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Can you move that? Can you move your uh thing out of the middle of the uh that's better. OK, everyone. Welcome to the meeting. My name is Raj Kiani. I'm a cardiologist. I work in London and in Milton Keynes. Um I'm going to talk about heart failure. There seems to be a wide audience from different levels of training and different healthcare settings. So this is really, this is really focused on heart failure in the UK. Um And I hope it is of some value, but it's really a developed world setting that we're really talking about. Um what I'll do is I'll do the talk. And then at the end, if you want to put some questions in the chat, I'm happy to answer any questions at the end, I should talk for about 50 minutes, 55 minutes. We say we have 5, 10 minutes of questions at the end. Good. So um heart failure is a very significant burden for the NHS in the UK. 1 to 2% of overall spending, nearly nearly two thirds of a billion pounds per year is spent on heart failure. These, these statistics are from 2016. So that number will only be increasing. Nearly a million people are living with heart failure in the UK 10 million across Europe with a prevalence of 10% in those over the age of 70. So as the population ages, the prevalence of the condition is increasing. The esc the European Cardiac Society, uh heart failure pilot showed that the 12 month mortality even in the modern era remains high at 12% and a 44% rate of hospitalization. So these are very sick patients with high risk of hospitalization and death. This is a chart of the aging of the population across the world. If you look in the European section, you can see in 2012 22% of the population were over the age of 65 by 2050 more than 34% of the population in Europe will be over the age of 65. So this is a real significant aging of the population. And as people reach retirement age, their comorbidity increases particularly cardiovascular disease and cancer. But heart failure is one of the mm most important diseases of an aging global population. This prevalence of heart failure is truly global really there. It's around 1 to 2% in all healthcare settings. Certainly advanced healthcare settings. Probably the variation depends a little bit on how developed the healthcare setting is and how much, how good the infrastructure is to count these sort of patients as well. But across North America Europe and many parts of Asia, we're looking at prevalence rates of 1 to 2%. The definition of heart failure has changed and this is the European Cardiac Society definition. These are the latest definitions. Um And now we used to call it left ventricular systolic dysfunction. And we used to call it diastolic dysfunction with heart failure with preserved fraction. We now call it he heart failure with reduced ejection fraction. With those patients with ejection fraction less than 40%. And that represents at least 50% of the population of heart failure. Then the old fashioned diastolic dysfunction is now called he Pff heart failure with preserved ejection fraction. Those patients with an ejection fraction greater than 50% and about 40% of the overall population of heart failure patients and then the group in between with, with an ejection fraction on trans echo between 40 50% is now called he. So uh heart failure with mildly reduced ejection fraction. Uh And so that's uh a min minority of patients and these patients move between the HFPF and the HFRF population as you follow them up over time as well. So uh the causes of heart failure, it's a very busy slide. There's an enormous list of causes of heart failure. I think the most important ones for you to remember is in the developed world is really ischemic heart disease with myocardial infarction or stunned myocardium uh with scar related to my infarction causing left ventricular dysfunction. Hypertension is an important cause of heart failure and dilated cardiomyopathy, which is often familial, often inherited uh in which you get dilated left ventricle poor function. Often there's very little in the way of scar or there's patchy scar on cardiac MRI uh which is a very increasingly recognized and increasingly important cause of heart failure. Uh And of course, there's a huge array of causes. I've listed some of them here on these slides. But um valvular disease, tachycardiomyopathy with fast af pacing induced heart failure. The these are, these are more niche um areas. And uh as long as you remember, the first three, those are the critical um populations. So, the complications of heart failure. Well, if you've seen the heart patients with heart failure, the most common complaint is fatigue and breathlessness and exertion and their exercise capacity is often significantly reduced. Um but there are a huge array of complications of heart failure. They may, they are at risk of arrhythmias including atrial fibrillation, v ventricular arrhythmia such as VF and VT. And we risk stratify our patients for ICD, implantable defibrillator, uh implantation to try and identify those patients at risk of sudden cardiac death from VT or VF. Um stroke is not uncommon in heart failure patients, particularly with um particularly those patients with um atrial fibrillation, for example. Uh but also you can get left ventricular dysfunction from uh with the left ventricular dysfunction, you can get left ventricular thrombus, which can cause a stroke as well. Depression is not as completely understandable because the exercise capacity and what they can achieve is much reduced. Sexual dysfunction and cachexia are also important uh causes of