Alex Hajduczok, MD, is an advanced heart failure and pulmonary hypertension specialist at Oklahoma Heart Institute. 

Philip Adamson, MD, MSc, is the chief medical officer of CVRx.

Rethinking Advanced Heart Failure: Treat the Disease, Not the Symptoms

, host Alex Hajduczok, MD, a cardiologist and heart failure specialist at Oklahoma Heart Institute, sits down with Philip Adamson, MD, MSc, chief medical officer at CVRx, to discuss ongoing paradigm changes in heart failure care and prevention.

Check out the full episode on Adamson’s full cardiology career

The discussion focuses on the evolving understanding of advanced heart failure and the need to move beyond symptom-based treatment paradigms toward earlier, mechanism-driven intervention. The guest argues that current clinical practice often allows left-sided heart failure to "metastasize," with progressive pulmonary vascular disease and right ventricular dysfunction developing long before patients meet conventional definitions of advanced heart failure. He explains that therapies are typically initiated only after patients become overtly symptomatic, despite the underlying pathophysiology having progressed for months or years. To address this gap, he describes the rationale behind the Team HF trial, which is designed to identify physiological markers that can better define the transition to advanced heart failure and determine which patients may benefit from earlier left ventricular offloading before irreversible disease progression occurs.

The speakers discuss the limitations of relying on traditional clinical assessments such as New York Heart Association (NYHA) functional class, noting that congestion and elevated filling pressures may be present regardless of symptom burden. They emphasize that symptoms often poorly reflect the severity of the underlying disease because the body is capable of compensating for substantial physiological disturbances before decompensation becomes clinically apparent. This disconnect, they argue, has led clinicians to justify treatment primarily on the basis of symptom relief rather than targeting the biological processes responsible for disease progression.

Building on this concept, the conversation explores the broader implications of adopting a mechanism-based approach to heart failure management. The guest reflects on his recent work investigating the autonomic nervous system, highlighting its central role in driving the progression of heart failure. Rather than focusing on downstream surrogate markers, he advocates for therapies that directly modify maladaptive autonomic signaling, suggesting that advances in neuromodulation may offer opportunities to fundamentally alter the disease trajectory. He draws parallels to emerging neurotechnology in other fields, arguing that cardiovascular medicine should similarly embrace innovative approaches capable of modifying the underlying mechanisms of disease.

The discussion also examines secondary pulmonary hypertension as a frequently overlooked consequence of left-sided heart failure. The guest cites findings demonstrating that a large proportion of patients with relatively mild, NYHA class II heart failure harbor significant pulmonary hypertension despite appearing clinically stable, underscoring how conventional symptom-based assessment may fail to identify patients at risk for progressive right ventricular dysfunction. Because these patients often would not undergo invasive hemodynamic evaluation in routine practice, important pathological changes may remain undetected until advanced disease develops.

The episode concludes with an overview of emerging therapeutic strategies targeting the pulmonary circulation, including pulmonary artery denervation to reduce maladaptive sympathetic tone. The speakers discuss the potential for these approaches to slow disease progression, attenuate secondary pulmonary hypertension, preserve right ventricular function, and ultimately redefine the treatment of advanced heart failure by intervening earlier in the disease course. Collectively, they emphasize that future advances in heart failure care will depend on identifying physiological mechanisms of progression and developing therapies that address these processes before irreversible clinical deterioration occurs.

Editors’ Note: Hajduczok reports disclosures with CVRx, Edwards Lifesciences, and Impulse Dynamics. Adamson reports employment with CVRx.

Videos

The latest episode of Moving the Needle in Medicine features Philip Adamson, MD, MSc, as he discusses ongoing changes in the way heart failure is treated and prevented.

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Heart Failure

The HCPLive heart failure page is a resource for medical news and expert insights on HF. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for heart disease, reduced and preserved ejection fraction, and more.

As the treatment landscape for IgAN continues to expand, clinicians are increasingly focused on identifying patients earlier, accurately assessing progression risk, and intervening before irreversible kidney damage develops.

In this Q&A, Ramy Hanna, MD, associate professor, disease expert, and clinical trial principal investigator in nephrology, discusses the challenges of early recognition in glomerular disease, evolving approaches to IgA nephropathy (IgAN) management, and the importance of timely evaluation to preserve kidney function.

