Latest news with #HFpEF
Medscape
13-05-2025
- Health
- Medscape
Few Patients With Diastolic Dysfunction Progress to HFpEF
In a 4.3-year follow-up study, few asymptomatic patients with preclinical left ventricular diastolic dysfunction (LVDD) progressed to heart failure with preserved ejection fraction (HFpEF), with a higher incidence noted in women. High blood pressure and decreased kidney function were associated with elevated levels of N-terminal pro–B-type natriuretic peptide (NT-proBNP). METHODOLOGY: The progression of LVDD may lead to the development of HFpEF over time. Despite the similar prevalence of LVDD in both sexes, HFpEF is more common in women than in men. Researchers evaluated longitudinal changes in markers of LVDD severity and HFpEF in men and women from a cohort of individuals who were at a high cardiovascular risk. They included 146 individuals with preclinical LVDD and no symptoms of HF at baseline (mean age, 63 years; 58% women) and reassessed them after a median follow-up duration of 4.3 years. Follow-up measurements included blood pressure, biomarkers such as NT-proBNP, kidney function, and echocardiography. HFpEF was assessed on the basis of signs, symptoms, and echocardiographic abnormalities. An LV ejection fraction below 50% was considered HF with reduced ejection fraction. TAKEAWAY: Overall, 10% of individuals developed HF, with 13 classified as those with HFpEF (nine women and four men). The annual incidence of HFpEF was 2%. Median NT-proBNP plasma levels increased from 71 to 100 pg/mL over the follow-up period. A significant rise was observed in terms of the presence of major functional abnormalities in both men and women and the presence of major morphologic abnormalities in women ( P for sex interaction = .03). for sex interaction = .03). Each SD decrease in the estimated glomerular filtration rate resulted in higher NT-proBNP levels in men and women (beta for change over time, 0.12; 95% CI, 0.01-0.22). Overall, a rise in systolic or diastolic BP led to an increase in NT-proBNP levels over time, with a higher systolic BP in women and a higher diastolic BP in men associated with an increase in NT-proBNP levels. IN PRACTICE: "High blood pressure and decreased kidney function were associated with higher levels of NT-proBNP. This highlights the need to further explore cardiorenal protection as a method to prevent HFpEF," the authors of the study wrote. SOURCE: This study was led by Anne Margje Lisa Naomi van Ommen, Utrecht University, Utrecht, the Netherlands. It was published online on May 04, 2025, in Open Heart . LIMITATIONS: The moderate sample size resulted in insufficient power to draw definitive conclusions about sex differences. A potential risk for measurement biases existed. The relatively low prevalence of comorbidities and the potential selection bias towards healthier individuals may have limited the generalisability of the findings. DISCLOSURES: This study received financial support from the Dutch CardioVascular Alliance, supported by the Dutch Heart Foundation. The authors declared having no competing interests.
Yahoo
02-04-2025
- Health
- Yahoo
ACC 25: tirzepatide influences clinical trajectory of patients with HFpEF and obesity
At the American College of Cardiology's 74th Annual Scientific Session in Chicago, further results and analyses were presented from the SUMMIT trial. SUMMIT was the first trial in patients with heart failure with preserved ejection fraction (HFpEF) and obesity with heart failure outcomes as the primary prespecified endpoint. The trial examined the effect of Eli Lilly's glucagon-like peptide-1 receptor agonist (GLP-1RA) tirzepatide, which is marketed as Mounjaro, on the clinical trajectory of patients with HFpEF and obesity. The study had previously identified that tirzepatide was able to reduce the composite of cardiovascular (CV) death and worsening HF events by 38% (P=0.026), an effect that was consistent across various definitions of events. Obesity often leads to both HFpEF and chronic kidney disease (CKD); CKD may influence the clinical course of obesity-related HFpEF, and incretin-based drugs may influence renal function. This study had dual objectives: 1) to evaluate the influence of CKD on the clinical responses to tirzepatide in patients with obesity-related HFpEF; and 2) to investigate