heart failure. It's important to identify depression because social isolation and depression are negative prognostic signs. So those patients have a poor outcome with heart failure. So how do you assess a heart failure patient? Well, you as in all patients, uh history, examination and investigation history is critically important with every patient including um heart failure patients. So you go through the previous medical history. For example, if they had hypertension, if they're known to have uh previous stenting or c car cardiac bypass grafting or my infarction, uh if they're cancer patients, if they've had chemotherapy agents, which may cause left ventricular dysfunction, um symptoms that are very suggestive of heart failure are orthopnea. So they or they need uh heart failure. Patients feel very breathless when lying flat because the palm edema is more um prevalent throughout the lung fields when you're lying flat flat, when you sit up, of course, the gravitational effect will reduce the edema to the lung base and the rest of the lung fields will be clear. So, orthopnea where they, where they feel very breathless, lying flat and they need two or three pillows or even four pillows, five pillows at night to sit up m make improves their breathing. This is highly suggestive of heart failure and P MD where they wake up gasping for breath in the middle of the night, they often have to go to an out uh open window just to get some fresh air. These are highly suggestive. And if you take the history and you, you have these features in the history, then um I'm sorry, excuse me, if you have these features in the history, then um then you should be highly suspicious of heart failure. Of course, in examination, you're looking for raised jugular venous pressure, sign of raised right atrial pressure with congestive cardiac failure. If the left ventricle is impaired, there will be secondary pulmonary hypertension and secondary right heart failure, which will raise the left, the right atrial pressure crackles at the basis ankle edema or sacral edema. Uh uh and uh other signs like um a gallop rhythm, for example. And uh other other signs like an atrial fibrillation can all be suggestive of heart failure. The ECG any abnormality on the the ECG can be normal in patients with heart failure, but any abnormality of the ECG should be taken seriously if you've got uh adverse clinical history or examination findings. Um Can I just check the chart cause? Uh Yeah. Ok. That yes. Ok. So the most important uh test that you can do in a heart failure patient is BNP, brain na peptide or NT pro BNP, which is a precursor of BMP. These uh these um na peptides are circulated. Uh They're, they're secreted from the heart, the chambers of the heart including the left atrium, um and are elevated in patients with serious cardiac disease, including heart failure. If the B MP is negative, then it's highly unlikely that the patient has heart failure. And other non-cardiac diagnosis should be considered Poe emol COPD pneumonia. There's a whole host of anemia, a whole host of causes that should be considered if the B MP is positive and it's highly positive. So, NT pro B MP, more than 2000 that is highly suggestive of heart failure. And those patient uh uh and, and um and these patients should all have an echo. Any patient with a raised BMP should have an ech A to confirm the diagnosis and also to work out what the etiology of the heart failure is whether this is valvular disease, severe aortic stenosis, severe mitral regurgitation or he or he and you'll work out the etiology from the echocardiogram. There are a few false negative um causes of uh uh so, so the B MP can be falsely negative uh in patients who are obese or those patients who are already on diuretics, perhaps for hypertension or any other heart failure medication. Again, for hypertension, for example, uh and these can cause a drop in the B MP. And so you may be falsely reassured by a negative reading of B MP in patients who are on these medications. These are the European Cardiac Society guidelines. So we've discussed BM 12 lead ecg. These are and transthoracic echo. These are essential uh diagnostic tests for all patients with heart failure. But really most patients will be going on to have routine blood tests as well as well as a chest x-ray as well to confirm palm edema, uh or to look for other non-cardiac causes of breathlessness. Uh and the routine blood test that you'd be doing for most of your patients, but include uh thyroid function, glucose diabetic cardiomyopathy is increasingly recognized as an important cause of he and iron studies because iron iron deficiency is a reversible substrate in patients with heart failure as well. And I introducing iron uh intravenous replacement of iron therapy can help reduce hospitalization with patients with um heart failure syndromes if they're iron deficient, um many of you will know about the three pillars of heart failure medication, but we're actually now moving to four pillars. But if we just start with the basics. So, ace inhibitors, beta blockers and uh Mra A S mineralocorticoid receptor antagonists have been the three pillars of heart failure for 2030 years now. And they've all been shown beta blockers and ma s such as spirolactone or eplerenone have been particularly uh important in showing reductions in mortality as well as symptoms of heart failure. So, these are critical drugs that all heart failure patients should be considered for. But now we're moving on and we now have four pillars of heart failure. So SGLT two inhibitors which are diabetic drugs are now also being