Samuel Asirvatham, MD, discusses contemporary management of artial fibrillation in heart failure.
thank you for the opportunity to talk about the uh complex area where a tra fibrillation, heart failure coexist and how management of one can affect the other. So we spend about 20 minutes to look at this very specific area of overlap. So these are the great epidemics often impacted by atherosclerosis of heart failure, metabolic syndrome in atrial fibrillation. There is this area where if eb and heart failure coexist and as a cardiologist will have to think about unique issues in what we recommend for managing the defibrillation in these patients, this is a common problem. Not only do both these conditions coexist, but the more severe the heart failure and the more longstanding the fibrillation and the more additional comorbidities a patient has. It can get close to being the majority of patients who have this coexistence in the syndrome. And it is important to appreciate that although these two entities are diseases in their own right, in this overlapping scenario, a vicious cycle, positive feedback cycle where the heart failure and ventricular dysfunction itself may make atrial fibrillation more difficult to manage and it atrial fibrillation per se, and especially with rapid rates, can make heart failure more difficult to manage. So one side of this equation is what's been established now for decades that heart failure is pra arrhythmic for the atrium, this maybe as a result of left atrial pressures being high regurgitation in the mitral valve stretch of the pulmonary veins as well as actual fiber optic changes that happen in the atria perhaps as a result of the condition that led to heart failure itself. The opposite side of that scenario, which makes this a vicious cycle is the eight of fibrillation from high rates irregularity in the rhythm, poor ventricular filling the loss of atrial sisterly can make heart failure in addition to ventricular dysfunction. Also, heart failure, symptom ecology worse in this patient population and both together, the arrhythmia and the poor perfusion can give rise to neuro hormonal activation and the more this happens the worst heart failure, the worst date population. Now, if we think about whether the temporal relationship is important, this goes back to one of the earliest studies that explored this relationship. If we think about the chance of heart failure developing an impatient who had atrial fibrillation first, then the incident heart failure diagnosis is fairly high, regardless of gender. On the other hand, if the index event is heart failure and we look at the cumulative incidence of atrial fibrillation, then the impact is less in men, but similar in women. So in other words, foreman, if you start off with heart failure or you don't, the chance of developing atrial fibrillation in the age group of this study was quite similar. Later, this was explored more in a little bit more detail in a relatively small study, to again understand which is the key driver here for morbidity, mortality, hospitalization and in this, if we look at this until date, this is among the best data that we have, it's always worse when the index diagnosis is heart failure. On the other hand, if it was atrial fibrillation and heart failure happening at the same time, often these patients have better outcomes because not only is the two fibrillation possible cause of the heart failure symptoms and hospitalization, but treating it has a good chance to improve outcomes. Now, our priorities are a little different when we are managing heart failure and managing it for fibrillation, NATO fibrillation is a lot about stroke prevention and improving symptoms in heart failure, a largest preserving ventricular function, improving forward flow, preventing pulmonary edema and patient symptoms. But there is a significant degree of overlap and for example, controlling rate or maintaining sinus rhythm often becomes a key decision in this patient population to help with the heart failure symptoms. We should note that there is also an interplay when it comes to stroke risk. Just heart failure alone is a trombone genic state and one of the well established risk factors in patients with atrial fibrillation is coexisting heart failure. So at this point before we think about our decision making in the patient, we understand that there is this potential positive feedback and we have to think about what's the optimal therapy and we'll spend the next few minutes to talk about options and what we can do about heart failure itself by managing atrial fibrillation and then we'll finish with a few differences between Beth and Beth now, one of the old ideas is that faster the heart rate, the less the life expectancy. And this is kind of like a theological type argument. But it is key to remember that all trials that looked at sinus rhythm maintenance sources, rate control for atrial fibrillation. We make this decision independent of managing stroke risk with anti coagulation or other therapy. And rate control itself may require rhythm control to be successful. What I mean by that is we have to recognize what is a good rate. What good rate control is degree of symptoms with inadequate rate control and the option of maintaining sinus rhythm for rate control. Over the years, most of you are aware that uh strict rate control, like resting rate, less than 80 beats per minute is rarely required. And most of the time all commerce with a profit relation, as long as the patient does not have symptomatic palpitation, relatively lenient heart heart rate control, 100 to 100 and 10 beats per minute. Uh, is reasonable. Now, this, however, can be different in heart failure and in general heart failure symptoms are less well managed when the rates are consistently higher. So although we don't uh maximize rate control with medical therapy because of side effects bradycardia. Uh, in the heart failure population, we tend to target heart rates a little closer to resting heart rate of 80 beats