the complexity of tirzepatide-related changes in renal function. Key opinion leaders (KOLs) interviewed by GlobalData have often commented on the need for a therapy that can achieve a broader cardiometabolic approach in treating disease such as CV-kidney metabolic syndrome, which the SUMMIT trial investigates, and tirzepatide's success in treating this broader metabolic syndrome is likely to achieve favourable opinion and uptake from physicians. The SUMMIT trial randomly assigned 731 patients with HFpEF: chronic HF, left ventricular failure (LVEF) 50% or higher, and body mass index at or above 30kg/m2. Patients were also required to have one of the following: 1) left atrial enlargement; 2) elevated left ventricular (LV) pressures; or 3) NT-proBNP greater than 200pg/mL in sinus rhythm or greater than 600pg/mL in AF. Patients received either placebo or tirzepatide for a median of 104 weeks and were followed for cardiovascular death or worsening heart failure events and for changes in the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) after 52 weeks. Because of the confounding variables produced by obesity, and changes in muscle mass, estimated glomerular filtration rate (eGFR) was assessed at the point of randomisation and after 12, 24, and 52 weeks by both creatinine-based and cystatin C–based eGFR calculation formulae. The enrichment criteria used to identify participants at high risk of events included: 6 minute walk test (6MWT) ≥100 and ≤425 meters, KCCQ-CSS ≤80 and HF decompensation within 12 months or eGFR <70m/min/1.73m2. If they met these criteria, participants were then randomised for the duration of double-treatment and follow-up. Patients were on a starting dose of 2.5mg/week, which was uptitrated by 2.5mg every four weeks, as tolerated, until it reached 15mg/week by 20 weeks, and the double-blind treatment was maintained until the last patient completed 52 weeks. Patients with CKD (based on creatinine or cystatin C) had greater severity of heart failure, as reflected by: 1) worse functional class, KCCQ-CSS scores, and 6-minute walk distance; 2) higher levels of NT-proBNP and cardiac troponin T; and 3) a two-fold increase in the risk of worsening heart failure events. CKD did not influence the effect of tirzepatide to reduce the relative risk of major adverse heart failure events and to improve KCCQ-CSS, quality of life, and functional capacity, but the absolute risk reduction in the primary events was numerically greater in patients with CKD. Regarding renal function assessments, baseline eGFR-cystatin C was consistently approximately 9mL/min/1.73m2 lower than that of eGFR-creatinine, with significant individual variance. Furthermore, tirzepatide increased eGFR at 52 weeks, assessed by both creatinine-based and cystatin C–based formulae, but with considerable discordance in individual patients. Tirzepatide produced a decline in eGFR at 12 weeks with eGFR-creatinine (but not eGFR-cystatin C), and it led to an improvement in eGFR at 52 weeks in all patients (when assessed by cystatin C), but only in patients with CKD (when assessed by eGFR-creatinine). This substudy from the SUMMIT trial demonstrates long-term tirzepatide improves renal function (both by cystatin C and creatinine), but the measurement of eGFR in patients with obesity receiving GLP-1RAs is likely to be skewed by the effects of fat and muscle mass and the changes in body composition on the synthesis of both cystatin C and creatinine. GlobalData predicts that tirzepatide is likely to be increasingly prescribed for broader cardiometabolic disease and beyond the traditional prescribing of GLP-1RAs for type 2 diabetes (T2D), steadily becoming one of the leading GLP-1 therapies in the market. "ACC 25: tirzepatide influences clinical trajectory of patients with HFpEF and obesity" was originally created and published by Pharmaceutical Technology, a GlobalData owned brand. The information on this site has been included in good faith for general informational purposes only. It is not intended to amount to advice on which you should rely, and we give no representation, warranty or guarantee, whether express or implied as to its accuracy or completeness. You must obtain professional or specialist advice before taking, or refraining from, any action on the basis of the content on our site.
