearly be to identify agents that improve the function of the HDL rather than the amount of cholesterol that’s carried within the HDL sub-fraction. For more interviews please visit www.cardio-debate.com
Views: 225 Cardio Debate
PET versus Cardiac MRI for Diagnosis of Myocardial Ischaemia and Microvascular Dysfunction | ESC2016
Professor Ornella Rimoldi from San Raffaele Hospital in Milan, Italy, speaks to Cardio Debate & Radcliffe Cardiology about the PET and Cardiac MRI for diagnosis of myocardial Ischaemia and microvascular dysfunction, during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* PET and Cardiac MRI have been around for many years. What are the different contributions they make to assessing myocardial ischaemia and acute myocardial infarction? Let me point out that PET is Positron Emission Tomography, which is a nuclear technique that has been around since the early eighties. Magnetic Resonance came around years after. So PET is a mature technique to assess fully quantitative myocardial blood flow and myocardial perfusion. As to Magnetic Resonance, the assessment of quantitative myocardial perfusion is possible but it is still in its teens, so is mainly a tool for research. As to myocardial ischaemia, there was a paper published and the first author is L. Gould in 2013, reporting around 5000 studies with positron emission tomography to assess myocardial ischaemia. And it is an expensive technique, but it is the best technique to assess myocardial blood flow and myocardial flow reserve. Magnetic resonance is better suited to assess a previous silent myocardial infarction and to quantify the extension of the MI. So let’s say that they are two techniques that can be complimentary. There are many papers on infarct size assessment with MRI, and the technique is very, very sensitive because you can detect two per cent of the LV mass infarction, and this has prognostic implications. The same can be said for flow reserve assessed with PET. It has prognostic implications – mainly in diseases that are diffuse impairment of the microvasculature, like hypertrophic cardiomyopathy, be it primary, congential or hypertensive cardiomyopathy, and also in heart failure with reserved ejection fraction. This is still a field that needs to be explored, because it’s still an ill-defined disease and we are trying to characterise it. Are there also cost-effectiveness considerations that should be contemplated? Cost is the Achilles Heel of positron emission tomography. So it’s a sort of third-level investigation. In Europe it is in-between €1500 and €2000 per investigation. So you need to highly select the patients. There is no point prescribing a PET scan if you just want to see if there is a significant stensosis. This is not the tool to use. It is cost-effective in patients with microcirulatory dysfunction, because these are patients who undergo endless invasive investigations. And there is no significant stenosis, but you go back home and you still have pain and symptoms, and this is the best indication for this type of patient. For magnetic resonance the cost is less, between €500 and €1000. It depends on what the investigation is. And it’s cost effective, again if you are looking for a better definition of infarction. If you want a qualitative assessment of ischaemic all in one session. I use both techniques. I think we need to increase awareness of the prescribing cardiologists of the limitations of the technique, and what you want to obtain. They are not to be used as a shot in the dark – “I don’t know what this patient has, have a look and tell me what is going on.”
Views: 205 Cardio Debate
Cardiac imaging in CAD: Too much of a good thing? Prof Udo Sechtem - ESC2016
Professor Udo Sechtem from Robert-Bosch Hospital, Germany, speaks to Cardio Debate & Radcliffe Cardiology about cardiac imaging in CAD during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* Is cardiac MRI overused? Well that’s a very difficult question to answer because cardiac MRI is used in different health systems in very different ways. It is not used often in the US, it is used in some institutions in the UK, and is used in some institutions in Germany. And in Germany it’s not even paid, so the major health insurers don’t pay for cardiac MRI, just as for cardiac CT in Germany. Now I think the general question is imaging overused? And this may be the case, because patients with chest pain, whatever kind of chest pain they have they will receive imaging, and only five per cent of all studies are currently pathologic. Meaning that 95 out of 100 studies basically do not give any answer, apart from confirming what the doctor may have suspected right at the beginning – that the patient doesn’t have any serious disease. Is it counterproductive to have so many options of cardiac imaging modalities? I think it may be quite confusing for the GP who has the patient with chest pain sitting in front of him and he needs to make a choice. He has to send the patient somewhere, and he has heard many lectures about the benefits of this and that, and that would make it more difficult. But it certainly doesn’t contribute to the overuse of imaging, I believe. What is the right strategy for young people with suspected myocarditis? (Echo versus MRI) The right strategy to diagnose whether they have myocarditis or not is sending them for an MRI exam. That makes most sense in patients who have some troponin and some ECG changes, but if MRI us normal you can reassure the patient that they don’t have any serious disease. And if it is abnormal then you have to care for him and forbid sports and work, etc, and then reimage him after three months.