demonstrated to be very good drugs for heart failure patients. And we'll talk a bit more about that later. And Sacu Valsartan, which is known in the UK as Entresto is the trade name is, has both uh an A two blocker with a Valsartan and SACU which is a Nepro inhibitor. We'll talk a bit more about that in a minute, have also been shown to reduce mortality in heart failure, both of these drugs. So now we have four pillars of heart failure. So, cubital Valsartan is hitting both the the ace inhibitor pathway, the the renin angiotensin pathway as well as the Nepro lyin pathway. SGLT two inhibition with dapagliflozin or empagliflozin um Aldosterone antagonist such as spirolactone or Eplerenone beta blockers as well. So the the four pillars of heart failure critical for all heart failure patients. This is the paradigm HF study which was a landmark study. It was actually published several years ago. 2014, I think um it was a multicenter study, a global study actually uh 47 countries, nine more than 900 sites, more than 8000 patients were randomized and they were randomized to both to ace inhibitors or Cubital valsartan. Now, the cubital component of the drug inhibits nepro lysin. Now, Nepro sin is uh uh an enzyme that degrades nati peptides to their um degradation pro products such as nap peptide A. By inhibiting that drug, you increase the dose of uh na the, you increase the circulating naic peptides, which have a beneficial effect on the renal angiotensin system. They also have a natural diuretic effect as well. And this was the landmark study in which the drug was with, with um paradigm uh in which Enalapril was compared with Entresto LCZ 696 is the uh investigator's name for uh Entresto. Uh And there was a significant reduction in both hospitalization for heart failure and cardiovascular death uh as well. On top of maximum medical therapy including ace inhibitors, this effect was seen across all age groups. Uh On the top lefthand slide, you can see that uh and both for cardiovascular death in the top right hand corner or cause death, the bottom, right hand corner and heart and le and bottom left heart failure, hospitalization as well across all age groups. From the young to the more elderly patients as well. So it's uh it's really uh a game changer in heart failure drugs and these patients all had optimal medical therapy with beta blockers, ace inhibitors um and um uh Eplerenone or Spirolactone on board as well and is on top of that. So nice. I is the UK um committee which looks at new technologies and really it's a sort of a cost effectiveness committee. It decides whether a drug is effective and whether it's cost effective and whether it should be introduced into the National Health Service and they prescribed on Entresto several years ago now. And they have and we are using Entresto widely in the National Health Service for patients with chronic stable heart failure, ejection fraction, less than 35% is still symptomatic with heart failure. Um And the uh who are on maximum medical therapy, we do need to remember that Valsartan is in the drug. So these patients are often already on ace inhibit inhibition. So there needs to be a washout period of at least 36 hours, whether the ramipril or enalapril is washed out before you initiate the drug. Otherwise you'll be doubling it, doubling up on the uh a renin angiotensin inhibition. The say these drugs are generally quite safe and the safety profile is similar to ace inhibitors. So, hypotension renal dysfunction, particularly hyperkalemia are the main side effects. It's a very effective as an antihypertensive. So, if you've got a patient with significant hypertensive heart failure and normal or near near normal renal function, it's highly effective in and, and he with reduced infection, it reduces the h infection. It's highly effective in um in get in controlling the BP and improving the ejection fraction. OK. I'll just move on here. So this is the next study which is called DAHF. This was published just before COVID in the um European Cardiac Society meeting 2019. Uh it got lost in translation because of COVID really. But then has, has really taken off since COVID in terms of prescription rates in the UK. This is a diabetic drug and it was first used in diabetic patients and diabetic patients with normal renal function. It has, it's actually quite a poor diabetic drug, but they noticed that the incident rate of heart failure in the diabetic patients was reduced. Uh It acts as a and so they tried to use it in non-diabetic patients with heart failure to see if it improved outcomes. It's a sodium glucose transporter, it acts in the renal tubule tubule increases the renal excretion of glucose and sodium. Um And uh and um you can see it has a natural diuretic effect because it's allowing the nas of both sodium and glucose into the urine. So, there is a diuretic effect, a modest diuretic effect with the drug itself because of the glycosuria, urinary tract infections also increased uh with this drug. So you just need to be cautious and counsel the patients about urinary tract infections or genital fungal infections as well. But they're, but they're uh the mechanism of action of the drug. It has multiple um you know, basic science mechanisms of actions, but we don't really understand how it's working in heart failure patients. But we know that it's having effects on both the heart, the kidney, the vasculature, the whole body. It's having a modest BP effect. That doesn't seem to explain the heart failure uh improvement effect, but it's uh it's having multisystem effects. And we were trying to tease out the exact mechanism of action at the moment. This was the randomized control trial, Dapa HF. And this was the landmark study. Uh another randomized placebo control trial. 