Yahoo
29-03-2025
- Health
- Yahoo
Imbria Presents Positive Clinical Data from Phase 2 IMPROVE-DiCE Trial of Ninerafaxstat in Patients with Cardiometabolic HFpEF at ACC.25
– Ninerafaxstat improves cardiac energetics, cardiac reserve capacity, 6-minute walk distance and heartfailure-related health status (KCCQ) in cardiometabolic HFpEF – – Findings support further development of ninerafaxstat in HFpEF and adjacent CV indicationssuch as non-obstructive hypertrophic cardiomyopathy (nHCM) – BOSTON, March 29, 2025 (GLOBE NEWSWIRE) -- Imbria Pharmaceuticals, Inc., a clinical stage, cardiometabolic company developing novel therapies designed to enhance cellular energetics, today announced positive clinical results from Part 2 of the IMPROVE-DiCE Phase 2 trial demonstrating that ninerafaxstat improved cardiac energetics, left ventricular reserve capacity, exercise capacity and patient-reported heart failure symptoms and physical limitations in patients with cardiometabolic heart failure with preserved ejection fraction (HFpEF). The results were presented at the American College of Cardiology's Annual Scientific Session & Expo (ACC.25) in Chicago, IL during the moderated poster session titled 'Innovations and Insights in Heart Failure With Preserved Ejection Fraction: Emerging Therapies, Biomarkers and Mechanistic Studies.' 'These findings validate the mechanistic rationale for targeting impaired myocardial energetics in HFpEF and demonstrate ninerafaxstat's potential to restore resting cardiac energetics and enhance functional cardiac reserve,' said Oliver Rider, MRCP(UK), DPhil (Oxon), Professor of Cardiovascular Medicine, University of Oxford. 'Importantly, these results suggest ninerafaxstat could improve daily symptoms and physical capacity for people living with HFpEF, a condition with few effective treatments available today.' Key findings from the trial include: Treatment of patients with cardiometabolic HFpEF with ninerafaxstat for 12 weeks resulted in a statistically significant (P=0.02) increase from baseline in cardiac phosphocreatine to adenosine triphosphate (PCr/ATP) ratio, consistent with an improvement in cardiac energy reserves and meeting the trial's primary objective. Of note, the largest energetic responses to ninerafaxstat were observed in those with the most severe energy deficit at baseline. Significant improvement in left ventricular (LV) systolic reserve capacity with exercise, reflecting an increase in the heart's ability to augment its stroke volume during exercise (P=0.03), a key abnormality in patients with HFpEF. Consistent with enhanced LV reserve capacity, an increase in 6-minute walk distance of ~14 m (P=0.02) was observed. Statistically significant and clinically meaningful improvements in heart failure-related health status, measured by the Kansas City Cardiomyopathy Questionnaire-Clinical Summary Score (KCCQ-CSS), were observed in patients most symptomatically limited at baseline, pre-specified as those with KCCQ-CSS ≤80 (~8 points; P=0.04). 'Approximately 50% of heart failure cases are related to HFpEF. In the U.S. alone, the prevalence is expected to rise to 8.5 million by 2030. Within the HFpEF population, at least 80% are living with type 2 diabetes mellitus (T2DM) and obesity. There are no current treatments aimed at targeting mitochondrial energy generation to improve patient symptoms, quality of life, and functional capacity. We believe these validating results pave the way to support further investigation of ninerafaxstat in cardiometabolic HFpEF,' said Jai Patel, MRCP(UK), Chief Medical Officer at Imbria. 'Ninerafaxstat's unique therapeutic profile has the potential to make a meaningful impact in cardiometabolic HFpEF and pathophysiologically adjacent disease states such as nHCM.' A copy of the poster will be available in the 'Media Center' section of the Imbria website at About ninerafaxstatNinerafaxstat is an innovative treatment for cardiac disorders characterized by an imbalance of energy supply and demand in the heart. To maintain normal contractile function, the heart requires substantial amounts of energy, which is produced primarily by the mitochondria in the form of adenosine triphosphate (ATP). The heart normally uses two main fuels for energy generation: fatty acids and glucose. Ninerafaxstat, a partial fatty acid oxidation (pFOX) inhibitor, acts to shift the heart's preference from fatty acids towards glucose. This shift in metabolism leads to more efficient mitochondrial energy generation with the potential for improved cardiac function both at rest and during exercise. Ninerafaxstat is a simple orally administered compound with no dose titration or monitoring required, no clinically significant drug-drug interactions and can be used on top of standard of care cardiovascular treatments. About IMPROVE-DiCEIMPROVE-DiCE is the first clinical trial utilizing multi-nuclear spectroscopy, including