Views: 221 Cardio Debate
Oestrogens, microvascular angina & possible treatments in HF - Prof Giuseppe Rosano
Giuseppe Rosano, visiting Professor at Medical School, St George's Hospital, University of London, UK, talks to Cardio Debate about oestrogens, microvascular angina & possible treatments, and new therapeutic treatments in heart failure. For more interviews please visit www.cardio-debate.com *TRANSCRIPT* Oestrogen and coronary artery disease (CAD) and microvascular angina in women: is it a pathogenic mechanism? Why? Is there a treatment? Oestrogens are very important to women, and are important throughout their life. What is important is the balance between the oestrogen and progestin. After menopause, there is a drop in oestrogen levels. And oestrogen is a naturally occurring calcium antagonist. So basically, after the menopause there is a loss of the vasodilatory effect of oestrogens, and this causes an increase in blood pressure on one side, on the other side an increase in vascular resistance. On the other hand, oestrogens have at least 300 different actions at the genome level that influence activities like the renin-angiotensin-aldosterone system, the release of naturetic peptides, the release of vasoconstricting factors, and therefore all the changes that occur after the menopause, altogether coexisting, cause an increase in vasomotor tone. Now this increase in vasomotor tone is increasing vasoconstriction, causing an increase risk – or increased prevalence – of microvascular angina. And part of the changes that are occurring with the oestrogens are evidenced in some women before the menopause. For example, women with catamenial migraines, so migraines that occur before the menstrual cycle. These are women that are more prone to develop these vasomotor changes with the drop of oestrogens. Regarding the mechanisms, it’s not just related to one single factor, there are several factors that are related to oestrogens. Regarding the treatments, we were shown a long time ago that oestrogen replacement therapy is effective in improving symptoms and exercise capacity in women with microvascular angina. What is important with hormone replacement therapy, is that it is started early after the menopause. Because if it is started too late it may be helpful, but if it is started early after the menopause it confers some benefit. And in those women with microvascular angina, it may give them significant symptomatic benefit. Which are the current effective treatments for Heart Failure? What are the new drugs with different mechanisms of action for heart failure? Regarding heart failure, we have two different faces of the coin. On one side we have acute heart failure where we don’t have any new treatment that has been shown to be effective for the past 15 years. And so we are still looking for effective treatments that may be effective in the acute phase. But patients that survive the acute phase, patients that become chronic, then in these patients we have several drugs that have been proven effective in the past 20 years, like ACE-inhibitors, Beta-blockers and mineralocorticoid receptor antagonists Now, these three class of drugs are extremely effective at reducing mortality and morbidity. After these three drugs are implemented, in patients with sinus rhythm ivabradine is a drug that is effective at reducing the composite end point of mortality and morbidity. So it is a drug that should be considered in all patients who are still symptomatic despite treatment. There’s a new treatment that has been shown to be effective, and it is the combination of valsartan and sacubirtil. This is a new molecule. Basically they took two molecules and bonded them together into one chemical entity. So in theory they are two different drugs that have been put into one single molecule. This combination has been shown to be effective in reducing mortality and morbidity in patients with chronic heart failure with increased levels of naturetic peptides, or who were still symptomatic after maximal therapy with background therapy. The effect of valsartan/sacubitril, or LCZ696 was more significant at that which was achieved with a sub-optimal dose of enalapril – an ACE-inhibitor. So it is a very promising drug. What is important for valsartan/sacubitril is to understand in which patients it can be used safely, because of course the sign of the study identified a very specific patient population - which patients can tolerate the drug that may induce hypertension. But once these two main problems are solved, it will be a very important drug that will further improve the benefits that we already have in heart failure. Now together with drugs, we have devices. And we are learning that resynchronization therapy is extremely effective, implantable cardioverter devices are extremely effective. Now the new trials testing the effect of mitraclip that basically repairs the dysfunctional mitral valve should give us results soon, and if proven positive then could be suggested for clinical indication.
