Cardiometabolic Health Advances Using GLP-1 Receptor Agonist

Find out how GLP-1 receptor agonists may improve cardiometabolic health and aid in effective weight management.

Abstract: A New Paradigm in Cardiometabolic Care

As a healthcare provider with a deep commitment to integrative and functional medicine, I am constantly seeking to understand and apply the latest advancements in patient care. This educational post explores the evolving landscape of treating complex cardiometabolic conditions, with a particular focus on the intersection of diabetes, heart disease, and chronic kidney disease. We will journey into the deep physiological connections between these conditions and explore the revolutionary medication classes—specifically SGLT2 inhibitors and GLP-1 receptor agonists—that offer profound cardiovascular and renal benefits beyond just glucose control. We will also delve into two detailed case studies that highlight the challenges and opportunities in managing patients with overlapping conditions, including complex scenarios such as Type 1 diabetes. I’ll share my perspective, informed by leading researchers and my clinical experience, on how we can leverage these powerful new medications, the rationale for their use, and the importance of a collaborative, multi-specialty approach.

At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, we embody this collaborative spirit. I lead our team, including Dr. Alex Jimenez, and our esteemed Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is Board Certified in Internal Medicine and brings over 40 years of invaluable experience. Her expertise (NPI #1164426749, Texas MD License #J2933) provides the essential medical direction that allows our multidisciplinary clinic in El Paso, Texas, to offer a comprehensive suite of services. Together, we integrate chiropractic care, functional medicine diagnostics, internal medicine, personal injury care, rehabilitation, and advanced medical protocols to address the root causes of our patients’ conditions, not just their symptoms. This post will illustrate how this integrated model is perfectly suited to navigate the complexities of modern cardiometabolic care.

Bridging Heart Failure and Diabetes: A New Era of Integrative Care

As a clinician with diverse training across chiropractic, nursing, and functional medicine, I am always seeking to understand the intricate connections within the human body. One of the most critical and complex relationships we see in modern healthcare is the link between type 2 diabetes and heart failure. For too long, these conditions were often treated in separate silos. However, emerging research is not only illuminating the deep physiological ties between them but also revolutionizing our treatment paradigms. Join me as we delve into these exciting developments and understand how we can better support our patients’ cardiometabolic health.

The Vicious Cycle: How Diabetes and Heart Failure Are Joined at the Hip

As a clinician who focuses on the body’s interconnected systems, I’ve always been fascinated by how one disease process can trigger another. Diabetes and heart failure are a classic example of this—two conditions that are truly joined at the hip. Diabetes isn’t just a risk factor for cardiovascular disease; it’s an independent cause of heart failure, a condition we call diabetic cardiomyopathy. This means a person can develop heart failure directly from the metabolic chaos of diabetes, even without the classic clogged arteries of atherosclerosis.

So, how does this happen? The journey begins with the core features of type 2 diabetes:

• Hyperglycemia: Chronically elevated blood sugar levels.
• Insulin Resistance: The body’s cells become less responsive to insulin, the hormone that helps shuttle glucose into cells for energy.
• Hyperinsulinemia: To overcome this resistance, the pancreas works overtime, pumping out excessive amounts of insulin.

This trio creates a pro-inflammatory environment that wreaks havoc throughout the body. The excess insulin and adiposity (especially in individuals with obesity) fuel chronic inflammation. This inflammation, in turn, causes dyslipidemia (unhealthy cholesterol levels) and endothelial dysfunction, which is damage to the inner lining of our blood vessels. This damaged lining becomes a fertile ground for the formation of atherosclerotic plaques, setting the stage for coronary artery disease.

Simultaneously, the heart muscle itself is under attack. The body responds to this metabolic stress by:

• Developing left ventricular hypertrophy (LVH), in which the heart muscle thickens and becomes stiffer.
• Activating the renin-angiotensin-aldosterone system (RAAS), a hormonal cascade that raises blood pressure and causes fluid retention, further straining the heart.
• Causing autonomic dysfunction, impairing the nervous system’s control over heart rate and blood pressure.
• Promoting fibrosis (scarring) in both the heart muscle and blood vessels, leading to further stiffening.