state-of-the-art hyperpolarized MR spectroscopy, and MRI to quantify the cardiac energetic, metabolic and functional responses to an investigational metabolic modulator in cardiovascular disease. It is a two-part, Phase 2 clinical trial evaluating the safety, tolerability and pharmacodynamic effects of ninerafaxstat. Part 1 enrolled pre-HFpEF patients with type 2 diabetes and obesity and demonstrated normalization of cardiac energetics, significant reduction in cardiac steatosis and improvements in left ventricular diastolic filling rate, an important component of heart failure. The results of Part 1 were presented at the European Society of Cardiology Congress in August 2022. Part 2 of IMPROVE-DiCE enrolled symptomatic patients with cardiometabolic HFpEF and assessed the impact of ninerafaxstat on cardiac energetics, cardiac reserve function, exercise capacity and heart failure symptoms. The trial was conducted at the Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Radcliffe Department of Medicine at the University of Oxford, UK and was led by Professor Oliver Rider. For more information, please visit (Identifier: NCT04826159). About heart failure with preserved ejection fraction (HFpEF)Over half of all patients with heart failure have preserved ejection fraction, a clinical syndrome characterized by an inability of the heart to pump blood adequately to the body without pathological increases in filling pressures at rest or during exertion. As with other forms of heart failure, HFpEF is associated with cardiac energy deficiency resulting from impaired mitochondrial energy generation. This leads to impaired cardiac functional reserve on exertion and is associated with exercise-induced pulmonary congestion, resulting in hallmark heart failure symptoms of exertional breathlessness, fatigue, and markedly reduced exercise capacity leading to severe impairment in quality of life. Despite being associated with severe morbidity and mortality, HFpEF has few evidence-based therapies. Within the clinical syndrome of HFpEF, the cardiometabolic HFpEF phenotype, in which chronic cardiometabolic stress resulting from type 2 diabetes and obesity are key drivers of heart failure pathophysiology, is rapidly emerging as the most prevalent form. About ImbriaImbria is a privately held, clinical stage company developing novel therapies for patients with life-altering cardiometabolic disorders. Our clinical pipeline is focused on restoring or improving the cell's ability to produce energy in cardiometabolic disorders where energetic impairment is a fundamental contributor to disease pathogenesis, symptoms and functional deficits. The lead product candidate, ninerafaxstat, has completed multiple Phase 2 clinical trials in three indications: nHCM, stable angina, and HFpEF. In Phase 1 and 2 clinical trials, ninerafaxstat was shown to be well tolerated. For additional information, please visit ContactKomal JoshiImbria Pharmaceuticals, in to access your portfolio
Yahoo
12-03-2025
- Health
- Yahoo
Rivus Pharmaceuticals Announces Publication of Phase 2a HuMAIN Trial of HU6 in Patients with Obesity-Related Heart Failure in JAMA Cardiology
–Treatment with HU6 led to significant reductions in body fat and abdominal visceral fat while preserving skeletal muscle in patients with obesity-related heart failure with preserved ejection fraction (HFpEF) – – HU6, a novel, once-daily, oral therapy in Phase 2 clinical development, is a Controlled Metabolic Accelerator, a new class of investigational therapies designed to selectively reduce body fat while maintaining muscle mass – CHARLOTTESVILLE, Va., and SOUTH SAN FRANCISCO, Calif., March 12, 2025 /PRNewswire/ -- Rivus Pharmaceuticals, Inc., a clinical-stage biopharmaceutical company dedicated to treating cardiometabolic diseases driven by obesity, today announced the publication of results of the Phase 2a HuMAIN clinical trial of HU6 in patients with obesity-related heart failure with preserved ejection fraction (HFpEF) in JAMA Cardiology. The study met the primary endpoint of reduction in body weight with HU6 compared to placebo over the 19-week period. This reduction was driven by decreases in fat mass and visceral fat while preserving lean mass, highlighting improved body composition with HU6. Overall rates of serious adverse events (AEs) and treatment discontinuation with HU6 were low. HU6, a novel, once-daily, oral investigational medicine, is part of Rivus' portfolio of Controlled Metabolic Accelerators (CMAs). HU6, the company's lead program, increases metabolic rate in a controlled manner enabling sustained fat loss while preserving muscle mass, the primary engine of caloric utilization in the body. Excess body fat plays a key role in the underlying pathology of HFpEF, an increasingly common disorder that affects a growing population of patients for whom few effective treatments are available. "I am excited to