4000 patients, symptomatic heart failure, ejection fraction, less than 40% randomized to 10 mg of dapagliflozin or placebo. On top of optimal medical therapy for heart failure, 18 months follow up and less than half of the patients were diabetic. Majority of patients were non-diabetic. And you can see uh really very nice couple of my curves here. If you look top left hand corner placebos in red dapagliflozin is in blue, you can see a reduction in the primary outcome of heart failure, hospitalization and cardiovascular death. Top right heart failure, hospitalization was significantly reduced. But as bottom left was cardiovascular death and bottom right. Death on many cause was also reduced. So really very impressive results on top of uh optimal medical therapy, it's quite a small slide, but it was just to really show that um the complication rate of the drug was very low um volume depletion with hypovolemia because of the diuretic effect. A small uh renal uh urinary tract infections. Um and uh acute kidney kidney injury can occur with the drug because of the diabetic effect. Uh the diuretic effect. Um non-diabetic ketoacidosis as well with the renal function, although there's a short term dip in the renal function over the long term, it's renal protective. And so if they can get through the short term dip, it will actually slow the decline in the renal function towards endstage renal failure. So we try and uh get patients through that short term dip by reducing the furosemide or other diuretic dose. While we introduce the drug to try and minimize the short term acute kidney injury, so that they can get the long term benefit of prevention of endstage renal failure or slowing of decline towards end-stage renal failure. There were some concerns about thorne's gang gangrene or amputation and these don't seem to have been laid out in the study as significant concerns. And so it's really relatively safe drug other than the side effects, we've talked about the primary outcome of cardiovascular death and hospitalization was reduced really very significantly. Um from 21% to 16%. These are absolute figures which are enormous in heart failure studies. So very impressive reductions. And if you look at cardiovascular death, nearly a 2% reduction in cardiovascular death and a 3% reduction in um heart failure hospitalization as well. Ok. So what does optimal medical therapy look like to me in 2023? Now, these are the target doses that I'm aiming for for all of my patients. Uh very few patients will re reach target dose of all of these drugs because of hypotension or renal failure. But we try and cautiously up titrate the drugs towards these target doses. Uh Bisoprolol, we're aiming for a resting pulse less than 70 10 mg of bisoprolol. Sometimes they use it five BD in patients who are hypotensive to allow, to try and mitigate the hypotension, ramipril five mg BD. It's not really a once daily medication. It's half-life is too short for that. So it can be used once daily, but it's better used uh as a BD drug. We're aiming in he E we're aiming for a blood systolic BP, less than 100 and 10 millimeters of mercury, uh spironolactone or eplerenone. We often start at 12.5 or 25 mg once a day. But we're again aiming for 50 mg dosing once a day, furosemide, we titrate to edema and once out of the acute setting, if they're edema free, we down titrate or even withdraw the Fufu and just keep it on standby because um it gives you more BP and renal function to introduce the other drugs. And uh then on top of that, in these days, in 2023 we would certainly use Dapagliflozin 10 mg uh for both he fre and now there's also data for he PF as well um for either Dapagliflozin or empagliflozin uh uh and Entresto with Cubital Valsartan aiming for target doses of 97 100 and three. But we often start at much lower doses and titrate it up. So this is uh so we'll stop, we'll, I think we'll stop on he E now and move on to HPF. Um heart failure with preserved ejection fraction. As you saw, this is a significant, about 40% of heart failure patients have HPF. And the mortality of HPF patients is high and as severe as he graf patients, you can see here five year mortality on this study approaching 70%. So really very significant mortalities. I think in the modern era, we may get better results on this but still very high five year mortalities. Certainly heart failure syndrome. Patients, mortality is traditionally regarded to be worse than most cancer diagnoses. Although the mortality is improving with modern medical therapy. Um So how do you diagnose he pe heart failure, preserve infection. It's often it's a Cinderella diagnosis. It's often uh poorly diagnosed or often missed. Um And the way I diagnose is, I'm looking for signs and symptoms of a heart failure syndrome. So the patient's breathless, they've got orthopnea P and D peripheral edema. They've got elevated B MP levels. And although the echo ejection fraction is preserved, more than 50% the echo is still abnormal. Often they have signs of raised filling pressure. So the left atrium may be dilated, they may have left ventricular hypertrophy, thickening of the left ventricle and they have what we call diastolic dysfunction parameters. Uh Basically, we look at the filling of the left ventricle through the mitral valve. And there's abnormal filling patterns of the left ventricle. And we can see that when we do Doppler pulse, way Doppler patterns of the filling of the mitral