Views: 398 Cardio Debate
ESC 2015: Dual antiplatelet therapy in unstable angina - Prof Gislasen
Professor Gunnar Gislasen, Gentofte University Hospital, Denmark, talks to Cardio Debate about his recent study that investigates the differences in dual anti-platelet treatment for acute coronary syndrome in patients undergoing PCI or not. For more in-depth insight and analysis on issues in cardiology visit the Cardio Debate website: www.cardio-debate.com TRANSCRIPT Well this is a register-based nationwide study from Denmark. We wanted to look at the persistence with dual antiplatelet therapy in patients with acute coronary syndrome. We know that the guidelines recommended at least 12 months period of dual antiplatelet therapy for all patients after acute coronary syndrome. We have done a similar study in the early clodipogrel period, where we found that especially patients not undergoing revascularization, had no persistence on dual antiplatelet therapy, shorter treatment duration and less often started on therapy. Now we have three different ADP receptor blockers available – clopidogrel, prasugrel and ticagrelor. So what we did, we identified all patients admitted with acute coronary syndrome – that is myocardial infarction and unstable angina – and we included in total 9700 patients, mainly patients with myocardial infarction, 90 per cent (8700 patients), and 1100 patients with unstable angina. What we found, that patients not undergoing revascularization were less seldom started on dual antiplatelet therapy, especially among patients with unstable angina. And in total 30 per cent of patients were not started on dual antiplatelet therapy. When we looked at the persistence we found that approximately 30 per cent of patients stopped dual antiplatelet therapy after the first 60 days of treatment, especially among patients not undergoing revascularization. So the conclusion of the study is that we need to be more focused on using dual antiplatelet therapy, starting patients on treatment and improving persistence, especially among patients not undergoing revascularization. How will these findings impact on clinical practice? Well the impact is that this is a treatment that we know prevents recurrent vascular events. We need to focus on patients where they are more likely to start treatment. We also need to focus on the individuals that we are not starting on therapy, and identify the reasons among doctors and health care personnel why they are not starting treatment. And then to secure long-term treatment – at least for most patients 12 months of treatment – we now need to focus on those patients that are most likely to discontinue treatment prematurely.
Views: 142 Cardio Debate
Devices for managing Heart Failure - Prof Francisco Leyva
Cardio Debate talks to Prof Francisco Leyva from Aston University, Birmingham, UK, about his presentation in the Heart Failure section during the Cardiology Update 2016 meeting, organised by St George's, University of London on the 2nd December 2016 at the RSA in London, UK. For more interviews please visit www.cardio-debate.com -TRANSCRIPT- What were the key messages in your speech today? I concentrated on the incidence of sudden cardiac death in patients with heart failure, and the role of device therapy in patients with heart failure. The recent Defibrillator Implantation in Patients with Nonischaemic Systolic Heart failure (DANISH) study [1], which concentrated on patients with nonischaemic cardiomyopathy has shown that there is no benefit from adding defibrillator therapy in patients with heart failure and nonischaemic cardiomyopathy. Now this has led to a lot of questions because the current indications are there, both in terms of UK guidelines, NICE guidelines and European guidelines. But it’s important really to appreciate that the DANISH trial may have been underpowered to answer that question. It dealt with just under 1100 patients, and we know that with a meta-analysis we need about 14,000 patients to demonstrate a beneficial role of ICDs in patients with noniscaemic cardiomyopathy. There are other aspects, of course, in that nonischaeimic cardiomyopathies can be very varied – can be valvular, can be hypertensive, can have scar or no scar, and they have different rates of sudden cardiac death. So one noniscaemic cardiomyopathy can be very different from another. So I have gone through some various data sets in order to show that, and I think that further studies will be needed, because it is likely that the guideline groups will take notice of the excellent DANISH study, but it is not the definitive answer. I also reviewed some of the evidence for remote monitoring in heart failure. These are monitors within cardiac devices, defibrillators and CRT devices, and largely they’ve not shown to be of benefit in terms of hard end points – mortality and morbidity. However I think they are of definite benefit to patients. I do wonder whether the heard end points are the right way to measure the effect, because effectively a remote monitor is a diagnostic adjunct and it’s always difficult to demonstrate a mortality benefit from a diagnostic tool. I also touch upon some of the studies on device therapy using quadripolar leads, which are now a standard of care in most centres, and really have been shown to be of benefit to most patients, and to virtually eliminate the need to bring patients back for the repositioning of left ventricular leads. References: 1. http://www.nejm.org/doi/full/10.1056/NEJMoa1608029