All these pathways converge, leading to either ischemic cardiomyopathy (heart damage from blocked arteries) or the aforementioned diabetic cardiomyopathy. In patients who already have heart disease, diabetes acts as an accelerant, making their heart failure worse.

Understanding the Two Faces of Heart Failure

When we diagnose heart failure, we classify it based on the heart’s pumping ability, measured by the ejection fraction (EF)—the percentage of blood the left ventricle pumps out with each beat. This distinction is crucial because the underlying physiology and treatment approaches differ significantly.

Heart Failure with Preserved Ejection Fraction (HFpEF)

• Definition: EF of 50% or greater.
• The Problem: This is not a pumping problem but a filling problem. The heart muscle, particularly the left ventricle, has become so thick and stiff (concentric remodeling) that it can’t relax properly to fill with blood between beats. Think of it like trying to fill a thick, rigid water balloon—it just doesn’t expand easily.
• Who It Affects: This type is more common in older adults, women, and individuals with obesity, diabetes, and hypertension.
• The Drivers: Systemic inflammation, endothelial dysfunction, and fibrosis are the key culprits. That epicardial adipose tissue—the fatty layer sitting directly on the heart—is a major source of localized inflammation driving this stiffness.
• Traditional Treatment: Historically, HFpEF has been notoriously difficult to treat. Management focused on controlling symptoms (decongestion) and managing risk factors like blood pressure and diabetes. For a long time, we had no medications that could definitively improve outcomes.

Heart Failure with Reduced Ejection Fraction (HFrEF)

• Definition: EF of 40% or less.
• The Problem: This is a classic pumping problem. The heart muscle is weak, and the ventricle often becomes enlarged and dilated (eccentric remodeling). The heart can’t contract forcefully enough to pump adequate blood to the body.
• Who It Affects: This type is more common in men and is often the result of ischemic heart disease (e.g., a prior heart attack).
• The Drivers: Overactivation of the neurohormonal systems, especially the RAAS and the sympathetic nervous system (“fight or flight” response), drives the progression of HFrEF.
• Treatment: We have a well-established “quadruple therapy” for HFrEF, often referred to as the four pillars of care: an ARNI (or ACE inhibitor/ARB), a beta-blocker, an MRA, and now, an SGLT2 inhibitor.

A New Pillar of Treatment: The Rise of SGLT2 Inhibitors

For years, we treated diabetes with the primary goal of lowering blood sugar. But a revolutionary class of drugs, the SGLT2 inhibitors, has completely changed the game. These medications have demonstrated profound benefits for the heart and kidneys, so much so that they are now a cornerstone of heart failure therapy, regardless of whether the patient has diabetes. Research has shown that SGLT2 inhibitors are highly effective at slowing the progression of heart failure, reducing the risk of atherosclerotic cardiovascular disease (ASCVD), and minimizing myocardial fibrosis (the stiffening or scarring of heart tissue).

How Do SGLT2 Inhibitors Work?

SGLT2 inhibitors act in the proximal convoluted tubules of the kidneys. They block the sodium-glucose cotransporter 2, a protein responsible for reabsorbing glucose from the urine back into the bloodstream. By blocking this transporter, these drugs cause the body to excrete excess glucose—and with it, sodium and water—in the urine.

This simple mechanism triggers a cascade of powerful benefits:

• Fueling the Sick Heart: This is one of the most fascinating aspects. A failing heart is metabolically inefficient; it struggles to use glucose for energy. SGLT2 inhibitors promote a mild state of ketosis. Ketones are a super-fuel for the heart. By providing the heart with a more efficient energy source, these drugs help it function better.
• Reducing Cardiac Stress: By promoting the excretion of sodium and water (natriuresis), SGLT2 inhibitors act like a gentle diuretic, reducing fluid volume and preload on the heart. This lowers the heart’s workload and reduces metabolic demand.
• Protecting the Kidneys: They reduce pressure inside the glomeruli (the kidney’s filtering units), slowing the progression of chronic kidney disease (CKD)—a common and deadly complication of both diabetes and heart failure.
• Combating Inflammation and Fibrosis: These drugs reduce systemic oxidative stress and inflammation. They have been shown to decrease myocardial fibrosis (heart scarring), which is particularly beneficial in HFpEF by reducing stiffness.
• Reducing Epicardial Fat: They help reduce that pro-inflammatory epicardial adipose tissue, directly targeting a key driver of cardiac dysfunction in patients with obesity and diabetes.