see the potential of HU6 in significantly reducing visceral adiposity and total body fat without affecting lean mass in patients with obesity and HFpEF," said Ambarish Pandey, M.D., a cardiologist, lead-author of the publication and member of the HuMAIN study Steering Committee. "As we know, visceral adiposity is causally implicated in the development and progression of HFpEF and having a therapy that can directly target this could be transformative in HFpEF treatment." The published HuMAIN study results showed that HU6 resulted in a significantly greater reduction in body weight (-6.8 lbs vs -0.5 lbs, p=0.0026), total fat mass (-7.4 lbs vs. -0.88 lbs with placebo, p=0.0003), percent visceral fat (-1.5% vs. -0.2% with placebo, p=0.0028) and percent reduction in body fat percentage (-4.8% vs. -0.45% with placebo, p=0.0002) at 19 weeks compared with baseline. Other measures of body composition showed: No significant change in lean body mass or skeletal muscle mass with HU6 vs. placebo or with HU6 at 19 weeks compared with baseline. A reduction in abdominal visceral adipose tissue with HU6 vs. placebo (-0.19 L) in patients whose body composition was assessed by MRI. Although this Phase 2a study was a short duration of 19 weeks, additional secondary endpoints were assessed to evaluate the impact of HU6 on a number of cardiac markers. The findings showed: Significant improvements from placebo in left ventricular systolic function (increased left ventricular ejection fraction [LVEF] of 3.76% and decreased left ventricular end-systolic volume of -5.64 ml) and right ventricular function (right ventricular systolic [RV S'] velocity of 2.10 cm/s) as assessed by echocardiography. Significant reductions from placebo in resting systolic blood pressure (-8.7 mm Hg) and diastolic blood pressure (-4.9 mm Hg), which was observed early and persisted throughout the study. No significant differences in changes in cardiac safety parameters in participants who underwent a cardiac MRI or in resting heart rate or respiratory rate. No significant difference was noted in peak exercise oxygen uptake between HU6 and placebo arms. The safety profile of HU6 was consistent with previous studies. HU6 was well tolerated in study participants, who were on average elderly, obese, had multiple comorbidities, and were taking 15 concomitant medications. Overall rates of serious AEs were low. Four patients taking HU6 and one patient taking placebo experienced a serious AE, all of which were deemed unrelated to the study drug. "Although HuMAIN was a small study of short duration powered only for a reduction in body weight, the significant improvements observed in body composition and cardiac and metabolic secondary endpoints are meaningful," said Jayson Dallas, M.D., chief executive officer, Rivus Pharmaceuticals. "These positive study results, especially the improvements in cardiac structure and function, suggest that HU6 could be the first disease-modifying treatment for HFpEF, a debilitating disorder associated with poor quality of life and physical limitations." Data from HuMAIN study participants in the compliance population (i.e., those who complied with taking HU6 throughout the study based on a measure of a primary metabolite of HU6) are available on the Rivus website. In addition to the Phase 2a HuMAIN study, Rivus is evaluating HU6 in the randomized, double-blind, placebo-controlled, parallel-group Phase 2 M-ACCEL trial ( NCT05979779) in patients with MASH. The company remains on track to announce topline results from M-ACCEL in the second quarter of 2025. About the Phase 2a HuMAIN TrialThe multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-escalation Phase 2a HuMAIN trial ( NCT05284617) evaluated the efficacy and safety of oral HU6 in patients with chronic, stable obesity-related HFpEF. In the intention-to-treat (ITT) population, 66 study participants were randomized to HU6 (starting at 150 mg/day and potentially up-titrated to 450 mg/day based on safety and tolerability) or placebo. Study participants were over age 30 (average of 64.5 years; range: 38 to 87 years) with a body mass index (BMI) >30 kg/m2 (average of 39.4 kg/m2) and an average body weight of 110.9 kg (245 pounds). The primary efficacy endpoint was the change in body weight from baseline to Day 134 (19 weeks). The key secondary efficacy endpoint was the change in peak oxygen uptake (VO2). Exploratory secondary endpoints included changes in body composition, 6-minute walk distance (6MWD), Kansas City Cardiomyopathy Questionnaire (KCCQ) score, N-terminal pro b-type natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (Hs-CRP) and safety/tolerability. HuMAIN was conducted at 14 clinical sites in the United States. About Heart Failure with Preserved Ejection Fraction (HFpEF)Heart failure with preserved ejection fraction (HFpEF) is a chronic debilitating syndrome characterized by severely reduced