Author: RankTribe

This transcript has been edited for clarity.

Michelle M. Kittleson, MD: Welcome to Medscape InDiscussion: Heart Failure. I’m your host, Dr Michelle Kittleson. This is the seventh episode of our 12-part series. In the second half of the series, we’re dealing with special concerns, and today we’ll talk about cardiac amyloidosis: What are the red flags and pitfalls in making an accurate, timely diagnosis? What about treatments for transthyretin (TTR) amyloidosis? What will the future look like for expert guidance on these questions? We’ve invited Dr Mat Maurer. He directs the Clinical Cardiovascular Research Laboratory for the Elderly at Columbia University in New York City. He also directs the Cardiac Amyloidosis Program at the New York Presbyterian Hospital, Columbia Campus. Welcome, Mat. I’m so happy to have you here.

Mathew Maurer, MD: Thank you so much. I’m very excited to talk to you today about amyloidosis, one of my favorite topics, obviously.

Kittleson: Speaking of being one of your favorite topics, you have achieved the holy grail of academic medicine, where your name is synonymous with expertise and a clinical condition — in this case, cardiac amyloidosis. In fact, I think you were interested in amyloidosis back when most clinicians were fatalistic about a condition with few treatment options. Cardiac amyloidosis has undergone a renaissance in the past decade. I’d love to know what inspired your initial interest in cardiac amyloidosis and what keeps you engaged today.

Maurer: Great question; I think the latter is easier. What keeps me engaged is the patients. They’re just lovely, wonderful people whom we all have the privilege of taking care of, but they are really a special group of individuals. The question about engagement is a little more difficult. I’m maybe not the brightest person, as Milton Packer once said, but I’m the most persistent. He hired me in 1999 for what was one of the first heart failure programs in the country. Jokingly, he said, “Everyone’s doing systole, so why don’t you go do diastole and relax?” And those individuals in the country who specialize in the clinical syndrome of heart failure with preserved ejection fraction (HFpEF) are much smarter than me and were able to embrace a lot more of complexity, I would say.

But I, fortuitously, began to see patients early on who had cardiac amyloid, was intrigued by the pathophysiology, and then made a few important connections, working with a guy named Jeffery Kelly. For those who don’t know, Jeff invented tafamidis, and he started a company back in the early 2000s called FoldRx. So, we did some seminal work with Jeff: natural history studies, developed a large registry. The rest is history, so to speak, but the motivation remains always the patient. Really, that’s what we’re here for.

Kittleson: I love that question, because I always learn something new, something I didn’t know, and I love the theme behind that, which is if your priority is to take great care of patients, you may not know where the adventure will lead you, but it will lead somewhere good. Let’s dive in, so our guests will leave this podcast knowing everything they need to know about cardiac amyloidosis: from diagnosis to treatment to new advances. It’s a particularly challenging diagnosis to make because it will not be uncovered on routine testing. You need to know to order the right tests to make the diagnosis. If you don’t look for it, you will not find it. Let’s start with those clinical clues that should make a clinician suspect that cardiac amyloidosis might be afoot.

Maurer: Yes. It’s not that hard a diagnosis to make. We develop these appropriate, if you will, algorithms and protocols, and the key thing is you need to be prepared as a clinician to think about it and be aware of it. One of the misnomers in the field is the idea that this is really a rare condition. The provider’s impression is that they’re kind of looking for a needle in a haystack, and the available data that are out there suggest, for example, that among hospitalized patients, if you have HFpEF with an increased wall thickness, you’ve got a 16% chance or some odd of having a cardiac amyloid. If you underwent a transcatheter aortic valve replacement (TAVR), it’s a similar percentage. In the community, it’s a little less common, about 6%, and is quite commonly mistaken for hypertrophic cardiomyopathy (HCM). So, probably about 5% of patients who have HCM are misdiagnosed and probably have amyloid. In those over the age of, say, 65 or 70 years, it could be as high as one quarter; it’s quite common as people age.