valve, the details you don't need to know about, but just, just be aware that there's abnormal filling patterns uh of the heart, particularly the left ventricle, as we've already said, by definition, the eject traction has to be greater than 50%. But the pop patient is often comorbid they're often elderly, they're often female, they're often diabetic, they usually have previous ischemic heart disease or obesity or hypertension in the background. And uh these are all contributing to the heart failure syndrome. Until recently, there was no randomized control trial to show improved cardiovascular outcomes in um he e and we'll discuss the first study that showed an improved outcome recent, which should been published recently. We'll discuss that in a minute and the treatment of he is really, you control the underlying comorbidities. You treat the hypertension, aiming for very tight BP control. You get good diabetic control. If their patients in A F, you try and restore normal sinus rhythm or if you're unable to restore sinus rhythm, you opt to a rate control strategy. Certainly getting the heart rate controlled. Certainly. Um I aim for less than 70 beats a minute in this population. Use diuretics in a similar way as you would in He e to obtain your vole to offload the patient's um to offload the patient's uh edema completely. Uh balancing against hypotension and renal dysfunction. And exercise has been shown to be very helpful. Once the patient is discharged home, an exercise program or cardiac rehabilitation program can be very helpful in improving outcomes in terms of quality of life and symptom control in heart failure with, with he EFPF patients, beta blockers. We used to think that beta blockers were good for this population and we used to slow the heart rate down to try and improve the left ventricular filling time because the left ventricle is often stiff, noncompliant in these patients. So the filling of the ventricle is poor. So the theory was that by improving, by slowing the heart rate, you improve the diastolic filling time, you improve the filling of the left ventricle, thereby increasing the straight volume. Uh And we still do use beta blockers in this population. But recent data suggest that they may actually in some patients, withdrawal of beta blockers may actually improve symptoms. And some of these patients may have undiagnosed sinus node disease. So you've got chronotropic incompetence because the S A node, the intrinsic pacemaker is not increasing the heart rate properly when they're exercising and the beta blocker is exacerbating that. And so pacemakers and things are being studied in this population to see whether withdrawal of beta blockers or even pacemakers themselves may be helpful in this group. So just be aware that although beta blockers are used, sometimes they can actually exacerbate the syndrome, particularly in patients who got undiagnosed sinus node disease, spirolactone has been shown to improve exercise capacity in this group. And so we do use uh spironolactone, often we're using it to treat the BP or it may be a weak diuretic as well and we're using it for these reasons as well. Ok. So this is the next study called um Emperor Preserved. So this is empagliflozin used in heart failure with preserved ejection fraction. And this was a large randomized double double blind placebo control study. Nearly 6000 patients, symptomatic heart failure with preserved ejection fraction. They defined it as ejection fraction greater than 40%. They randomized the patients to 10 mg of empagliflozin or placebo in addition to their usual heart failure drugs. And there was a significant reduction in the primary outcome of cardiovascular death and heart failure hospitalization again, led by um heart a reduction in heart failure hospitalization rather than cardiovascular death, but really very significant improvements. So we now use empagliflozin, another SGLT two inhibitor in patients with heart failure with preserved ejection fraction and dapagliflozin. There's a similar study with dapagliflozin in preserved ejection fraction. So the SGLT two inhibitors are now used across the spectrum of heart failure from he to he PF and even patients with mildly reduced ejection fraction has these studies included those populations as well. So really SGLT two inhibitors are critic in all patients across the entire spectrum of heart failure. So we've talked about everything in green has data behind it to show improvements in mortality. Everything in yellow has improvement in morbidity but not mortality. Um But we've talked about these, this is sort of the p the ladder of heart failure, escalate uh escalation. We talked about medical therapy, which is really the and the four pillars of medical therapy. SGLT two beta blockers, mineralocorticoid aist and uh uh cubital valsartan. Um In addition to that, we use icds, implantable defibrillators or cardiac resynchronization therapy in selective patients with heart failure, we then move on to in niche areas. We use drugs like ivabradine, digoxin hydrALAZINE isosorbide. Um And they've been shown to be beneficial in certain niche areas. We haven't got time to discuss that today. And then really the apex of advanced heart failure therapies include mechanical circulatory support devices such as left ventricular assist devices or right ventricular assist devices or both or heart transplantation in a highly selective number of patients um as well. So this is the ladder of heart failure escalation and you should be thinking about the whole ladder when managing your patients. But certainly those in green should