Views: 210 Cardio Debate
Direct Oral Anticoagulants (DOACs) and the impact of 'antidotes' - CardioEd Lecture
In this free-access CardioEd resource from the recent Cardiology Update 2016 meeting organised by St George's University of London, UK, Dr Steve Austin, consultant haemotologist from St George's University Hospital's Foundation Trust talks about the use of DOACs and the impact of 'antidotes' in the treatment of atrial fibrillation. The Cardiology Update 2016 meeting focused on heart failure management and stroke prevention in patients with atrial fibrillation. For more free-access OnlineMedEd resources visit www.cardio-debate.com TRANSCRIPT What impact will having an ‘antidote’ have regarding the use of DOACs in real life clinical practice? You raise a very important question, what effect having a reversal agent will have on clinical practice, and there are certainly a number of implications. But the first thing that is important to remember is the Direct Oral Anticoagulants (DOACs), these new agents that we use, basically have a much safer profile than the previous agent – warfarin – than we were using. And this is so important to appreciate, because people were reluctant to prescribe it without a reversal agent. So it raises the issue of whether the presence of a reversal agent will actually improve prescribing. But indeed it probably won’t be used nearly as much as people might think. So the reluctance to prescribe is somewhat influenced by anxiety over bleeding, but the data doesn’t support that. So the first thing is it might influence people to prescribe a little bit more, because they think there is something they can use. And certainly that is important. But actually what is really important, that will have a big implication on clinical practice, is certainly that this agent can be used in urgent situations – whether it be in a patient with uncontrolled, life-threatening bleeding, which is a rare problem for these patients on this drug, but it can occur – or whether it can be use to simplify and streamline the management of a patient who requires an urgent procedure or surgery. So you can imagine if a patient comes in and they have been on dabigatran, which is the one agent that we do have a reversal agent for, if they have been on dabigatran and they can be given the agent and sent off to theatre if they have fractured their hip, for example. There’s no waiting around, or giving them lots of plasma products, or things like that. So it will certainly change that practice. It will also certainly change the way we think about people who might not have been put on an anticoagulant previously because of problems with bleeding. If they have a very high HAS-BLED score, for example, or whatever tool you’re using to determine bleeding risk. People can be reluctant to put them on anticoagulant. And so high-risk patients at higher risk of bleeding than the standard patient, people might be more happy to prescribe say dabigatran because there is idarucizumab – a reversal agent. So I think it will slowly influence that. But beyond that, will influence when these patients have procedures because they come in needing something urgent and they don’t have to wait. It will reduce bed time, in terms of stays in hospital, because the whole thing will be much less complicated. So there are big implications for clinical practice. What proportion of AF patients in the UK are now receiving DOAC treatment? That’s a very important question, and the first thing I would say to you is not enough. The second thing I say to you is it is completely variable. It depends on what region of the UK we’re talking about. If we look at the national median from last year’s reports we get around 16 per cent of patients are on DOACs for AF and stroke prevention. That’s versus all the rest being on warfarin. But that’s not really enough. There is still a proportion of patients who are either not treated at all, or who are on aspirin which we know is not an adequate treatment for stroke prevention. So basically we need to improve that uptake still, and I hope that over the years to come people will get more confident in the use of these agents, and patients will be put on appropriate preventative strategies.
