It's a Catch-22: morbid obesity can keep patients with advanced heart failure from getting a new heart, but advanced heart failure can also keep them from getting weight loss surgery.
How can clinicians manage such patients? Andrew Perry, MD, finds out in this episode of the AP Cardiology podcast through a conversation with Radha Gopalan, MD, of Banner-University Medical Center in Phoenix.
A transcript of the podcast follows:
Perry: In this episode, I am visiting with Dr. Gopalan from Banner University in Phoenix to discuss bariatric surgery in patients with heart failure. He shares an interesting experience and perspective of working with morbidly obese patients who are declined from heart transplant due to their obesity. We discuss the risks of the surgery and the benefits of bariatric surgery on functional capacity. I thought it was super interesting and hope you do so as well. Thanks for listening.
Perry: This is AP Cardiology and this is your host, Andrew Perry. Thank you for meeting with me today, Dr. Gopalan. Can I have you say your name and your title for our listeners?
Gopalan: Thank you, Andrew. I'm Dr. Radha Gopalan. I'm the Medical Director of Heart Transplantation, Mechanical Circulatory Support, Total Artificial Heart, and Advanced Heart Failure at Banner-University Medical Center in Phoenix, Arizona.
Perry: Perfect. Thank you. I am visiting with you today about a topic that doesn't get a lot of attention. We had some questions regarding bariatric surgery in patients with heart failure, so to frame our discussion I'm going to present a case.
We saw a 55-year-old woman with obesity, a BMI of 38, who is insulin-dependent diabetes and hypertension, and she presents with a few months of exertional dyspnea and fatigue. During her workup, she ends up getting a resting echocardiogram demonstrating a normal ejection fraction of 55%, and the diastology, when you look at it, is most consistent and suggests elevated left atrial filling pressures. She's put up with a diagnosis of heart failure with preserved ejection fraction.
As a lot of people know, the heart failure with preserved ejection fraction, a lot of these patients are fairly obese. My first question for you is how obesity can contribute to heart failure, both preserved and reduced ejection fraction?
Gopalan: I'm glad to note that you had framed the BMI at 38, and actually, that falls into morbid obesity paradigm. Heart failure has different ways of looking at obesity, so I'm going to quickly just give you an overview of how we look at patients with heart failure who are obese.
Perry: Perfect.
Gopalan: Obviously, we like patients that have a BMI less than 30, ideal for our situation. But when patients' BMI falls between 30 and 35, we have this obesity paradox concept where the obesity itself appears to protect these women and men with regard to the adverse effects of heart failure with regard to mortality and morbidity.
But most of the studies of retrospective analysis have shown that once you cross a BMI of 35, then the adverse effects are enhanced or increased. They . Their hospitalization increases, the trajectory and rapidity of clinical deterioration increases, and they just don't do well. There are several reasons for that and I think that is still being explored.
Having said that, how does obesity contribute? One of the issues, especially looking at obesity, is it's a metabolic disease process. So as a result of metabolic alterations, especially these patients tend to have other comorbidities such as obstructive sleep apnea, diabetes mellitus, either insulin-dependent or non insulin-dependent, and hypertension. When we looked at this... interestingly, you framed the patient at age 55.
Hypertension, men tend to have more hypertension under age 45 and then women start getting more. Incidence of hypertension in women increases as the age increases, and then they surpass men after age 65 in having hypertension. As a result of it, if you extrapolate that, they have heart failure with preserved ejection fraction incidence higher as the age progresses in women.
Having said that, the molecular etiologies and pathways that lead to heart failure with preserved ejection fraction in men and women with obesity is still in the exploratory phase where we are trying to figure out what pathways exactly lead to heart failure as such. In clinical experience, we come across both. We do have patients who have morbid obesity and don't have heart failure; and we do have patients who have obesity and have heart failure.
Obviously, obesity is one of the contributing factors, but we are beginning to think obesity is a manifestation of a similar molecular and neurohormonal pathway that leads to heart failure. We are in the clinical phase, as specialists, looking to see -- the obesity is as much of a manifestation as heart failure is a manifestation of probably the same underlying molecular pathway alterations or genetic alterations. That is the thought process.
Perry: Interesting. I guess that frames that concept a bit differently as opposed to obesity being a risk factor and perhaps a driving causative mechanism. But you're suggesting that there may be a separate underlying mechanism that results in both obesity and heart failure. Is that correct?
Gopalan: Correct, and I think what I'm trying to say is the mechanism that drives obesity also contributes to heart failure rather than you have to first develop obesity to have heart failure.