The Evidence: Landmark Clinical Trials

The shift in practice didn’t happen overnight. It was driven by a series of groundbreaking trials that consistently showed incredible results. The initial goal of these trials, mandated by the FDA in 2008, was to prove new diabetes drugs weren’t harmful. What researchers found was astonishing. The 2015 trial for empagliflozin (Jardiance), as published by Zinman et al. (2015) in the EMPA-REG OUTCOME trial, was the first to show not just safety, but a 14% reduction in major adverse cardiovascular events. This was a landmark moment.

• McMurray et al. (2019) and the EMPEROR-Reduced trial: both studies evaluated dapagliflozin and empagliflozin in patients with HFrEF. Both showed a remarkable ~25% reduction in cardiovascular death or hospitalization for heart failure, cementing their role as a pillar of HFrEF therapy for patients with and without diabetes.
• Anker et al. (2021): The EMPEROR-Preserved trial was a true game-changer. It was the first to show a clear benefit for any drug in patients with HFpEF. Empagliflozin significantly reduced the risk of hospitalization for heart failure in this notoriously hard-to-treat population, with a 27% relative risk reduction in the composite endpoint of cardiovascular death and hospitalization for heart failure.
• The EMPA-KIDNEY Collaborative Group (2022) and Perkovic et al. (2019) focused on patients with CKD. Both empagliflozin and canagliflozin demonstrated a powerful ability to slow the progression of kidney disease and reduce the risk of kidney failure, cardiovascular events, and death.
• Bhatt et al. (2021): The SCORED trial with sotagliflozin further confirmed the class effect, showing significant reductions in cardiovascular death and the total burden of heart failure events.
• Voors et al. (2022): A key question has always been whether these medications are safe and effective in acutely ill, hospitalized patients. The EMPULSE trial confirmed that the benefits translate directly to the inpatient setting, meaning we can safely initiate these therapies in patients who are either stable (compensated) or actively experiencing symptoms (decompensated).

These trials collectively proved that the benefits of SGTL2 inhibitors are a class effect, transforming them from simple diabetes drugs into essential cardiometabolic and renal-protective agents.

A New Frontier: GLP-1 Receptor Agonists and Cardiovascular Protection

Now, let’s shift our focus to another revolutionary class of drugs: Glucagon-Like Peptide-1 (GLP-1) receptor agonists. The American Diabetes Association guidelines now place SGLT2 inhibitors and GLP-1 agonists at the forefront of treatment for patients with established cardiovascular disease, heart failure, or chronic kidney disease (American Diabetes Association, 2023).

While SGLT2 inhibitors are often preferred for patients with heart failure and kidney disease, GLP-1 agonists are favored for those with established ASCVD. In my practice, for high-risk individuals, the ideal approach is often to use both concurrently, if insurance and patient tolerance permit. This combination targets multiple pathological pathways simultaneously, offering comprehensive cardiometabolic protection.

How Do GLP-1 Agonists Work?

GLP-1 agonists, such as semaglutide (brand names include Ozempic and Rybelsus), have a multifaceted mechanism of action. One of their primary effects is delaying gastric emptying. While this can cause side effects like nausea, it’s also a key therapeutic benefit.

• Increased Satiety: Slowing digestion helps patients feel fuller for longer, thereby naturally reducing calorie intake and promoting weight loss.
• Lower Postprandial Glucose: By slowing the release of food from the stomach, these drugs prevent sharp spikes in blood sugar after meals.
• Reduced Inflammation and Endothelial Dysfunction: GLP-1 agonists have been shown to reduce low-grade systemic inflammation and improve endothelial function (the inner lining of blood vessels).
• Plaque Stabilization: They help stabilize atherosclerotic plaques, reducing the risk of rupture and heart attack or stroke.

A crucial safety feature of these drugs is that their glucose-lowering effect is glucose-dependent. They primarily work when you eat, meaning they stimulate insulin release only as blood sugar rises. This significantly reduces the risk of hypoglycemia (low blood sugar), a major concern with older diabetes medications.