definitely be used in in all patients who are eli eligible. This is an implantable defibrillator. Um So you can, it's, it's a very similar to a pacemaker. It's slightly larger and bulkier than a pacemaker and uh the conventional defibrillator has transvenous leads, passing through the vein i into the heart, uh and attached it into the heart. You can see little screws at the end of the leads. So we screw into the heart muscle itself. And this is why we do it for abortion of sudden cardiac death. And this is a strip from a defibrillator. And you can see the patient has gone into what looks like polymorphic VT. Normally, they would either black out or have sudden cardiac death. At the end of the strip, you can see what looks like a pacing artifact which is a shock artifact from the defibrillator. And then straight after that artifact, you can see uh a sinus beat and the patient is restored to sinus rhythm. So these are lifesaving devices aborting sudden cardiac death or syncope in patients who are at risk of VT or ventricular fibrillation. They work by first to trying to pace the patient out of these arrhythmias using very aggressive anti tachy anti tachycardia pacing algorithms if which are completely painless. If they work great, the patient is painlessly resuscitated. But if they don't work, then the shock is delivered which is uncomfortable for the patient but potentially lifesaving. This is one of the landmark studies from many years ago, Scud Heft, 2.5 1000 patients uh with severe heart failure with action, less than 35% they were randomized to medical therapy, placebo, amiodarone or single shock single cha I CD, which was a shock only device in those days uh without an tachycardia pacing. And you can see that the amiodarone curves and the placebo curves cross over completely. So actually the benefit of amiodarone while we do use amiodarone, particularly to try and reduce the number of shocks patients may get from defibrillators. There's no evidence that amiodarone improves mortality over placebo in these patients with HEP A. Um and uh but ICD therapy in the Green Dash Line, you can see a very significant reduction in mortality uh at um five years with uh ICD implantation. Um And actually this in this particular study, um it benefited both patients with ischemic cardiomyopathy and non ischemic cardiomyopathy. There's more recent study that conflicts with this. But uh in this early study, it showed benefit in both groups and it showed benefit. The most benefit was seen in patients with MHA class two heart failure. So these are the patients who are minimally symptomatic, they're walking around. They're often working. They may be doing gentle exercise or light exercises and they seem well with their heart failure. But although they do seem well, they're still at risk of sudden cardiac death. They still should be considered if they've got severely reduced ejection fraction, less than 35% they should still be considered for I CD implantation. These are expensive devices they're used while while widely in the UK and the US and Germany. But they are very expensive devices when I first started implanting these 20 years ago. Oh, gosh, even longer now. But uh they were 30,000 lbs per device. So 40 $50,000 they've now reduced significantly. And you can get a good I CD for less than 10,000 lbs. So 12 to $13,000 for a, a high quality I CD good. So this is um I think we're running out of time so I might just quickly go through a couple more and then uh I'll stop for questions. This is cardiac resynchronization therapy. You can see in the top left, there's a lead in the right atrium, there's a lead in the right ventricle and the third lead pacing. The left ventricle from the coronary sinus, which is the venous supply of the heart. You can see an x-ray here showing the I CD lead and the Coronary sinus lead. And what we're, what we're doing here is pacing in patients with re and left bundle branch block. They have a rocking heart. We call it synchronous heart. It's basically rocking. It's very inefficient and it's an electrical disturbance of the heart heart failure patient. What we do by pacing both the right ventricle and the left ventricle by pacing the venous supply of the heart, the outside of the heart, outside of the left ventricle, we pace them synchronously. We eliminate the electrical disturbance of left bundle, we eliminate the rocking motion of the heart, the disy and that improves the stroke volume. And it actually has a very significant effect on improving the cardiac output and reducing hospitalization for heart failure and reducing death from heart failure as well. And this is one of the landmark studies that showed the benefit of the di biventricular defibrillator, otherwise called cardiac resynchronization therapy because we are resynchronization, the heart uh with a defibrillator over and above the benefit of a defibrillator, only in patients with heart failure with reduced ejection fraction and left bundle branch block. So um I think just for time reasons, I'm going to quickly skip through this. And just to say that the ESC guidelines are easily available on an app form or by emailing the ESC and you can get a little poster, little, you know, quick pocket guidelines, but the app is very easy to download on your phone and it's also available on their website. So it's definitely worth either using their website. Um Just to the documents are very bulky, very detailed. But if you just go to the flow charts, you'll get very quick guidelines. Summaries of all the ese guidelines and this is useful for all cardiology, not just heart failure. So