Q&A: Early Detection and Treatment Advances in IgA Nephropathy, With Ramy Hanna, MD

HCPLive: What are some of the biggest challenges with recognizing glomerular diseases early, including IgAN?

 The problem with most glomerular diseases is that the only signs that you're going to have initially, and even into the medium term, are laboratory signs. You're going to have hematuria and proteinuria as the 2 cardinal signs, and that's early on.

Then, if you wait a little bit longer, you start to see a decline of kidney function. We call that GFR. We usually measure that through one of several measures, whether it be creatinine or cystatin C.

The problem is by the time that you actually have the decline in kidney function, it has been a long time — decades often — and when you look at biopsies, you see irreversible tissue death and fibrosis. So you're dealing with tissue that is no longer viable.

There are people walking around with 1000 mg of protein, 500 mg of protein. Those are significant biopsy thresholds. If they're not going to see a doctor, their doctor is not well informed, or they are not willing to undergo an invasive procedure for diagnosis, those patients are going to be missed.

The gold standard for glomerular diseases, most of them — not all of them at this point; there are a couple exceptions — would be kidney biopsy. It is an invasive procedure that does come with some risks. However, it is the only way to actually detect the immune involvement, and then in doing so, triage it, stage it, and plan treatment.

That's the problem. You have to catch people early. Patients have to go to the doctor. Their doctor has to be well informed. After that, they have to get a proper biopsy, and that's a lot of ducks to line up in a row. Sometimes those ducks don't line up perfectly.

HCPLive: What early warning signs should clinicians and patients be watching for, and when should a patient be referred to a nephrologist?

 There are 2 different sets of things you have to worry about as a patient.

I think patients need to look out for blood in the urine. That could actually be tiny little drops that we catch on a laboratory test. We catch 2 to 3 RBCs, or 4 RBCs, in a urinalysis, and that needs to be looked into.

In many cases, though, the urine will just turn bright red, and that obviously brings people in quickly. I imagine especially as a man, you see that and think, "Whoa, okay."

The other thing you look for is foam or protein in the urine. Now, I have to be careful because I have a couple cases in my mind of people who had organic acids, who were producing what looked like foam, or where the actual stream of urine was disrupting the water and CO₂ was mixing in and creating a panic.

I don't want to create a mass panic for everybody who generates foam in the toilet bowl. But if you are urinating into a steady collecting surface, like a cup when you provide a sample, or you're pretty sure you are not agitating the water as much and you are seeing lots of foam — almost like the head on a beer — realize that is what happens to protein when this process occurs.

It precipitates, and when it precipitates, it creates that head. That is when you think, "Okay, this is actually protein coming out of solution."

When you get that foam, or when you get blood in the urine, those are immediate warning signs.

Also, if you have chronic kidney disease and nobody knows why, that should prompt curiosity. I have a very high bar for physicians personally. We should be able to diagnose almost everything at this point. Not everything — there are always things beyond our ability to figure out — but we should make an effort to diagnose everything.

We can't cure everything. We should certainly try. And as physicians, we need to have the mindset of kidney success rather than kidney failure.

Editor’s Note: Hanna reports relevant disclosures with Alexion Pharmaceuticals, Novartis, AstraZeneca, and others.

Stamellou E, Seikrit C, Tang SCW, et al. IgA nephropathy. 

 2023;9(1):67. doi:10.1038/s41572-023-00476-9.

Lee M, Suzuki H, Nihei Y, Matsuzaki K, Suzuki Y. Ethnicity and IgA nephropathy: worldwide differences in epidemiology, timing of diagnosis, clinical manifestations, management and prognosis. 

 2023;16(suppl 2):ii1-ii8. doi:10.1093/ckj/sfad199.

Articles

Early recognition of IgA nephropathy is impeded by a long asymptomatic phase in which abnormalities are primarily laboratory-based, notably hematuria and proteinuria. Declines in GFR often reflect decades of injury and may coincide with irreversible fibrosis on biopsy. Meaningful proteinuria can go uninvestigated due to limited access, variable clinician awareness, and reluctance to undergo invasive diagnostic procedures. Kidney biopsy remains central for confirming immune-mediated pathology, staging disease, and guiding therapy. Gross hematuria and persistent foamy urine warrant prompt evaluation.

Ramy Hanna, MD, discusses early IgAN recognition, biopsy decisions, and how emerging therapies are reshaping disease management.