Views: 390 Cardio Debate
Coronary microcirculatory pathophysiology: Can we afford it to remain a black box?
Professor Axel R. Preis, Charite-Universitatsmedizin, Berlin, Germany, speaks to Cardio Debate & Radcliffe Cardiology about coronary microcirculatory pathophysiology and if we can afford for it to remain a black box, during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* Could you briefly describe why the coronary microcirculation plays an important role in CAD/myocardial ischaemia? The microcirculation is actually the ‘business end’ of the circulation, because in the smallest vessels, which distribute all the materials, the oxygen and nutrition, and everything, you have a very small diffusion distance to the actual working myocyte. So you need a very working microcirculation to have a well-supplied myocyte array. It’s a little bit like small roads in a town. You couldn’t supply a town only by big roads, you need the small roads to reach every single house. And over the last 10, 20 years there’s more and more evidence that problems in microcirculation underlie a number of diseases that lead to myocardial problems. Many people come into the hospital and you look at the large vessels, and the large vessels are okay. But still they have angina and have problems with the heart. And then the assumption is that the microvessels are disturbed and there is somehow a problem with the microvessels. What research should be conducted to help us understand its role better and guide medical therapy? That’s an interesting question. Over the last 30 years there has been a shift from mechanistical research in animals in addition to what we do in man, towards imaging research mostly in men. Which is good on one hand because we want to use as little animals as possible. But on the other hand we lose the capacity to find out what is really the mechanisms. And that can only really be done in the model when you can change things. And therefore what I think is needed is something we want to call a Coronary Microvascular Observatory, where you can look into the microvessels of a beating heart and see what kinds of problems appear. Are they occluded? Are there leukocyte-endothelium interactions? Are they compressed by the tissue pressure? Are there inflammatory processes? And these days this can be done very well by modern microscopic techniques. During the last 10 or 15 years the development of two-photon microscopy, of photo-acoustic microscopy, of light-sheet microscopy have all enlarged the array of possible investigation tools so much that we can now focus on these things. But you need to bring together experts from the functional cardiac site or the vascular site, and these people who can deal with these modern microscopes. It’s really like an astronomical observatory where you need one guy to fix the lense and deal with all the physics, and another one having to question, with respect to science. And this should come together on a large scale, creating groups – with one group bringing the questions and another group saying how they can address these questions.
Views: 237 Cardio Debate
Genetics of sudden death: mendelian diseases, SIDS and SADS - Lia Crotti
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 216 Cardio Debate
What's New in the Management of Diabetes? - Prof Nikolaus Marx - ESC2016
Professor Nikolaus Marx from Aachen University, Germany, speaks to Cardio Debate & Radcliffe Cardiology about what's new in the management of Diabetes during the ESC2016 Congress held in Rome, Italy. For more interviews like this please visit www.cardio-debate.com *TRANSCRIPT* The most critical point that we learned over the past few years is that therapy should be individualised, with Hb1c targets below seven as the regular target, and more stringent targets in young patients without cardiovascular disease, and more loose targets in subjects with higher age or comorbidities. In addition to that, we learned that we should avoid side effects such as hypoglycemia or weight gain. Why do we have anti-diabetes drugs improving CV outcomes and what are the mechanisms of action that makes them effective? For years we haven’t seen trials reducing cardiovascular events with anti-diabetic drugs. But only recently the EMPA-REG OUTCOME trial testing empagliflozin and SGLT2 inhibitors versus placebo showed a reduction in cardiovascular events, driven by cardiovascular death and hospitalization and heart failure. In addition to that GLP-1 analogue reduced cardiovascular events in the LEADER trial. The mechanisms are unclear, but as far as we know today it is not glucose-lowering, or glucose-lowering alone, but additional effects such as weight loss, or as of yet unknown effects may have contributed to the results. Is there anything on the horizon in terms of further CV outcome data? There are a couple of cardiovascular outcome trials that are coming – trials with the agents that I mentioned, with the SGLT2 inhibitors and the GLP-1 analogues. In addition to that there is the CAROLINA trial comparing Linagliptin, a DPP-4 inhibitor - versus a sulphonylurea, so challenging our current concept that the second important drug after metformin is sulphonylurea, and the study is testing whether Linagliptin may be more beneficial.