if you want to refer to these guidelines, I would strongly uh recommend this. They're very helpful these flow charts, for example. And this is a summary. It's a busy slide. It's a summary, but I just want to bring out some of the things we've discussed today that heart failure, patients with heart failure with reduced ejection fraction. We should be really looking at the four pillows at the top with um the ace inhibitors, angiotensin uh and ani um entresto sacu valsartan beta blockers, mini uh spironolactone or Eplerenone with mineralocorticoid antagonists and SGLT two inhibitors. Of course, we should be using diuretics to offload the patients. And once you've optimized them with the four pillars of heart failure, then you should consider a cardiac device, either cardiac resynchronization therapy with the RV lead and the left ventricular lead or I CD only therapy in patients who've got reduced ejection fraction without left bundle branch block. There's a whole host of other therapies that can be considered. We haven't got time to go in detail into these today. But just to say that you should be consider is considering some of these options such as a f ablation or cardiac bypass surgery or uh Tavis or aortic valve replacements in selected patients with heart failure, for example, a aortic valve replacements in those with severe aortic regurgitation. Uh And you should also consider mechanical circulatory support devices or heart transplantation depending on your health care system. But exercise rehabilitation now that can be in the UK that we try and do that with physiotherapists, psychologists and so on. But it can just be the patient just going on their own exercise program and just increasing their exercise distance every day. And exercise has been shown to be really helpful in heart failure patients. So do encourage exercise as soon as the patient's out of acute heart failure and able to mobilize good. I'm just conscious of time. So I'm gonna stop there and uh allow some time for questions if I may. Uh ma are you moderating? Do you want to moderate the questions? If currently there's no questions in the chat. So if anyone has any questions, please raise your hand or just pop it in the chat? So lovely. Thank you very much. We've got one person as that raising his hand. Yeah, go ahead, please. Uh Yes. Could you see the side? Did you skip? No, when you skip, got it. Uh the whi which one do you mean the one where the leads were in the heart or the atrium? And just prior to that? Yes. And, and this one, yes. And before this, there was a description of this uh S MS D slide number 45 right? Scott Scott have study. Yes. OK. Yeah. Do you have any questions about that? No, I just wanted to like if you could just go in a small brief man. So you want me to go through these here? Hello? Sorry. Do you want me to? Uh Yes, yes, yes, yes. Like in a short, yes, you uh OK. Was, I mean, I think we've already discussed this but uh really Scud Heft was showing these were, these were patients with eject fashion, less than 35% uh randomized to placebo amiodarone or I CD therapy. And I CD therapy had a very uh important improvement in mortality in these patients in both ischemic and non ischemic cardiomyopathy, uh particularly in patients in men with H A class two heart failure. And the studies show that amiodarone was not beneficial in terms of survival. Although we do use amiodarone from time to time for niche benefits, particularly patients who are having recurrent shocks on their ICD to try and reduce the frequency of shocks, for example, uh but it will not have a mortality improvement over five years over placebo. Um And then this is the I, this is the CR T slide and this is the CR TD slide. You can tell this is AC RT D because the size of the IC the generator is much larger than a pacemaker. And if you look in the SVC here, you can see this bright coil, you can also see a coil in the right ventricle as well. And these are the coils from an ICD lead. This is the atrial lead here and this is the left ventricular lead. So, you know, immediately from the x-ray, this is not a pacemaker and this is a defibrillator because of the presence of this dual coil I CD lead. And the fact that the pace the device is about twice the size of a standard pacemaker as well. Um And this is the left bundle branch bo pattern that we were looking for? Good. Does that answer is that, is that what you were looking for? Is that, does that help? Yeah, excellent. Any other questions? We got two more questions in the chat doctor. Um One person says, what does SND mean? Oh So what is the node, signal, node, defibrillator, sinus node snd means sinus node disease. What that means is um so that was let's go back to that. So this is, yeah, this is half ef um so half PF heart failure with preserved ejection fraction. Uh beta blockers have historically been used in heart failure with preserved ejection fraction to lower the BP and to slow the heart rate down and to increase the filling time of the ventricle by increasing the filling time when you've got a stiff ventricle, um you improve the filling of the ventricle and that can improve the stroke volume and the cardiac output. However, there's a recent study that showed that actually when you withdrew the beta blockers, some patients symptoms of heart failure improved and we don't know why that is, but we think it may be because they've actually got sinus node disease. What that means is the pacemaker, the intrinsic pacemaker, which is in the right atrium in the sinoatrial node uh is firing off at 50 60 70 beats a minute, whatever the base