The Journey of Discovery: From Safety Trials to Shocking Benefits

The story of GLP-1 agonists is a testament to scientific rigor and unexpected discovery. Following the landmark SGLT2 inhibitor trials, the 2016 LEADER trial for liraglutide (Victoza), a GLP-1 agonist, was published. This study, involving over 9,000 patients, demonstrated a 13% risk reduction in the MACE composite (Major Adverse Cardiovascular Events: cardiovascular death, non-fatal heart attack, and non-fatal stroke) (Marso et al., 2016a).

Subsequent trials for other GLP-1 agonists continued this thrilling trend:

• SUSTAIN-6 (semaglutide/Ozempic): 26% risk reduction in MACE (Marso et al., 2016b).
• REWIND (dulaglutide/Trulicity): 12% risk reduction in MACE (Gerstein et al., 2019).
• PIONEER 6 (oral semaglutide/Rybelsus): 21% risk reduction in MACE (Husain et al., 2019).

Expanding the Benefits: Obesity and Heart Failure Without Diabetes

The next logical step was to ask whether these benefits could extend to people without diabetes. The SELECT trial provided the answer. This groundbreaking study evaluated semaglutide (at the 2.4 mg Wegovy dose) in over 17,000 overweight or obese patients without diabetes but with pre-existing cardiovascular disease. The results were definitive: a 20% reduction in the composite risk of cardiovascular death, non-fatal heart attack, or non-fatal stroke (Ryan et al., 2024).

Further studies, like the STEP-HFpEF trial, reinforced these findings in obese patients with HFpEF but without diabetes. Treatment with semaglutide showed substantial improvements in heart failure symptoms, exercise function, as well as significant weight loss (Kosiborod et al., 2023). It’s becoming clear that the benefits are driven not just by weight loss but also by a reduction in visceral obesity—the metabolically active fat surrounding our organs that produces inflammatory markers.

The Deep Science: Why These Medications Are So Effective

So, what are the deep physiological mechanisms behind these remarkable outcomes? It’s more than just weight loss or glucose control.

Cardiometabolic and Hemodynamic Effects

Weight loss and improved glycemic control directly reduce the strain on the heart. Lower adiposity and less insulin resistance mean a reduced hemodynamic load. Modest but sustained reductions in blood pressure and improvements in lipid profiles add up to a significant reduction in long-term risk. Furthermore, by improving kidney outcomes, these drugs reduce downstream cardiovascular risk by improving blood pressure regulation, volume status, and inflammation.

Cellular and Vascular Mechanisms

GLP-1 receptors are found throughout the cardiovascular system. They work to:

• Reduce Endothelial Activation: Inflammation makes the lining of our blood vessels “sticky.””GLP-1 agonists calm this process, slowing plaque formation.
• Reduce Macrophage Infiltration: By limiting the migration of immune cells into the vessel wall, these drugs prevent the formation of foam cells, which drive plaque growth.
• Lower Oxidative Stress: They reduce inflammatory cytokines and improve the bioavailability of nitric oxide, a crucial molecule for healthy vascular function.
• Reduce Platelet Activity: Some evidence suggests GLP-1 agonists may reduce platelet aggregation, contributing to the lower rate of thrombotic events.

Direct Myocardial and Electrical Effects

Perhaps most fascinating, GLP-1 receptors have been identified directly in heart tissue, including the sinoatrial (SA) node, the heart’s natural pacemaker. This suggests direct cardiac effects, such as enhancing cardiomyocyte survival and improving myocardial energetics. A heart that can generate energy more effectively is a stronger, more resilient heart. When you layer all these mechanisms, it becomes clear why these medications so powerfully reduce cardiovascular events.

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Integrating Advanced Pharmacology with Chiropractic and Functional Medicine

At Injury Medical Clinic, our multidisciplinary team is dedicated to integrative care. While these advanced medications are powerful tools, they work best as part of a comprehensive strategy. This is where our integrative model shines.