exercise capacity, which degrades quality of life. Obesity is a strong risk factor for HFpEF and key contributor to the increasing worldwide prevalence of this disorder, with as many as 80% of patients with HFpEF in Western countries either overweight or obese. Specifically, systemic inflammation generated by visceral fat deposits is believed to contribute significantly to the development and progression of HFpEF. Studies have shown that the five-year survival rate in the United States for people hospitalized with HFpEF was 24.3%. Weight loss approaches that involve dieting, bariatric surgery and GLP-1 agonists work by decreasing energy intake rather than by increasing energy expenditure. In addition to loss of fat, these approaches result in marked reductions in muscle mass, which can lead to impaired function in patients with HFpEF, who are typically elderly and frail and already have reduced muscle mass. About Controlled Metabolic Accelerators (CMAs)Rivus is advancing a new class of investigational therapies called Controlled Metabolic Accelerators (CMAs) that have the potential to improve metabolic health for people with obesity and associated metabolic diseases. Rivus' CMAs are oral small molecules in development to increase resting metabolic rate, which results in increased consumption of energy, primarily from fat. The loss in fat mass may address multiple cardiometabolic conditions driven by adiposity. CMAs increase metabolism in a manner that is consistent and imperceptible to the patient by leveraging the natural metabolic process of mitochondrial uncoupling. In preclinical studies, mitochondrial uncoupling was shown to account for a significant portion (20% to 50%) of daily energy expenditure. Caloric-restriction strategies, on the other hand, reduce energy input and result in loss of muscle mass as well as fat. Initial data in humans has demonstrated that CMAs provided fat-selective weight loss, improved insulin sensitivity, and significantly reduced oxidative stress and inflammation. About HU6HU6, a novel, oral, once-daily investigational therapy, is Rivus' lead CMA. It is a purposely designed investigational oral small molecule that is intended to be a foundational monotherapy for cardiac, liver, diabetes and obesity indications. HU6 has been demonstrated to promote sustained body fat loss by imperceptibly increasing resting metabolism, which results in fat burn, while preserving muscle mass. The current clinical development of HU6 is focused on metabolic diseases with the most morbidity and greatest treatment needs: obesity-related heart failure with preserved ejection fraction (HFpEF) and metabolic dysfunction-associated steatohepatitis (MASH)/metabolic dysfunction-associated steatotic liver disease (MASLD). To date, more than 400 patients have been treated with HU6 as part of the clinical development program. Results of a Phase 2 metabolic study in patients with a high body mass index (BMI) and MASLD showed that once-daily HU6 significantly reduced liver fat content and body weight with no loss of lean muscle mass and improved key markers of systemic inflammation and metabolism.1 HU6 was well tolerated in this trial; side effects were mainly mild or moderate in severity. Results from the Phase 2a HuMAIN study ( NCT05284617) of HU6 in patients with obesity-related HFpEF showed the trial met its primary endpoint, demonstrating that treatment with HU6 resulted in statistically significant weight loss. The rationale for the use of HU6 in HFpEF and the design of the HuMAIN trial were published in the European Journal of Heart Failure in June 2024.2 About Rivus PharmaceuticalsRivus Pharmaceuticals, Inc., a leader in mitochondrial biology, is dedicated to improving metabolic health by advancing a new class of investigational therapies called Controlled Metabolic Accelerators (CMAs). Rivus' lead CMA is the investigational small molecule HU6 in clinical development to treat obesity-related heart failure with preserved ejection fraction (HFpEF), metabolic dysfunction associated steatohepatitis (MASH)/metabolic dysfunction-associated steatotic liver disease (MASLD) and Type 2 diabetes. In addition to HU6, Rivus is developing a pipeline of oral small molecule CMAs. For more information, please visit Contact:Sheryl SeapyReal Chemistry sseapy@ References Noureddin M, Khan S, Portell F, et al. Safety and efficacy of once-daily HU6 versus placebo in people with non-alcoholic fatty liver disease and high BMI: a randomised, double-blind, placebo-controlled phase 2a trial. Lancet Gastroenterol Hepatol. 2023;8(12):1094-1105. Kitzman DW, Lewis GD, Pandey A, et al. A novel controlled metabolic accelerator for the treatment of obesity-related heart failure with preserved ejection fraction: Rationale and design of the Phase 2a HuMAIN trial. Eur J Heart Fail. June 26, 2024. View original content to download multimedia: SOURCE Rivus Pharmaceuticals
