Part one of three. An interview with Nir Uriel, MD, Director of Advanced Heart Failure and Cardiac Transplantation.
Part 1: Heart Failure
The raising rates of heart failure in the U.S. are pretty staggering. With a growing population over age 65, diabetes and obesity on the rise, studies project the rate will continue to climb. Talk to us about heart failure deaths, why the rise?
You know, this is a critical question not enough people are addressing. I will tell you something, heart failure historically was a disease that a primary physician or cardiologist could treat, or theoretically, every doctor could. But it's evolved. Unfortunately, in the mindset of the majority of physicians, it has not evolved yet. Instead, they think they can take care of these patients and when they identify that they cannot anymore and the patient is too sick, they offer the patient hospice care. Yet that patient missed out on the near entirety of treatment.
The sad truth is that the majority of heart failure patients are not taken care of. Only 20 percent of heart failure patients are treated by cardiology. Instead, the majority are taken by primary physicians, and of that 20 percent I just mentioned, only 8 percent are treated by a heart failure specialist.
This is the first problem that we face. If you look at the recent journal paper that came out about compliance, we wanted every heart failure patient—even without going on a sophisticated therapy—to at least be on three medications. Only a minority of patients get them, and of that minority, only 1 percent gets the right doses. That’s how bad it is.
Wow. Tell us about these medications—What’s new in the treatment of heart failure?
The treatment of heart failure has gotten a significant boost in the last few years. First of all, we understand that we're dealing with multiple diseases. So, each one of the diseases started having a path of their own in order to treat it.
Speaking of two of the most exciting medications that have come into the market—one is a group called SGLT2, it's a medication, actually, we used to use for diabetes and it just causes you to pee more sugar out. But when we pee more sugar out we pee a lot of fluid out, so it can be a treatment for heart failure. And a recent study showed that a group of medication, the SGLT2—and specifically dapagliflozin—reduce significant mortality and readmission of patients with heart failure by 20 percent. So this is a big jump and something that we can very simply adjust with medication.
That’s incredible.
And the other medication that’s made lots of headway in the last few years is Entresto. This is actually a combination of two medications, one called valsartan, which is an ARB [Angiotensin Receptor Blockers] that we used to treat heart failure, and another twist ingredient called sacubitril. The combination of the two of them makes like a hemodynamic medication. And in the study that was published in NEMJ, we actually saw a real paradigm shift because it was superior to all the other therapy that we have given up to now. So it's completely changed our practice.
Even with the simple heart failure patient that comes to the office today, this is not the old, narrow therapy that they get. We have a lot of new treatments, and those are just two examples of what we have available.
Have any specific conditions or diseases within the heart failure patient population seen transformative shifts in treatment?
Oh yes, within the heart failure population sometimes we tier out other patients. For example, patients who developed heart failure due to cardiac amyloidosis, and that’s a disease where protein actually gets stuck to the heart. And it was very sad for us for a long time because eventually we always had to say to them, "You know, we don't have any more to offer to you." But today we do.
Now, we have multiple therapies for amyloidosis, and unfortunately, most people still don’t know about them. They think it's a death sentence. But, even here at Columbia, we were the leader in the study to evaluate Tethamalsis, the new medication that shows significant reduction. It has changed completely the way we look at amyloid right now because we can save those patients.
How important is early detection, or early treatment rather?
Oh, that’s such a good question—we need patients to know that treatment is available and to come to get therapy as soon as possible after diagnosis because the earlier you get it, the better the results.
How does medical therapy for amyloidosis work?
So Tethamlis is interwoven with the protein that's supposed to be stuck to the heart. And it's actually blocking its creation. It's actually a very simple mechanism, and this is only one example in heart failure.
Heart failure treatment has also changed completely for sicker patients, the ones who really require a significant amount of attention. And those patients sometimes will come in and out of the hospital, having a tough time adjusting to treatment. But today we can implant a small chip into their pulmonary artery, a chip called CardioMEMS.
Amazing, tell us about this chip implant.
So this chip is probably something like one centimeter big, and we send it through a femoral vein and go into the pulmonary artery and drop the chip in. Then we calibrate this chip with a catheter called a swan. A swan catheter gives us the pressure in the pulmonary artery. And after this calibration, we send the patient home. Patients go home with this chip, and of course, it doesn't feel like anything. The recovery is simple. It's an ambulatory procedure, and they go home the same day.