Perry: Gotcha. Very interesting. Okay. I had not heard that.
Related to obesity, it's hard to help patients and guide them along weight loss programs and strategies through either pure lifestyle changes and/or assistance with medications. That's where bariatric surgery has come in and has been a huge player in patients, at least in terms of non-heart failure patients, just a pure obesity population, in helping with large amounts of weight loss and sustained weight loss over long periods of time. One question with these overlapping paradigms of obesity and heart failure is a question of whether bariatric surgery in patients with heart failure with preserved ejection fraction would improve their clinical outcomes, such as heart failure hospitalizations and/or even survival.
Gopalan: Interesting question. One of the things that... as you can see in heart failure, the obesity now is in the radar for us. Especially in our program, we have been successful in . Those are patients who are normally turned down by most of the bariatric programs as being high-risk. As a result of this... and I'm going to share with you some of the observations as an advanced heart failure guy and the difficulties we have faced, which will sort of set the tone for the subsequent discussion.
What we find is that we have women and men, mostly women... and I'm going to say most women tend to... the incidence of obesity in women is more than in men. Most women who have obesity, because of the physiology differences, they tend to have more heart failure with preserved ejection fraction, as opposed to men having heart failure with reduced ejection fraction. That's because of the physiology difference.
The physiology difference is one of those that have been identified being women with obesity, or even without obesity, any afterload stressors such as hypertension or other afterload stressors, women tend to develop concentric hypertrophy as opposed to men who have eccentric hypertrophy of the heart.
There is a difference. Eccentric hypertrophy mostly leads to systolic dysfunction and concentric tends to, at least at the initial phases, before it becomes burned out, results in preserved ejection fraction. But nevertheless both are heart failure.
What we had felt and experienced is that these tend to be young men and women between the ages of 30 to 50 who unfortunately develop heart failure. Mostly, my world has been exposed to reduced ejection fraction. That's when I get patients in to me for transplant evaluation. Unfortunately, they are not transplant candidates if their BMI is more than 35, so most transplant programs in the country it is an exclusion criteria to transplant. That is based on the database that came out of International Society of Heart and Lung Transplant, where they looked at obese patients who underwent heart transplantation. They had increased complications and their morbidity and mortality was higher compared to people who were not obese. As a result, we draw the line at BMI of 35.
What is the next step for these patients who have what we consider end-stage heart failure to improve quality of life and extend their life? Naturally, we gravitated with the development and advances of mechanical circulatory support. We gravitated to implanting mechanical circulatory support, especially left-ventricular assist devices in these patients, hoping that will improve their ability to lose weight because it will improve their functional capacity. But most of the retrospective studies, the finding is the opposite. In other words, their obesity worsened...
Perry: Interesting.
Gopalan: ... after the implantation. As perceived, exercise capacity was not the driver of obesity. It's just the behavior of the patient. Even though they were able to exercise, it just didn't get done. There were other factors that were restricting and limiting the patient from going through it.
We started seeing these patients with left ventricular assist device who are now not candidates for transplant still. Even after being implanted with the device, they don't lose weight to a BMI less than 35. In fact, they started having more complications with the device because of the belly obesity. When it increased in size, the abdominal girth increased. Anyone who had seen a left ventricular assist device, the device itself is implanted within the chest cavity, but there is a driveline that's connected to the device that comes out of your belly, abdominal wall to be connected to the batteries of the driver.
What we experienced is when the abdominal girth increased with increasing obesity after device implantation, their complications of driveline infection increased. When they had driveline infection at some point in time, we were not able to rescue them from developing sepsis and device infection and subsequent hospitalization.
We started seeing young patients with morbid obesity dying without a doorway or a pathway for them to actually go to transplant, which then left us to think about, "Hey, how about we make them lose weight by bariatric surgery?"
Perry: Sure.
Gopalan: Then the barrier there is the most bariatric surgeons won't touch these patients, even if they have a left ventricular assist device. From a cardiology perspective, we cardiologists think once you have a device your circulatory system is taken care of, so you should be able to go for the surgery. We will clear it. But surgeons are not familiar with it and they will decline these patients unless the surgeons are working with a heart failure specialist who can then support them. That's what happened.