1. Medical Management (Dr. Cardenas): Dr. Cardenas provides crucial medical oversight, prescribing and managing medications such as SGLT2 inhibitors and GLP-1 agonists when indicated. Her extensive experience in internal medicine ensures that these advanced therapies are initiated safely and effectively, with monitoring for potential side effects and dosage adjustments as needed.
2. Functional Medicine Investigation (Dr. Jimenez): I use my functional medicine training to look beyond the diagnosis. We might run advanced tests to assess inflammatory markers, nutrient deficiencies, gut health, and metabolic function. This helps us identify and address the root drivers of inflammation and insulin resistance.
3. Chiropractic and Neuromusculoskeletal Care (Dr. Jimenez): As a Doctor of Chiropractic, I see the profound connection between the nervous system, structural integrity, and systemic health. Chronic pain, poor posture, and spinal misalignments can contribute to a state of chronic stress and inflammation. This elevates cortisol and other stress hormones, which can worsen insulin resistance and blood pressure. Through precise spinal adjustments and neuromuscular rehabilitation, we can:

• • Improve Neurological Function: Correcting spinal misalignments can alleviate nerve interference, promoting better communication between the brain and the body, including the organs involved in metabolism. This can help down-regulate the sympathetic nervous system (the “fight or flight” response).
  • Reduce Pain and Inflammation: By addressing biomechanical sources of pain, we can reduce the body’s overall inflammatory load, thereby complementing the anti-inflammatory effects of medications.
  • Enhance Mobility and Exercise Tolerance: By restoring function and reducing pain, chiropractic care empowers patients to exercise, which is essential for maximizing the benefits of these medications.

• Nutritional and Lifestyle Coaching: Our team provides detailed guidance on anti-inflammatory diets, targeted supplementation to support mitochondrial function (the “powerhouses” of our cells), stress management techniques, and personalized exercise programs.
• Rehabilitation: For patients whose conditions limit their physical capacity, our rehabilitation specialists design safe, progressive exercise regimens to improve strength, endurance, and quality of life.

This collaborative model ensures that, while we leverage the powerful benefits of modern pharmaceuticals, we also address the foundational pillars of health—nutrition, movement, and structural integrity—to help the body heal and function optimally.

Clinical Case Studies: Putting It All Together. Let’s consider two common scenarios to see how this integrated, modern approach works in practice.

Case Study 1: “James” and the Type 1 Diabetes Challenge

James is a 57-year-old man with adult-onset Type 1 diabetes (LADA), a BMI of 38 (obese), and a history of coronary artery disease, HFmrEF (EF 48%), and Stage 3A CKD (eGFR 48). His A1C is 7.9% despite a modern insulin pump. In my clinical observations, the stereotype of lean Type 1 patients is often untrue; they face the same struggles with weight as the general population. James is a perfect example.

The Challenge: SGLT2 inhibitors and GLP-1 agonists are not FDA-approved for Type 1 diabetes, making their use off-label. However, given his heart failure and nephropathy, the benefits are compelling.

Our Integrative Approach:

• Medication Optimization (Dr. Cardenas’s oversight):

• • Switch to a high-intensity statin, such as rosuvastatin, for aggressive lipid control.
  • Initiate an SGLT2 inhibitor off-label to protect his heart and kidneys. The main risk is euglycemic DKA, so meticulous patient education on ketone monitoring is paramount. We provide ketone test strips and teach “sick day rules”—never stop insulin and monitor ketones closely when ill or under stress.
  • Add a GLP-1 agonist off-label for cardiovascular protection, weight reduction, and improved glycemic control. We may seek insurance approval by documenting an alternative indication, like obstructive sleep apnea, which is common in this population.

• Functional and Chiropractic Care (Dr. Jimenez):

• • We’d use functional testing to guide a personalized anti-inflammatory diet.
  • Chiropractic adjustments would aim to modulate his autonomic nervous system and reduce systemic stress.
  • A personalized cardiac rehab and exercise plan would be crucial for weight loss and cardiovascular strengthening.

Case Study 2: “Karen” and Advanced Disease Management

Karen is a 70-year-old female with HFrEF (EF 30%), Stage 4 CKD (eGFR 24), Type 2 diabetes, and COPD. Her blood pressure is low (90/70), and her potassium is slightly elevated (5.2). Many providers would panic and stop her life-saving medications. I urge you: don’t follow that instinct.