Nephrology

The HCPLive nephrology page is a resource for medical news and expert insights on kidney disease. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments in nephrology, and more.

IgA Nephropathy

The HCPLive Berger disease page is a resource for medical news and expert insights on IgA nephropathy. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments in Berger disease, and more.

Early Detection and Treatment Advances in IgA Nephropathy, With Ramy Hanna, MD

University of Colorado Health Sciences Center

Quality of life (QoL) scores improved over 15 months in patients with 

 who treated breakthrough attacks with sebetralstat while on long-term prophylaxis (LTP), according to the recent KONFIDENT-S open-label extension analysis.

 Investigator Daniel F. Soteres, MD, MPH, a physician from Asthma & Allergy Associates, PC, discussed what those gains mean for patients already considered well-controlled.

“When you think about using a new medication, we want to know: Is it safe? Is it effective? And then our patients definitely want to know…what will it offer them in terms of improvement in their quality of life,” Soteres said.

Sebetralstat Shows QoL Gains on Top of HAE Prophylaxis in KONFIDENT-S

The analysis included 35 participants with type 1 HAE who experienced a total of 504 breakthrough attacks despite being on a long-term prophylaxis of either berotralstat (n = 16), lanadelumab (n = 13), or C1 inhibitor replacement (n = 6). With sebtralstat, the median time to the beginning of symptom relief was 1.3 hours for both berotralstat and lanadelumab and 1.8 hours for C1 inhibitor LTP.¹ Only 1.6% of the breakthrough attacks went untreated, and 22.3% of attacks required a second dose of sebtralstat within 12 hours.

The median time from attack recognition to sebetralstat administration was 6 minutes overall. This ranged from 1 minute in participants on C1 inhibitor LTP to 20 minutes in those on berotralstat. In this study, nearly 30% of attacks were treated while still mild.

Sebetralstat Improves Quality of Life in HAE

QoL scores were available for 34 participants. Among these patients, Angioedema Quality of Life Instrument scores improved by a squares mean of 10.3 points (−21.1 to 0.6) from baseline to month 15, exceeding the threshold considered clinically meaningful. The largest gains were in the fatigue/mood (-13.3), followed by gains in fears/shame (-11.2) and functioning (-9.6).¹ Treatment satisfaction was high, with 88.8% of sebetralstat-treated attacks rated satisfactory and 75.0% rated very or extremely satisfactory.¹

The Smaller C1 Inhibitor Subgroup in KONFIDENT-S

Effectiveness signals looked somewhat different among the 6 participants receiving C1 inhibitor (C1INH) LTP, whose median time to complete attack resolution was 16.6 hours versus 10.9 hours for berotralstat and 15.1 hours for lanadelumab.¹ Soteres cautioned against overinterpreting the small subgroup, noting patients on C1INH may be more accustomed to relief from injectable therapies, representing "a real paradigm shift" in understanding that a pill could offer comparable results. He added there could also be subtle differences in disease chemistry that respond more slowly, though efficacy still held for these patients.

Soteres said the findings reinforce existing guidance rather than change it: patients with HAE, including those stable on LTP, should keep 2 doses of on-demand therapy available at all times, a standard he has built into his own practice. He said sebetralstat's oral route remains a favorable on-demand option even for patients who continue to have it available alongside injectable choices.

Read part 1 of our interview with Soteres here: 

Sebetralstat Resolves Breakthrough HAE Attacks Despite Prior Prophylaxis.

Editor’s note: Reported disclosures for Soteres include KalVista Pharmaceuticals, BioCryst, CSL Behring, Intellia Therapeutics, Ionis Pharmaceuticals, Pharming, Pharvaris, and Takeda.

Kinaciyan T, Aygören-Pürsün E, Martinez-Saguer I, et al. Sebetralstat for breakthrough attacks in patients with hereditary angioedema receiving long-term prophylaxis in KONFIDENT-S. 

. 2026;5(5):100750. Published 2026 Jun 12. 