Views: 309 Cardio Debate
ESC 2015: PCSK9 a ‘game changer’ in the treatment of familial hypercholesterolaemia - Prof K Ray
Professor Kausik Ray speaks to Cardio Debate and Radcliffe Cardiology about PCSK9.
Views: 72 Cardio Debate
Can ablation prevent sudden death? - Magdi Saba
The A to Z of Sudden Cardiac Death - The latest in the prevention of sudden cardiac death for the clinician. Cardiovascular Sciences Research Centre 5th Annual Meeting Programme - 28th November 2014 - London UK
Views: 1113 Cardio Debate
HDL and Cardiovascular Risk - Prof Gillian Cockerill
Prof Gillian Cockerill, Head of the Vascular Biology Research Centre at St George's Hospital University of London, speaks with Cardio Debate & Radcliffe Cardiology about HDL and Cardiovascular Risk during the "Advances in the Pathogenesis and Management of Cardiovascular Disease" 2015 meeting, organised by the Cardiovascular Sciences Research Centre of St George's University and held at the Royal College of Surgeons of England in London, UK. Transcript HDLs have anti-inflammatory properties; which inflammation pathways are affected by HDL? Well that’s quite a good question. Just to paraphrase it, what I would like to tell you about are the inflammatory pathways that have currently been investigated at molecular level with regards to how efficient high density lipoproteins can be at ablating or reducing inflammation in diseases. Currently there’s an awful lot of data on raising HDL as being protective in sepsis. So the pathways of inflammation that are elicited in sepsis are very well characterised, and there’s a lot of molecular analysis information that we have on the way HDL interferes with the binding of LPS to CD14 on monocytes and endothelium. And another pathway that has been looked at with regards to HDL, which is a common pathway of many diseases, is the ability of high density lipoprotein to inhibit cytokine-induced adhesion molecules on endothelial cells. And so prevent monocyte-adhesion and inflammation through those pathways. And there are common cellular inflammatory pathways that are found in the etiology of a number of diseases. Why has CTP inhibition so far failed to show a beneficial effect in patients with coronary disease? The cholesterol ester transfer protein inhibitor class of drugs have thus far given unimpressive results. They are supposedly able to raise high density lipoprotein and some have the ability to also lower low density lipoproteins. Now so far the drugs tested which have significant high density lipoprotein raising abilities have given very negative results in clinical trials, where they have been used to look at the improvement in acute coronary syndrome patients. And it may be that the ability of this drug to raise the production of high density lipoproteins is not overcoming the ability of that high density lipoprotein to become affected by the factors that are involved in the inflammatory scenario of a chronic condition. We know that chronic disease alters the status of high density lipoproteins, and has been shown to be able to modify high density lipoprotein from protective to almost protagonistic. So in an acute coronary syndrome patient, the high density lipoprotein is no longer anti-inflammatory. Its complexity is adjusted in interacting with other lipoproteins in cell membranes, and results in a particle that is pro-inflammatory – or at least no anti-inflammatory. So perhaps the actual hypothesis is somewhat naïve in that raising HDL alone is the way to go. What we need to do is to find out what is the mechanism of raising HDL that is protective, rather than just simply raise HDL globally with these treatments. Currently there remain two products in market under trial – evacetrapib and anacetrapib – and they are due to report either this year or next year. But both those drugs not only have HDL raising ability, but they have further LDL-lowering abilities in addition. So benefits may come from further lowering of low density lipoprotein. But nevertheless it will be interesting to see what happens to the heterogeneity and complexity of HDLs in those patients treated with the drugs. For more interviews please visit www.cardio-debate.com
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