The first message is that we’re all seeing cases of cardiac amyloid, and all you need to do is start to let it into your differential diagnosis. As we say, “If you don’t think about it, you’ll never diagnose it.” But to your question about the clinical clues, the central phenomenon is that these individuals have an increase in left ventricular wall thickness. We in amyloid don’t call that left ventricular hypertrophy. We specifically say wall thickness because it’s not hypertrophy; it’s not muscle. The clues are numerous. You can have heart failure in an older adult, particularly an older adult male. We mentioned aortic stenosis. Often, these individuals do not have concomitant hypertension. Their ventricles are small; they have a low stroke volume, so their cardiac outputs are low. Over time, though, these individuals become hypertensive, so you’re cutting back on medicines.

There is neuropathic involvement in some individuals, either a sensory or peripheral neuropathy. They can even have subtle autonomic symptoms — in men, erectile dysfunction — or gastrointestinal upset. There’s the light chain (AL) form of amyloid, which we’re probably not focusing on much today, but those individuals have multisystemic involvement, so you can see proteinuria; you can see periorbital purpura. You don’t see that in TTR often — in fact, very, very rarely — or a big tongue. In TTR, there are all these orthopedic phenomenon that are just fantastic clinical clues, right? We all know about bilateral carpal tunnel syndrome, but there is the classic Popeye’s sign: a ruptured biceps tendon; hip, knee, and joint replacements. Mazen Hanna just reported about shoulder replacements as well. Then there’s a whole host of imaging findings that we can touch upon. But the classic phenomenon is low voltage on the cardiogram, or voltage that’s not necessarily low but just not in proportion to the wall thickness on the echocardiogram. Obviously, for those who have variant disease, taking a family history is quite helpful, because you can find that out on an EKG. Besides a low voltage, obviously a pseudoinfarct pattern would be another phenomenon. In fact, there are so many clues that it’s kind of amazing we don’t think about it or see it more frequently.

Kittleson: I love that, and it’s a great example of why we are all doctors first and subspecialists later. You don’t have tunnel vision on your organ. You can identify these seemingly disparate clinical clues and find a very satisfying, unifying diagnosis. So, say we’ve crossed the first hurdle. We’re thinking about the diagnosis. Now we need to order the right tests. Tell us your approach to a streamlined, accurate diagnosis and the common pitfalls you see in practice.

Maurer: With pitfalls lately — it’s a little bit because we’ve heightened awareness about amyloid. There are lots of people getting tested who may not even have a phenotype that’s suggestive. If we start randomly applying these diagnostic tests to people with a very, very low pretest probability, we’re going to end up with many false positives, and the positive predictive value is not going to be in a range that’s useful to anyone. That’s the first thing, and while I’m very happy about people being aware of this, there’s a constellation of findings. But it does usually start not only with the history that we talked about in those clues, but on echocardiography or MRI, a phenotype that’s suggestive of amyloid. It’s an increased wall thickness with a small chamber or a high relative wall thickness. The approach we use is straightforward. First and foremost, you should probably tell the patient what you’re thinking about. I think we forget to do that. It’s a little alarming for people. God forbid they utilize the internet and they read about amyloid. The first thing that still comes up is a dictum about AL amyloid that’s untreated that says they’re going to be in a grave in 4-6 months, so that’s not a thing you want to leave a patient to find out on their own, in their own home. There’s a lot of shared decision-making. For example, you may say, “I’m thinking about this diagnosis. This is what it entails. This is where my thoughts are.” That’s important, and it’s straightforward.

Regarding streamlining, it’s really a three-step process. You want to evaluate for AL amyloid, because that is quite malignant. That involves essentially three tests that assess for monoclonal proteins. It’s serum protein immunofixation, not just a serum protein electrophoresis (SPEP), but an immunofixation, looking for those small proteins: the kappa and lambda, chains, along with intact immunoglobulin. A urine immunofixation, which can be done on a spot urine; it doesn’t need to be a 24-hour urine collection. And then, obviously, the kappa lambda free light chain, which is probably the best biomarker we’ve ever developed, the reason being it’s a biomarker that’s diagnostic of the disease. It’s a biomarker that’s prognostic: the higher the difference between the involved and uninvolved light chain. It’s part of the Mayo score, and it’s the target for therapy. If only we had such biomarkers in all of medicine, it would make life easy. Those are the three tests to assess for a monoclonal protein.