Johnson V. Sebetralstat Shows Long Term Fast Relief of Breakthrough HAE Attacks. HCPLive. Published July 21, 2026. Accessed July 24, 2026. 

https://www.hcplive.com/view/sebetralstat-shows-long-term-fast-relief-breakthrough-hae-attacks

Soteres D. Sebetralstat Resolves Breakthrough HAE Attacks Despite Prior Prophylaxis. HCPLive. Published July 24, 2026. Accessed July 24, 2026. 

https://www.hcplive.com/view/sebetralstat-resolves-breakthrough-hae-attacks-prior-prophylaxis

Daniel Soteres, MD, discusses KONFIDENT-S data showing sebetralstat improved quality of life for HAE patients already stable on long-term prophylaxis.

Allergy

Allergy condition center page is a comprehensive resource for clinical news and insights on allergic and inflammatory diseases. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for food and seasonal allergies, as well as allergic asthma and related conditions.

Welcome to The HCPFive, your go-to roundup for the latest healthcare news and breakthroughs, curated specifically for busy healthcare professionals.

Each week, we highlight 5 key developments or headlines from healthcare that you need to know — whether it's a cutting-edge treatment, regulatory updates, or innovations shaping the future of medicine. This week's top stories include Agios’ discontinuation of tebapivat’s clinical development program for sickle cell disease, the US Food and Drug Administration (FDA) approval of olopatadine hydrochloride and mometasone furoate (Ryaltris) nasal spray, 665 mcg/25 mcg per spray, for the treatment of seasonal 

 symptoms in children aged 6 to 11 years, positive topline results for the global phase 3 SHASTA-3 and SHASTA-4 clinical studies of plozasiran in patients with severe 

, the FDA acceptance of BridgeBio’s New Drug Application (NDA) for encaleret for the treatment of 

autosomal dominant hypocalcemia type 1 (ADH1)

, and the FDA approval of MannKind Corporation’s furosemide injection (Furoscix ReadyFlow) for the treatment of edema (fluid overload) in adults with 

With The HCPFive, you'll get the essential takeaways to stay informed and ahead of the curve. Here's your quick dive into the top stories for the week of July 19, 2026 — let's jump in!

Agios Ends Tebapivat Development in Sickle Cell Disease After Phase 2

On July 21, 2026, Agios announced topline results from a phase 2 trial of tebapivat in patients aged ≥16 years with sickle cell disease showing improvements in hemoglobin and markers of hemolysis. However, the results did not demonstrate sufficient differentiation to support continued development of the pyruvate kinase (PK) activator, prompting the Company to discontinue the program.

"These phase 2 data further reinforce PK activation as a clinically validated mechanism in sickle cell disease, with tebapivat demonstrating hematologic activity consistent with this class of medicine," said Sarah Gheuens, MD, PhD, chief medical officer and head of research and development at Agios, in a statement. "However, the results did not establish the level of differentiation we believe is necessary to support continued development."

FDA Approves Ryaltris for Children Aged 6 to 11 With Seasonal Allergic Rhinitis

On July 21, 2026, the FDA expanded the approved use of olopatadine hydrochloride and mometasone furoate (Ryaltris) nasal spray, 665 mcg/25 mcg per spray, to include the treatment of seasonal allergic rhinitis symptoms in children aged 6 to 11 years. With the approval, the treatment is now indicated for adults and pediatric patients aged ≥ 6 years in the United States, broadening access to a younger population than the drug's original 2022 approval for patients aged ≥ 12 years.

Plozasiran Meets Primary Endpoint in SHASTA-3, SHASTA-4 sHTG Trials

On July 22, 2026, Arrowhead Pharmaceuticals announced topline results for the global phase 3 SHASTA-3 and SHASTA-4 clinical studies of plozasiran in patients with severe hypertriglyceridemia. Both trials successfully met the primary endpoint of triglyceride reduction versus placebo and met all prespecified secondary endpoints, including a statistically significant reduction in the rate of acute pancreatitis compared to placebo.

FDA Accepts NDA for Encaleret for Autosomal Dominant Hypocalcemia Type 1

Only July 22, 2026, the FDA accepted BridgeBio’s New Drug Application (NDA) for encaleret for the treatment of ADH1, assigning a Prescription Drug User Fee Act (PDUFA) date of May 8, 2027. If approved, encaleret will be the only therapy indicated specifically for patients with ADH1. The orally administered small molecule designed to selectively negatively modulate the calcium sensing receptor has previously received Fast Track Designation from the FDA and Orphan Drug Designation in the US, European Union, and Japan.