per minute or so. Now one of the questions that come up is our beta blockers, which are indicated for heart failure. Our drug of choice when there is a tree fibrillation and we need rate control. Intuitively this was thought to be the case. And in fact, some meta analysis studies which, however, had a lot of older studies that didn't have good monitoring for a tre fibrillation actually suggested that compared with placebo, if beta blockers are used in heart failure, you actually got leslie confabulation, but this is generally thought to be an artifact of the monitoring. The flip side is we know beta blockers across the board are beneficial and heart failure, but this is this was true when looked at independent of rhythm that is in sinus rhythm, not in arrhythmias. When we actually look at patients to look at the advantage of beta blockers, it's almost exclusively restricted to patients in sinus rhythm. So in other words, once atrial fibrillation, is there the big blocker benefit specifically for heart failure management is difficult to demonstrate translated. This means we should not feel hard pressed to reach first for beta blockers when we are trying to read control in coexisting syndrome of FM and heart failure. Another question that sometimes comes up in patients or colleagues is what can we do when there's coexistence and heart failure to uh have mortality benefit, since it's not that clear with beta blockers or other therapies, the only one debate is really a C inhibitors that regardless of sinus rhythm or arrhythmias, a mortality benefit in managing heart failure is seen Now, even though we accept that symptom management is key and we want to try to do this with rate control many, many patients. The question of rhythm control comes in either because we just can't rate control or because they still have symptoms despite rate control, especially in the heart failure population here, we may also see correlation of incident a film during heart failure, hospitalizations that makes us drive towards a rhythm control strategy. Now, how do we do this? So, one of the things that's uh difficult is standard drug therapy for a tribulation when there is heart failure. If there is a systemic heart disease infarction, we have contra indications for drugs like play tonight and pro pathan on because of heart failure being a low output state and coexisting renal insufficiency. It can be difficult to use primarily renal clear drugs and even less commonly used drugs can be almost uh impossible to use when we wind up having coexisting structural heart disease. Here's an example, One of the fears patients started on a potassium channel blocker. Heart failure worsens renal failure worsens previously stable drug. But now now take a cardio related cardiomyopathy. The typical syndrome is no real palpitations goes undetected for a while. But compared to other patients with a fib uh and heart failure, they're not quite as sick. So the a fib is asymptomatic. The heart failure is not that symptomatic. So patients come to attention quite late, There is multifactorial methods, although it is still primarily a disease of rapid rates. There are some patients where just the regularity or maybe coexisting drivers such as neuro hormonal hormonal that cause both to occur. There's also well described studies that just the presence of atrial fibrillation over time can increase ventricular fibrosis as measured during uh CMR should also be as clinicians aware of heart failure symptoms even though the ventricular function is normal and maybe even compliance is normal. But there's primarily atrial ventricular valve regurgitation. Just as we know, annular dilation can occur with ventricular enlargement. Some patients atrial fibrillation and massive atrial enlargement can also produce functional atrial ventricular regurgitation and these patients may benefit from restoration of sinus rhythm. Here's an example from our practice. Uh I'm sorry only difference. Uh Only difference that we see here is cardioversion and uh this uh cardioversion and some time for remodeling. What about evidence for uh specifically treating to maintain sinus rhythm in heart failure and when we look at combined endpoints we do get more benefit from catheter ablation than drug therapy in the heart failure population than when we think about all commerce. We should be aware though that non pharmacological therapy can really take two types in heart failure, maintaining sinus rhythm with catheter ablation if anti arrhythmic drugs have failed or getting a better handle on rate control with a V. Note ablation and pacing usually with crp in the heart failure population when rate control strategies are failing most of you are aware that ablation really was born Pareto fibrillation from the observation that the transition from sinus rhythm, atrial fibrillation. In some patients are from discrete areas that can be targeted for ablation. The vast majority of those discrete areas are from the pulmonary veins and pulmonary vein isolation with or without heart failure has a better than drug therapy alone, chance of maintaining sinus rhythm. On the other hand, we also know that in heart failure with atrial stretch atrial fibrosis, it may not be just the pulmonary veins that drive a truck population. So in these patients it may be likely that they may still need anti arrhythmic therapy along with treatment. And this is the notion of atrial fibrillation that substrate mediated longstanding heart failure valvular disease. Probably less benefit from ablation alone versus a patient with a relatively normal heart and paroxysmal atrial fibrillation when successful, even partially, there can be benefit in heart failure class and ventricular function. On the other hand, as a cardiologist. Following up patients who've had ablation, we should also be aware of something that happened at ablation that's made heart failure worse. One that we are should always be open to looking at his pulmonary vein stenosis, The symptoms of pulmonary vein stenosis