If someone has a monoclonal protein, then the noninvasive approach to diagnosis off bets. You can’t diagnose some AL amyloid without a biopsy, at least not yet, so you need to shift gears and move toward a kind of invasive approach. But for TTR, which is the majority of what most people are going to see. A vast majority, I would say, because of the aging of the population, If there are no monoclonal proteins, then you can get nuclear scintigraphy either a pyrophosphate or a hydroxymethylene diphosphonate scan. Both are available, and if that shows diffuse uptake, that’s confirmed by single photon emission CT imaging. It is really important to confirm that you don’t have a blood pool as the cause of what you’re seeing on planar imaging, then, basically, you’ve made a diagnosis of TTR amyloid. Now, you just need to genotype the patient. So, the three steps are monoclonal protein assessment, PYP scan, and genetic testing. Pretty algorithmic and straightforward.

Kittleson: I love how you start with “Tell the patient what you’re thinking about.” Then we need to remember, don’t just do SPEP urine protein electrophoresis (UPEP), do the immunofixation electrophoresis SPEP UPEP. If that’s not sensitive enough, if the monoclonal proteins are positive, then stop. Do not do your technician scan; biopsy something instead. Call your friendly hematologist and only interpret the technician scan, the bone stratigraphy, in the context of the negative monoclonal protein screen.

Now, let’s say we’ve successfully met the hurdle of accurate diagnosis, and we talk about treatment. When it comes to AL, again, we’re collaborating with our friendly hematologists and allowing them to direct therapy against those pesky monoclonal proteins. But what about TTR? Tell us the best treatment for TTR amyloid cardiomyopathy.

Maurer: Hopefully, the best treatments are still to come. Right now, we only have one FDA-approved treatment, unfortunately. That drug is tafamidis. This field is evolving so rapidly because amazing basic scientists like Jeff Kelly have really elucidated the biology. It’s very clear: We have a small protein produced predominantly in the liver, and its job is to transport thyroid hormone and vitamin A, hence the name transthyretin. It looks like a four-leaf clover. The protein dissociates into pieces either because of aging or because of variants in the protein, and those pieces basically agglomerate to form amyloid fibril. Once you understand that biology, it becomes almost like a kindergarten story. You can either shut off the protein or can stabilize the protein. We all hope that one day we could maybe do something at the amyloid fibril level. Those are the three big strategies. The one that’s been proven to work is tafamidis as a TTR stabilizer. It is a small unfortunately too expensive of a compound but a highly effective one that in the ATTR-ACT trial, it basically prevented mortality and reduced the number of hospitalizations. The numbers needed to treat (NNTs) are quite low: under 10 for both mortality over 30 months and for hospitalizations. It’s an NNT of four to prevent one hospitalization in a year. We still don’t need to pay a quarter of a million dollars a year for a small pill every day, of course, but that’s the standard-of-care approach. Thankfully, for all the bad things about the US health care system, tafamidis is widely accessible and relatively easy to get, although there are still a lot of patients who have significant out-of-pocket costs.

But people still progress on tafamidis therapy. It’s much better when given earlier in the course of the illness. We show that in the trial, in which the patients with class III heart failure tended to live longer but spent a little bit more time in the hospital. And that’s not how we all want to spend our time; it’s like the last place most of us want to be. So, obviously, with the success of tafamidis, there have been a whole host of newer treatment options that we remain very hopeful about, if not highly confident, that they’re going to be effective. For patients who have variant disease, for years, there’s been a silencer-based therapy option, since 2018, even before tafamidis. That’s for patients who have polyneuropathy with or without a cardiomyopathy. But they must have variant disease and a polyneuropathy. The two compounds in that space, which are now three, were patisiran, inotersen, and now, vutrisiran. So three different silencer-based therapies.

Kittleson: We owe so much to you Mat, being the person who spearheaded the ATTR-ACT trial, and I cannot emphasize enough what you said. Number one: The earlier you start it, the better patients will do; it doesn’t reverse disease, it only prevents progression. Number two: Those survival curves take a while to separate. So if you want to give your patient the best chance of doing well, start it as soon as possible so they can start to accrue benefits. And now, we’re going to move on to prediction time. I want you to tell us, where we will be in the next decade. Will we be screening communities at risk? How will we be treating asymptomatic carriers? What will be the algorithm for silencer plus or minus stabilizer therapy for our patients?