Then they get a special pillow. Where every morning when the patient wakes up, we ask them to lie on this pillow. And that is literally it—the pillow and the chip do the work. They lie down and the CardioMEM that is in them transmits the pulmonary pressure of this specific patient to the pillow and the pillow puts it into the cloud. And we in the office can see exactly how our patients are doing, right now in real-time. If the pressure is too high we can call them and say, "You know, I know that you feel okay, but something is blooming. Please increase your diuretics." Or the contrary, we can say, "You're too dry. Can you eat a bag of chips and don't take your diuretics today?”
You’re kind of blowing my mind a bit! Is this chip readily available? What have you learned by having this type of access to your patient’s immediate pressure readings?
Oh yes, it’s already an FDA approved chip. This remote monitoring technique has reduced the rate of heart failure hospital admission by more than 30 percent. And in actual real-life studies, not in the official champion study, by up to 70 percent. And really this is just the beginning, there are a lot more treatments coming down the road, and at Columbia, we are trying to participate in any study that is going to develop remote monitoring.
By doing this daily remote monitoring, have you found things that are really surprising to you?
All the time. I have to say, that in the beginning, you're sure that you are a very good clinician. You know, you look at your patient and you just know what their fluid status is. But what we learn is that we really count on ourselves too much. We actually did a big study, published in the Journal of Cardiac Failure, and we took a group of patients that came to the intensive care unit and we asked the residents, the fellows, and the attendings to examine the patient and tell us if the patient has a lot of fluid or not a lot of fluid. If they have a lot of blood flow and if the circulation is normal or not. And then after that, the patients were immediately taken to the cath lab and we evaluated the hemodynamics of those patients. And guess what, we were as good as the flip of the coin.
Whoa.
Medicine is evolving, and I think the big part of the evolution is the quantification of accurate data; not based on an assessment that is subjective to what I really feel and think. The big challenge right now in the medical field in general and in heart failure is to accept that there is so much data coming into the system, that even as smart as we think we are and as talented as we are, we don't have enough computing power or enough understanding to see it. And we need some help from technology.
The study turned out so positive, especially because all of us were a little bit skeptical. I remember the first patient I put a CardioMEM into. And I did it because almost every month they had to come in, they would call with discomfort, "I'm so bloated." So, we would increase the diuretic. And then there would be renal failure, and then they “was too dry.” Almost every month they were coming to the hospital.
After the CardioMEM implant, they were not admitted into the hospital for more than a year. Even when they called we were always able to assess risk. Patients are concerned and that’s a good thing, but when you have an objective prompt that can really guide your care accurately it changes everything for them. Even if our patients are traveling we can know what's going on with them. This is a huge, huge change, and we’re really taking it to the next level with centralized heart failure.
I have a feeling there’s even more technology you can drop here that will make our jaws drop a little.
Always. We constantly see more and more technology coming in, isn’t it wonderful? Here’s an example, this company called EKO—they do a simple 20-second EKG and by reading this simple EKG can tell you with 97.9 percent accuracy if a patient has heart failure with a low ejection fraction. Just by a simple EKG.
The difference is, we in cardiology will read this EKG and we'll just see whatever we read in the EKG. The machine can identify a very subtle pattern that we never saw. So, this machine learning is going to allow us to identify patients early, to identify which patient will be at risk, to identify which medication is the right medication for those patients. And I truly believe that earlier identification for disease will lead to much, much better treatment, longer life, and improved quality of life.
When you say better treatment, do you mean the earlier a heart failure patient is identified, the longer you will be able to treat them medically as opposed to more invasive procedures?
I’m saying it will change even that. So, the question that you're asking is very right—are we going to treat them longer or are we actually going to change the natural history of the disease?
And we know today that early intervention in heart failure can change the natural history of the disease. Intervention with medication that can induce what we call a reverse remodeling and progression of the disease is available and this is already something we use.
Incredible.
I know! I'm very excited about that. I'm very excited about the new technology that's coming in the field of acute decompensated heart failure too. We have multiple devices now being evaluated that are going to change everything completely. Unfortunately, when a patient comes in with acute decompensated heart failure right now, I treat them almost the same as I would have treated them 40, 50 years ago. I give them oxygen, I give them diuretics, I can give them morphine if they need it. But there is not a lot that you can actually give to those patients. Now we have a lot of devices that are going to try to change this philosophy across the board.
Would you say this is where you’re seeing the greatest change in treatment?
Well actually, we've seen a complete change in our two strongest modalities of advanced heart failure. One is LVAD, left ventricle assist device, and the other is heart transplantation.