We are seeing nationally, and I am sure internationally, more and more patients undergoing bariatric surgery with the collaborative work between bariatric surgeons and advanced heart failure cardiologists. That's what happened in our center. We have performed in excess of 50 bariatric surgeries in morbidly obese patients with reduced ejection fraction. If I counted preserved ejection fraction, the number is even more. We have performed bariatric surgery on patients with left ventricular assist device, but here is what I want to comment on: The interesting thing that has been published and being looked at is we had few patients who were transplant... the barrier to transplant for them, they were evaluated in transplant programs, and the barrier to transplant was the obesity. It's a single barrier and the patient was told, "If you get rid of this, you will be a transplant candidate."
They were referred to our center. We successfully got them through bariatric surgery and their BMI dropped to below 30. What we found out is they are no longer transplant candidates for another reason, because they are doing much better.
Perry: Oh, interesting. Okay.
Gopalan: So they don't need transplant. That allowed us to look at the . When bariatric surgeons and most of the programs follow these patients with regard to their other comorbidities, where we found heart failure improves, the requirement for diabetic medications decrease after bariatric surgery, the requirement for the amount of antihypertensives for these patients significantly decreased or even eliminated, and most of the obstructive sleep apnea patients don't even require CPAP anymore.
If you look at the benefits of it, it's multifactorial, not just not requiring transplant. As a result, there are initiatives in most robust bariatric programs to start developing bariatric surgery as a strategy to even treat these comorbidities and influence these comorbidities, rather than looking at obesity as a secondary product of these comorbidities.
I think they coexist. Going back to our initial conversation about obesity and heart failure, I think the underlying mechanism is perhaps very much linked together and heart failure is not a result of obesity. We just happened to find that. Now, the question one might ask in the academic world is, "How about patients who don't have heart failure who are obese?" Right?
Perry: Sure.
Gopalan: That question needs to be answered and we don't know whether it is a matter of time. It depends on how long you have had the obesity in order for you to manifest heart failure and the other is what degree of other comorbidities that coexist in an obese patient. We have not teased out that fine-tuned information to be able to answer that question.
Perry: Interesting. I'm certainly no expert on this topic, but I do recall coming across some data to suggest that bariatric surgery in obese patients does prevent the... or there was a reduced likelihood of developing heart failure in the future for some of those patients. But, of course, I don't know any of the caveats from that data or some of that.
Going back to what you said to kind of go over some more specifics is, so you're seeing patients who have end-stage heart failure and are not transplant candidates because of their obesity. They end up getting a bariatric surgery, losing weight, so they go from greater than BMI of 35 to less than 30. Then it sounds like most of them, or a lot of them, have an improvement in their functional class to the point where they are no longer transplant candidates. Does this also come with an improvement in more objective signs like in terms of ejection fraction or echocardiographic parameters, or even like measured exercise tolerance? Do you have any data or experience there?
Gopalan: We don't. We actually haven't. That is a great question, so I think one of the things is the two parameters you just mentioned -- ejection fraction and functional capacity -- these in the heart failure world are two main factors we focus on to predict longevity. Right?
Perry: Yes.
Gopalan: The question actually, in fact, extends into asking does this bariatric surgery and loss of weight, with its associated improvement in other comorbidities, produce longevity indicators for these patients? Have they improved their lifespan by losing this weight? It's something that needs to be looked at, but functional capacity significantly increases. Our experience is, when these patients who are transplant candidates, the single most parameter that the transplant centers use to tell them that you are too well for transplant is the functional capacity.
We do cardiopulmonary exercise testing, measuring the maximum or peak VO2, which is one of the cornerstones of the decision-making process for transplant. In most centers, if the VO2 is less than 12 in patients who are being treated with beta-blockers for heart failure that's an indication to consider transplant workup. If it is more than 12, then that is kind of the cutoff, where we don't. We continue to manage them medically.
If they are not on beta-blockers, then the cutoff VO2, maximum VO2, is 14. If it is less than 14, you will be worked up for transplant. We have seen improvements. I think across the retrospective analysis, across the literature world, we are beginning to see that improvement.
To my knowledge, I haven't seen a prospective study that did cardiopulmonary exercise testing before and after, something that we are designing at our program. And ejection fraction, anecdotally, we have seen improvement in ejection fraction after the bariatric surgery.
Most bariatric surgeons will perform surgery in patients who have an ejection fraction more than 30 without involving a heart failure guy. They are comfortable because the patients... most of the surgeries now are laparoscopic, they are not open abdominal surgeries, with very little fluid shift, so they are comfortable performing the surgeries. But when the ejection fraction drops below 30, most of the patients get turned down.