Maurer: Those are great questions. I’m convinced that there’ll be some type of guidelines, if you will: a screening or active ascertainment approach. We don’t know what the best one is. I mentioned the false-positive rate, but there are a whole host of approaches looking at people who’ve gotten carpal tunnel surgery, examining the tissue, and finding amyloid. It is the same as we’re doing now for a multicenter study. This has been recently published in JACC by Finn Gustafsson’s group in Denmark. They showed that you can identify people much earlier in the course of the illness when you were thinking about it and really going out and looking for folks. We have a screening program with Frederick Ruberg that’s focusing on minority populations because they’re disproportionately afflicted by the Val122Ile variant, which affects individuals of West African ancestry. That means individuals in the US who self-identify as Black or Caribbean Hispanic. Obviously, there are a lot of health disparities. We must be appropriately active in the idea that as medicine gets more precision-based, we want to make sure no one is left out, so that’s why Rick and I have been committed. They’ll be an active ascertainment, and we’ll have to figure out what the best approach is; we don’t know. There’ll be a whole host of new therapies. We’re kind excited about a new tafamidis called acoramidis. It’ll be reporting out later this year. All the silencers I mentioned, including some new ones, such as a drug called eplontersen, which is a subcutaneous silencer, are being tested in large studies. There’s even one that’s being tested in 1400 patients, which is kind of unbelievable for amyloid.

Most of us believe that these drugs will be effective at obviously knocking down or shutting off the production of transthyretin, which will translate into clinically meaningful outcomes. Patients want to live longer, feel better, and function better. We’re hopeful for all those. The “pie in the sky” that people are talking about, even in patients who unfortunately are still diagnosed too late, is whether any anti-amyloid therapy would be effective. There are three or four different companies that are conducting early-phase studies, in which there are kind of monoclonal antibodies that are active against an epitope of amyloid-activate macrophages, like a Pac-Man: just chew up the amyloid that’s disrupting the structure and the function of the organ. This is an exciting space, and there are lots of amazing scientists. The collaboration among investigators around the country and junior faculty is great. Most importantly, the patients are just all, like I said, not only lovely but also very engaged and easy to take care of. Almost all of them, about 85%, whom we approach enroll in a trial. It just makes the life of a clinical investigator like me very easy.

Kittleson: I love it. I think we’ve taken our listeners now on a whirlwind tour through the following: Should you heighten your clinical suspicion? How do you make the right diagnosis? What’s the right treatment, and what can we look forward to? Tell me, what’s the one thing you want listeners to do differently after hearing this discussion?

Maurer: I think it’s back to the first point, which is to put amyloid on your differential diagnosis. You’ve got to think about it to diagnose it. Every time you see someone, think about whether this potentially is amyloid. That’s the main starting point for clinicians and for patients to benefit from all these therapies.

Kittleson: I love it. What we’ve learned today is: (1) If you follow your passion and make patient care your priority, you will have a fulfilling career in medicine, (2) have a heightened suspicion, as Dr Maurer so beautifully told us, and (3) order the right tests. Don’t forget that you can’t diagnose TTR amyloid with a positive monoclonal protein screen and a positive technician scan. If your protein screen is positive, then you must biopsy something, and tafamidis is our best treatment for now. So thank you, Dr Maurer, for being here with us today. It’s been so much fun to talk to you.

Maurer: Thank you. Your enthusiasm is always wonderful, and your expertise in translating what sometimes is very complicated information to providers is enviable to everybody.

Kittleson: Well, I did not pay him to say that. I will say that Dr Maurer is one of my favorite people in the world — and not just because he answers my emails almost before I send them.

Thank you for joining us today. There’s much more ahead in the coming episodes, so be sure to check out the Medscape app, and share, save, and subscribe if you enjoyed this episode. I’m Dr Michelle Kittleson for Medscape InDiscussion.