are very similar to heart failure, exacerbation with the exception that cough is prominent. So if a patient has shortness of breath, but previous heart failure was not that prominent with cough then should think. In a post ablation patient of uh pulmonary vein stenosis. As cardiologists, we should also be aware of emerging changes in technology where non native that is not heating the tissue in the veins as a treatment for atrial fibrillation. One of these that is uh steadily gaining traction as an option is pulsed field or electro operation therapy should also be aware that post ablation bisney, a maybe from pericardial disease or inflammation. In addition to pulmonary vein stenosis, frantic nerve damage can happen especially with right side and ablation near the superior vena cava and a very important syndrome where left atrial pressures increase after ablation, even though ventricular function has not changed and is thought to be from increasing stiffness of the left atrium. Typical story, there is multiple ablation procedures should also appreciate that there are common drivers for atrial fibrillation and heart failure and this has to do with the autonomic nervous system. In fact, some studies have shown that a tre fibrillation begins as a neural phenomenon prior to what's happening in the pulmonary veins and and the atrium. And most of you are already aware of the critical role of the autonomic nervous system, particularly sympathetic drive in heart failure. The modulation of the autonomic nervous system is now actively investigated, both for treating heart failure as well as atrial fibrillation and for atrial fibrillation, the specific areas are where the autonomic merge onto the heart behind the atrium in the gangling. Now, outside of ablation, CRT therapy is also impacted by atrial fibrillation and the key take home. There is unless the rates are controlled were lose ground with CRT alone in patients with a fib and heart failure. So rate control will be important to allow for maximum pacing with by ventricular pacing. Many patients this winds up with a requirement for a V node ablation one second. Okay now if the rates are well controlled then we'd say a V node ablation and with adequate placement of CRT leads, there can be tremendous manifestation, patient symptoms and uh at times improvement in ventricular function and facilitation of uptight trading other medical therapies as well. It's an example of a patient with marked the synchrony in heart failure, atrial fibrillation and then much more improved synchrony along with rate control and crp. The key to remember though is we have to maintain rates. Unfortunately in some patients that means a V node ablation or a trial of sinus rhythm maintenance even though they may not have symptomatic palpitations. Few things about diastolic heart failure and atrial fibrillation. It's unequivocal that the stroke risk is very very similar. So heart failure, not the mechanism of heart failure is what we think about in adding stroke risk for patients with atrial fibrillation. When we look at this though, the emerging idea of a fib with ff is it's a biomarker. A fib is more a uh a marker that there is heart failure and atrial stretch. Uh and eventual treatment has to be with better methods of treating diastolic heart feeling. Now, one thing we should be aware of is that the heart of the symptoms in half with a fib may be much worse than in sinus rhythm with exercise. There's a shortening of diastolic time from inadequate rate control or short intervals. In irregular atrial fibrillation should also appreciate that mitral regurgitation and they left atrial myopathy may predispose to atrial fibrillation in patients who have have, so even if they are not in atrial fibrillation at that time, in addition to the pressures being elevated and actual myopathy, a problem in left atrial compliance can predispose to uh atrial fibrillation. Now, with preserved function and specific scenarios of cardiomyopathy is like hypertrophic cardiomyopathy, a pitfall to avoid is failure to recognize that can be extremely poorly tolerated and give rise to flash pulmonary oedema. So here uh sometimes just watching the weights is not enough and patients should be instructed with worsening shortness of breath or palpitations to present for care and at least attempts to control rate or maintain rhythm. The opposite issue may also occur where some patients after ablation, especially multiple abrasions when they have poor ventricular compliance, hypertrophy feel better in atrial fibrillation and markedly worse in sinus rhythm. So paradoxical worsening with sinus rhythm. It's not common. But the two things to think about. The stiff, left neutral syndrome, very difficult condition to manage. But those patients actually have atrial contraction that works against them and can worsen heart failure. The opposite is because of the atrial myopathy that's present in these population conduction intervals can be very long in the atrium and as a result, left atrial pacing may be required to optimize the timing between the left atrium and the left ventricle. So two things to think about is atrial the synchrony, electrically or stiff left atrial syndrome. If there's paradoxical worsening of symptoms in a stable rhythm invasive human dynamics can be done with different pacing sites To find the right place to place the lead in this patient. A left atrial lead gave rise placed surgically gave rise to improvement, marked improvement in the patient's symptoms. So, to summarize managing atrial fibrillation, even if we're thorough with the choices there and heart failure, we know how to treat the overlap of these conditions. Makes us think a little differently. We aim for better rate control anti arrhythmic drugs. We have to recognize the difficulties in managing post ablation complications. Can mimic heart failure, exacerbations and our options, including newer options for rhythm control, particularly in this population. Thank you very much for your attention