FDA Approves Furosemide Injection (Furoscix ReadyFlow) for Edema in HF, CKD

On July 24, 2026, the FDA approved MannKind Corporation’s furosemide injection (Furoscix ReadyFlow) for the treatment of edema (fluid overload) in adults with heart failure or chronic kidney disease, making it the first and only autoinjector delivering subcutaneous furosemide with IV-equivalent exposure (based on comparisons of AUC and PD endpoints), providing a full 80 mg/mL dose in a simple, patient-friendly format administered in < 10 seconds.

Key regulatory and pipeline updates span hematology, allergy, metabolic disease, rare endocrinology, and cardiorenal care. Agios halted tebapivat after phase 2 sickle cell data showed hematologic activity yet inadequate differentiation. FDA expanded Ryaltris intranasal olopatadine/mometasone to ages 6–11, extending the ≥12-year indication. Arrowhead reported SHASTA-3/4 phase 3 success for plozasiran in severe hypertriglyceridemia, including reduced acute pancreatitis. FDA accepted BridgeBio’s encaleret NDA for ADH1 with a May 2027 PDUFA. MannKind gained approval for Furoscix ReadyFlow with IV-equivalent exposure profiles.

Stay updated with the latest healthcare breakthroughs, including phase 3 plozasiran data in hypertriglyceridemia, the FDA approval of Furoscix ReadyFlow, and more.

Hematology

The HCPFive: Top News for Healthcare Providers from the Week of 07/19

Can We Stop Heart Failure at Its Source?

In this segment from the latest episode of 

, host Alex Hajduczok, MD, a cardiologist and heart failure specialist at Oklahoma Heart Institute, sits down with Philip Adamson, MD, MSc, chief medical officer at CVRx, to discuss Adamson’s perspective on the recent advancements in heart failure care and the ongoing trials of future treatment techniques.

The conversation begins with a reflection on the evolution of Adamson’s career and the continuity of his scientific focus despite transitioning across different areas of cardiovascular medicine. He explains that, although others have viewed these shifts as changes in specialty, his underlying objective has remained constant: understanding the fundamental mechanisms of disease. Emphasizing the importance of viewing medicine through the lens of pathophysiology rather than rigid sub-specialization, he argues that cardiovascular disorders cannot be fully understood in isolation. Instead, clinicians should recognize the complex interplay between the electrical, mechanical, autonomic, and circulatory systems that collectively influence cardiac function and disease progression.

The discussion then turns to the historical evolution of heart failure management, highlighting the shift from a hemodynamic model of disease to the now well-established neurohormonal hypothesis. Recalling the early 1990s, Adamson describes how the recognition that maladaptive neurohormonal activation drives heart failure progression fundamentally transformed therapeutic strategies. He reflects on the initial skepticism surrounding beta-blocker therapy, noting that many clinicians doubted the failing heart could improve structurally. Subsequent clinical evidence demonstrating reverse ventricular remodeling and improved survival, however, validated the concept that interventions targeting disease mechanisms could modify the natural history of heart failure rather than simply relieve symptoms.

Building on this framework, Adamson explains the physiologic role of the carotid baroreceptors as the body's primary sensors of circulatory status. He describes how reduced cardiac performance leads to diminished baroreceptor signaling, causing the brain to misinterpret heart failure as a state of hypovolemia or hemorrhage. This perceived threat initiates a cascade of maladaptive responses, including sympathetic nervous system activation, renin-angiotensin-aldosterone system stimulation, and inflammatory signaling. While current guideline-directed medical therapies effectively block many of these downstream pathways, he characterizes them as protecting target organs from the consequences of persistent neurohormonal activation rather than addressing its central origin.

The conversation subsequently focuses on baroreceptor activation therapy (BAT) as a novel strategy designed to intervene earlier in this pathophysiologic cascade. By electrically stimulating the carotid sinus nerve, BAT restores afferent signaling to central autonomic control centers, reducing sympathetic outflow, enhancing parasympathetic activity, and attenuating inflammatory responses. Adamson contrasts this approach with conventional pharmacologic therapies, describing it as an opportunity to reduce the neurohormonal "storm" itself rather than simply shielding organs from its downstream effects. He suggests that directly modulating the autonomic nervous system may provide a more comprehensive strategy for slowing heart failure progression.