Resources

Cardiac Amyloidosis: Evolving Diagnosis and Management: A Scientific Statement From the American Heart Association

Amyloid Neuropathies

Cardiac Amyloidosis

Transthyretin Cardiac Amyloidosis: A Cardio-Orthopedic Disease

Prevalence of Orthopedic Manifestations in Patients With Cardiac Amyloidosis With a Focus on Shoulder Pathologies

Low QRS Voltages in Cardiac Amyloidosis: Clinical Correlates and Prognostic Value

Pseudoinfarctions

Genotype and Phenotype of Transthyretin Cardiac Amyloidosis in the United States: The Transthyretin Amyloid Outcome Survey (THAOS)

What Is New in Diagnosis and Management of Light Chain Amyloidosis?

Serum Protein Electrophoresis

Immunofixation

The Role of Light Kappa and Lambda Chains in Heart Function Assessment in Patients With AL Amyloidosis

Comparison of Different Technetium-99m-Labelled Bone Tracers for Imaging Cardiac Amyloidosis

Transthyretin-Related Amyloidosis Treatment & Management

Transthyretin-Related Amyloidosis

Amyloid Fibrils

Tafamidis Treatment for Patients With Transthyretin Amyloid Cardiomyopathy

Genome Silencer Therapy Leading to “Regression” of Cardiac Amyloid Load on Cardiovascular Magnetic Resonance: A Case Report

Cardiac Amyloidosis Treatment

Two Decades of Cardiac Amyloidosis: A Danish Nationwide Study

Design and Rationale the SCAN‐MP (Screening for Cardiac Amyloidosis With Nuclear Imaging in Minority Populations) Study

Epigenomic Profiles of African American Transthyretin Val122Ile Carriers Reveals Putatively Dysregulated Amyloid Mechanisms

Efficacy and Safety of Acoramidis (AG10) in Subjects With Transthyretin Amyloid Polyneurophathy (ATTRibute-PN)

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CORVALLIS, Ore. – Oregon State University will graduate 7,338 students during its university-wide commencement ceremony at 10:30 a.m. on Saturday, June 17, at Reser Stadium on the Corvallis campus.

More than 3,700 students are expected to participate in the ceremony that will honor the university’s 154th class. The event is free to attend, open to the public and held rain or shine. Gates will open at 9 a.m. and tickets are not required. The ceremony will be livestreamed in English and Spanish.

The 7,338 graduates will receive 7,583 degrees. (There will be 238 students receiving two degrees, two receiving three degrees and one receiving four.) They will add to the ranks of OSU alumni, who have earned 287,469 degrees over the university’s history.

The commencement address will be given by OSU alumnus Dr. Charity Dean, who helped guide the state of California’s strategic response to the COVID-19 pandemic. Dean is the CEO and founder of The Public Health Company, which seeks to protect communities and businesses from infectious disease.

The university-wide commencement ceremony held in Corvallis on June 17 celebrates all OSU graduates including Ecampus and OSU-Cascades graduates. OSU-Cascades’ commencement ceremony for graduates attending OSU-Cascades will be held in Bend on June 18. OSU-Cascades students are welcome to attend both ceremonies.

Some facts and figures about Oregon State’s class of 2023:

• Of the 7,583 degrees that will be awarded, 5,961 will go to students receiving bachelor’s degrees; 1,190, master’s degrees; 285, doctor of philosophy degrees; 73, doctor of pharmacy degrees; 71, doctor of veterinary medicine degrees; and three, doctor of education.
• OSU’s 2023 graduates represent 34 of Oregon’s 36 counties, 50 states and 71 countries.
• A total of 1,335 identify as Asian; 702, Latinx; 245, First Nations including Alaskan Native; 187, Black or African American; and 113, Native Hawaiian or Pacific Islander.
• The oldest graduate is 72 years old; the youngest is 18 years old; the average age is 26.
• The graduating class includes 193 veterans of U.S. military service.
• A record total of 1,892 degrees were awarded to Oregon State students in 60 academic degree programs this year through Ecampus, the university’s online education provider. The graduates hail from 48 states and 18 countries.
• OSU-Cascades in Bend will award degrees to 248 undergraduate students and 62 graduate students on Sunday, June 18.
• OSU’s Honors College is graduating 245 students.
• The graduating class includes 1,216 students who are the first in their family to earn a college degree; 4,194 Oregon residents; and 3,145 non-resident students of which 724 are international students.
• The College of Engineering has the most graduates with 1,792, followed by: College of Liberal Arts (1,107); College of Business (866); College of Science (652); College of Public Health and Human Sciences (564); College of Agricultural Sciences (505); College of Forestry (250); College of Earth, Ocean, and Atmospheric Sciences (167); and College of Education (58). 