heart rate is, as you exert yourself that, that intrinsic pacemaker should increase the rate to increase to in because your workload is increasing, it increases your heart rate to cope with the increased workload. But in patients with sinus node disease, instead of the heart rate going from 70 to 80 to 90 to 100 it just stays flat and the heart rate stays at 50 60 70 it just stays at that level. And if you're on a beta blocker, that can make that even more exacerbate that problem. And that means that those patients with a very flat heart rate, feel very breathless when they're exerting yourself. And if you, because they've got sinus node disease, because the sinus node, the intrinsic pacemaker is not increasing the rate at which it fires. If you remove the beta blockers, then the sinus node starts working properly or at least tries to work as well as it can and then the heart rate will increase. There is some uh there is some data to suggest that putting a pacemaker into these patients may actually help them as well. And so we're looking at research at the moment to see whether we can pace these patients with heart failure, with preserved ejection infection, in particular, those with sinus node disease to improve their symptoms as well. I hope that explains uh a sinus node question. I've got 11 more last question in the chat. Uh Sorry, two more are dry cough. A side effect. In Sacco, sorry, say that again, dry cough cough. Is it a side effect in uh sacri L? Um Dr, yeah, it's similar to the um, you can get a dry, well, it's a Valsartan rather than uh an ace inhibitor. So dry cough is less common with sacu valsartan than with standard ace inhibition because it has less of an effect on bradykinin which is what the mechanism of dry cough with ace inhibition. So we don't really see dry cough as a major side effect. The main side effects we see are acute on chronic kidney injury, hyperkalemia, hypotension. Uh Those are the main side effects that we see. Um Next question is, does the I CD have three leads? If so, can you please reexplain how it works? Ok. Yeah, sure. Um There are two types of defibrillator. The first is uh a dual chamber I CD like this, which has two leads and this device simply has a pacing function and has the ability to shock a patient out of VT or VF. The second uh this is just a standard defibrillator, tran standard transvenous defibrillator and it treats the ventricular rhythm. The second type of device is cardiac resynchronization therapy, which can be either a PA which has three leads, it can either be a pacemaker or it can be a pacemaker with a defibrillator function and you can combine it with a defibrillator function if you wish the leads that it has with this and this is called cardiac resynchronization therapy or biventricular defibrillator. If it's combined with a defibrillator, the three leads are the lead in the right atrium, the lead in the right ventricle and the third lead in the left ventricle. And it's pacing the coronary sinus, which is the venous supply of the heart. And we put the lead in a branch of the great cardiac vein, the the the venous supply of the heart, we pace the left ventricular lead paces, the left ventricle and clearly this lead paces the right ventricle. This lead is in the endocardium. So inside the chamber of the right ventricle, this lead is on the epicardium, outside the heart pacing the left ventricle. And we're using these devices in patients with heart failure with reduced ejection fraction, who have got an electrical problem with their heart with left bundle branch block. So when you have left bundle branch block, what you have is early septal contraction of the left ventricle and delayed depolarization of the post lateral wall. So it's like a rocking motion of the heart. The septum contracts first and then the post lateral wall contracts late. So it's literally rocking. So it's taking a if you imagine taking a wine glass and putting a lot of energy, but you're putting the energy in a circular motion, none of the wine will come out of the glass. What we want to do is re synchronize the left ventricle. So you're pushing the wine forward, it all comes out very easily. And that's what we're trying to do with the left ventricle. And so by pacing the left ventricle from both this, the right ventricular surface and the left ventricular surface, we can pace both the, the septum and the post lateral wall synchronously. And we can remove this left bundle branch block and remove this walking motion so that the left ventricle contracts in a normal contraction pattern and that improves the stroke volume. So patients with he fre with e less than 35% and with left bundle branch block should all be considered for cardiac resynchronization therapy with or without a defibrillator with uh with a defibrillator, it will improve, it will improve mortality, both with a defibrillator and without a defibrillator. But in patients in ischemic cardiomyopathy with big scars, that's a focus for VT. And so we often use it with a defibrillator because there are also risk of VT in that group. Um I hope that explains it. Does that, does that make sense? I hope so. Thank you. Yes, we've got a thumbs up. Thank you very much doctor for such an amazing lecture and I thank everyone else for attending. Um Could I just please have everyone to fill out the survey and the feedback that is very crucial for us to continue. And again, thank you very much doctor for such an amazing lecture and hope to see you next time. Thank you. Thank you for the invite. It's a pleasure. You too. Ok. Bye bye. All right. Bye bye. Have a lovely day.