What we are beginning to see is if the ejection fraction is less than 20, the chances of recovery of the ejection fraction tends to be less compared to the ejection fraction higher, more than 30. In other words, what we are beginning to look at is if there is moderate LV dysfunction. I don't think we can still define very clearly from an ejection fraction perspective, but I think what we could do is talk in terms of moderate versus severe LV dysfunction. If there is moderate LV dysfunction and the weight loss efforts, including bariatric surgery, is instituted early, there is an increased potential for recovery of the LV function, as opposed to waiting till severe LV dysfunction occurs. The reason in our world is most likely fibrosis.
Perry: Sure.
Gopalan: If irreversible fibrosis has happened in the heart, reversing that process and recruiting mechanical ability for the ventricle to contract, even if you reverse the underlying neurohormonal molecular pathways that facilitated obesity, doesn't seem to produce a robust result. These are areas of exploration and great areas for research and studies that we are looking at.
Perry: Very interesting. Very cool. One last little question, just to be clear: It sounds like this is also safe for these patients. You've had a lot of patients go through this procedure and their outcomes and their surgical risks are acceptable, like they're not a prohibitively high surgical risk for undergoing this surgery.
Gopalan: Yeah. Another great question. Yes. If you look at... one of the things we do in cardiology is risk assessment for non-cardiac surgeries, so every resident, and fellow, and internist, and cardiologist are called upon by surgeons that say, "I need clearance." Then, at that point, our job is to assess the risk of developing cardiac complications during the non-cardiac procedures.
What we found is that I have not excluded any patient who had heart failure with reduced ejection fraction based on ejection fraction. In other words, we have performed bariatric surgery in patients who have an ejection fraction of 10%. But we have a process and we have successfully got them through the procedure because, as I mentioned, it's a laparoscopic procedure.
What we do is we get the patient ready and prepared. A couple of things happens and I want to... since we've worked with a bariatric surgeon closely, and I am in the operating room at the initial phase of anesthesia with the bariatric surgeon and anesthesiologist watching these patients.
The process we utilize at our center is if a patient has an ejection fraction of less than 25%, we bring the patient in. If they have demonstrated and confirmed heart failure, we admit the patient a couple of days before and insert a PA catheter to measure hemodynamics. That way we assess, because as you know, in obese patients, all your clinical examination's out the window. You can't even get a transthoracic echocardiographic image that tells you exactly where the patient is. We cannot look at the RV.
It's hard to look at the IVC diameter to evaluate volume. More importantly, we have no idea what the cardiac index is to supply the obese patient. We do a right heart catheterization with hemodynamics, and then based on that, if their cardiac index is less than 2.2 we place them on inotropic support, so they are being prepared with inotropes. This is under 25% ejection fraction.
Once we document normal cardiac index and diurese them to a CVP less than 10, and if they don't have RV dysfunction, they go for surgery. Because during surgery the most feared times are two instances. That's what you have to... if you get the patient through those two instances, most of them go through the surgery without a problem.
The first one is when you put the patient in reverse Trendelenburg. When you put the patient to prepare for the surgery on the surgical table, there is significant reduction in venous return because of pooling of blood in the veins due to the position.
At that time, the preload to the right ventricle is reduced and as a consequence, the preload to the left ventricle is reduced. As you know, based on our calculations, the stroke volume is reduced so cardiac output is reduced. They become hypotensive and they have a tendency to develop arrhythmias, so that is one.
The second instance is when the bariatric surgeon introduces air into the abdomen to separate the bowels and to be able to see clearly. That increases intra-abdominal pressure, thereby further reducing venous return by compression of the veins and the inferior vena cava. These are the two main barriers that I have to get my patients through. Once I get them through, after that, the procedure proceeds unimpeded to a successful outcome.
In our experience, we have not had a single complication in the OR or have lost a patient during the admission for bariatric surgery. I have lost patients afterwards because of non-compliance and progressive heart failure, but we have not lost a patient perioperatively because of considerably high risk.
Perry: Gotcha. Okay. Very cool. Very interesting. I'm, unfortunately, going to have to cut us off there, but a really interesting discussion and really cool experience to hear about what you're doing there with bariatric surgery and heart failure patients. I'm looking forward to hearing more about this. It sounds like you have some interesting studies and data collection that you're working on right now, so looking forward to hearing and reading more about it.
Gopalan: Thank you, Andrew. I wish you good luck with the continued service that you are providing to our young physicians.
Perry: Cool. No, I appreciate it. Thanks again, and hopefully I talk to you again.
Gopalan: Thanks for having me. Take care.
is a cardiology fellow at the University of Washington Medical Center in Seattle.