Each OSU graduate has a compelling story. For example:

• Javon Smith of Bellingham, Washington, will receive her bachelor’s degree in natural resources with a focus on policy and management from OSU’s College of Forestry. Smith has spent 20 years working in public affairs and currently runs a consulting practice specializing in renewable energy development. She decided to go back to school to learn new tools for communication, collaboration and consensus around contentious issues. She chose to earn her degree online through OSU’s Ecampus because she needed a program that would accommodate her schedule as a full-time working professional. “I could choose my path and tailor classes to my passions and the direction I’m going to steer my career,” Smith said. “I feel like I’m able to apply every class in my life in some way. And this degree will give me more confidence to speak with authority on these important issues.”
• Lucas Yao, who grew up in Portland and graduated from Ida B. Wells High School, hasn’t limited himself to one primary focus during his time at OSU. In fact, he’ll be graduating this June with undergraduate degrees in biohealth science and creative writing, along with minors in chemistry and public health, and a medical humanities certificate. Yao, an Honors College student who aspires to attend medical school, wants to approach health care and medicine from an intersectional perspective, and also believes communication is crucial to his future career. “OSU has exposed me to so many subjects and fields that I didn’t even know existed, much less that I would be interested in,” he said. “My understanding of what research is has expanded; my understanding of what is possible outside of STEM has increased; and I have learned so much about what I’m drawn to and why.”

• Kellen Copeland, who completed his Ph.D. in environmental sciences in November 2022, combines the fields of anthropology, sociology and philosophy to understand how human cultures shape societal outcomes for nonhuman participants. He recently helped launch Tap & Wag, a nonprofit whose mission is to raise money for animals in need by selling monthly memberships at a communal dog park, tap house, coffee bar, and training and boarding facility. This fall, Copeland will work as a postdoctoral scholar in the University of British Columbia’s animal welfare program. “My primary advisor, Michael Harte, has been an inspiration to me since the beginning of my Ph.D. program,” Copeland said. “Michael has a way of getting complex information across into simple terms and is unapologetically upfront about the issues that future generations must work to resolve. The support within my program has been instrumental to my growth.”

• Kellen Copeland, who completed his Ph.D. in environmental sciences in November 2022, combines the fields of anthropology, sociology and philosophy to understand how human cultures shape societal outcomes for nonhuman participants. He recently helped launch Tap & Wag, a nonprofit whose mission is to raise money for animals in need by selling monthly memberships at a communal dog park, tap house, coffee bar, and training and boarding facility. This fall, Copeland will work as a postdoctoral scholar in the University of British Columbia’s animal welfare program. “My primary advisor, Michael Harte, has been an inspiration to me since the beginning of my Ph.D. program,” Copeland said. “Michael has a way of getting complex information across into simple terms and is unapologetically upfront about the issues that future generations must work to resolve. The support within my program has been instrumental to my growth.”
• Alex Varela took a nontraditional path to higher education, working as an educational assistant in high school classrooms after dropping out of high school. The son of immigrants from Mexico, he knows firsthand how the public education system often fails to support students of color and wants to become a teacher to help provide culturally and linguistically competent instruction to students from diverse backgrounds. At OSU, Varela double-majored in education and history; served as a student ambassador within the College of Education, helping fellow education students navigate applications and exam prep; and was active in OSU’s Centro Cultural César Chávez and LGBTQ+ initiatives. Varela has already begun teaching language arts at McKay High School in Salem, where he spent fall term as a student-teacher and then accepted a temporary job in March. He plans to pursue a permanent post closer to his home in Portland, teaching high school social studies or language arts.