To conclude the discussion, attention shifts to the ongoing Benefit HF trial, which Adamson notes is expected to enroll approximately 2,500 randomized patients, making it the largest device-based heart failure trial conducted to date. He explains that the study aligns with emerging perspectives reflected in recent heart failure consensus statements, which emphasize defining heart failure according to impaired cardiac function and underlying pathophysiology rather than relying solely on ejection fraction thresholds. By evaluating BAT in patients with ejection fractions below 50%, the trial seeks to determine whether earlier autonomic modulation can improve clinical outcomes across a broader population of patients with heart failure and further redefine the role of device-based therapies within contemporary heart failure management.

The latest episode of Moving the Needle in Medicine features Philip Adamson, MD, MSc, as he discusses upcoming advancements in heart failure care.

The latest episode of Moving the Needle in Medicine features Philip Adamson, MD, MSc, as he walks through his long and successful career in cardiology.

Lessons From a Career Dedicated to Transforming Heart Failure Care

Daniel Soteres, MD, discusses KONFIDENT-S data showing sebetralstat quickly resolves breakthrough HAE attacks in patients on long-term prophylaxis

Sebetralstat Resolves Breakthrough HAE Attacks Despite Prior Prophylaxis

Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for 

. He is also the executive producer of two podcasts: 

. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

Sanofi has discontinued development of OX40L-targeting amlitelimab for atopic dermatitis, following the heels of Kyowa Kirin's similar rocatinlimab discontinuation.

Atopic Dermatitis

Atopic Dermatitis condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatitis research, treatment, and drug development.

Sanofi Announces Discontinuation of Amlitelimab for Atopic Dermatitis

Mandana Khalili, MD, is Chief of Clinical Hepatology and Director of Clinical and Translational Research in Hepatology at San Francisco General Hospital, and directs the UCSF T32 Hepatology Training Program.

Telehealth stepped alcohol treatment reduced weekly drinking, but not the primary endpoint, among patients with chronic liver disease.

Hepatology

MASH / MASLD

The HCPLive MASH & MASLD page is a comprehensive resource for clinical news and insights on metabolic dysfunction-associated steatotic liver disease and steatohepatitis. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for fatty liver disease, steatohepatitis, and more.

Telehealth Stepped Alcohol Care Reduced Drinking in Liver Disease

Jason Hawkes, MD, explains how new biologics and targeted therapies are advancing precision medicine and improving personalized care in atopic dermatitis.

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Q&A: How Is Precision Medicine Changing Atopic Dermatitis Care? With Jason Hawkes, MD

Abigail Brooks is a strategic content lead overseeing 

She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

The approval makes MannKind Corporation’s furosemide injection the first and only autoinjector delivering SC furosemide with IV-equivalent exposure.

Chronic Kidney Disease

FDA News

David Golden, MD, clinical associate professor of medicine at Johns Hopkins University School of Medicine.

David B.K. Golden, MD, of Johns Hopkins, discusses anaphylaxis counseling, the Anaphylm CRL, and why a new epinephrine guideline is still years away.

Anaphylaxis

The HCPLive anaphylaxis page is a comprehensive resource for clinical news and insights on acute allergic reactions. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for preventing anaphylaxis, and more.

Shared Decision-Making Guides Epinephrine Delivery Choice

GLP-1 receptor agonists show early promise for psoriasis and HS, but 3 experts urge caution on mechanism, durability, and long-term safety.

GLP-1s in Dermatology: Emerging Evidence and Unanswered Questions

Ron Blankstein, MD, is the associate director of the cardiovascular imaging program, director of cardiac computed tomography, and co-director of the cardiovascular imaging training program at Brigham and Women’s Hospital, as well as a professor of medicine at Harvard Medical School.

Ron Blankstein, MD, explains the value of PCD-CT and its consistency in both data collection and analysis of plaque with prior technology.

Atherosclerotic Cardiovascular Disease

Photon-Counting CT Plaque Analysis Consistent With Energy-Integrating Detector CT

IgA nephropathy shows a male predominance, but researchers have not identified why. Ramy Hanna, MD explores possible biological explanations.


Latest News

Rethinking Advanced Heart Failure: Treat the Disease, Not the Symptoms

Early Detection and Treatment Advances in IgA Nephropathy, With Ramy Hanna, MD

Sebetralstat Shows QoL Gains on Top of HAE Prophylaxis in KONFIDENT-S

The HCPFive: Top News for Healthcare Providers from the Week of 07/19

Can We Stop Heart Failure at Its Source?