Bold Treatment Decisions:

1. Absolutely Add an SGLT2 Inhibitor: Karen has powerful indications. We must anticipate the transient drop in eGFR that occurs when starting this drug. This is a sign the medication is working to protect the kidney long-term, not a sign of injury.
2. Reduce Diuretics, Not Other Key Meds: Karen is on a diuretic but isn’t congested. SGLT2 inhibitors have a natriuretic effect. We would reduce her diuretic dose by 50% when starting the SGLT2i.
3. Do Not Stop the MRA (eplerenone): Her potassium of 5.2 might seem scary, but SGLT2 inhibitors help blunt the potassium-elevating effect of MRAs, allowing us to continue this life-saving therapy.
4. Rethink Fluid and Salt Restrictions: Recent evidence shows rigid restrictions do not improve outcomes and often lead to malnutrition in these catabolic patients. With modern natriuretic drugs, we should empower patients to listen to their bodies.

Final Thoughts: A Collaborative and Proactive Future

The management of cardiometabolic renal disease is undergoing a revolution. The cases of James and Karen underscore several key principles: embrace collaboration, treat early and aggressively, don’t stop life-saving drugs due to fear of lab value shifts, and think in classes of medications that treat multiple problems at once.

Our ultimate goal is to create a future free from the devastating complications of these diseases. By combining the latest evidence-based medicine with a holistic, integrated, and collaborative approach—as we do at Injury Medical Clinic under the medical direction of Dr. Cardenas—we can make that future a reality for our patients in El Paso and beyond.

References

• American Diabetes Association. (2023). 9. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes—2023. Diabetes Care, 46(Suppl. 1), S140–S157.
• Anker, S. D., Butler, J., Filippatos, G., Ferreira, J. P., Bocchi, E., Böhm, M., Brunner–La Rocca, H.-P., Choi, D.-J., Chordà, J., Chuquiure-Valenzuela, E., Conte, C., DeMets, D., Doehner, W., Farmakis, D., Gaggini, M., Geller, N., Gotsman, I., Kitzman, D. W., & Lonn, E. (2021). Empagliflozin in heart failure with a preserved ejection fraction. The New England Journal of Medicine, 385(16), 1451–1461.
• Bhatt, D. L., Szarek, M., Steg, P. G., Cannon, C. P., Leiter, L. A., McGuire, D. K., Lewis, J. B., Riddle, M. C., Voors, A. A., Metra, M., Lund, L. H., Komajda, M., Testani, J. M., Sun, Y., Pastor-Navarro, H., Tereshchenko, L. G., & Ponikowski, P. (2021). Sotagliflozin in patients with diabetes and recent worsening heart failure. The New England Journal of Medicine, 384(2), 117–128.
• The EMPA-KIDNEY Collaborative Group. (2022). Empagliflozin in patients with chronic kidney disease. The New England Journal of Medicine, 387(19), 1–12.
• Gerstein, H. C., Colhoun, H. M., Dagenais, G. R., Diaz, R., Lakshmanan, M., Pais, P., Probstfield, J., Riesmeyer, J. S., Riddle, M. C., Ryden, L., Xavier, D., Atisso, C. M., Dyal, L., Hall, S., Rao-Melacini, P., Wong, G., & Avezum, A. (2019). Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomized placebo-controlled trial. The Lancet, 394(10193), 121–130.
• Husain, M., Birkenfeld, A. L., Donsmark, M., Dungan, K., Eliaschewitz, F. G., Franco, D. R., Hovingh, G. K., … & Buse, J. B. (2019). Oral semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine, 381(9), 841–851.
• Kosiborod, M. N., Abildstrom, S. Z., Borlaug, B. A., Butler, J., Christensen, L., Davies, M., … & STEP-HFpEF Trial Committees and Investigators. (2023). Semaglutide in patients with heart failure with preserved ejection fraction and obesity. New England Journal of Medicine, 389(12), 1069–1084.
• Marso, S. P., Daniels, G. H., Brown-Frandsen, K., Kristensen, P., Mann, J. F., Nauck, M. A., … & LEADER Steering Committee. (2016a). Liraglutide and cardiovascular outcomes in type 2 diabetes. New England Journal of Medicine, 375(4), 311–322.
• Marso, S. P., Bain, S. C., Consoli, A., Eliaschewitz, F. G., Jódar, E., Leiter, L. A., … & SUSTAIN-6 Investigators. (2016b). Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine, 375(19), 1834–1844.
• McMurray, J. J. V., Solomon, S. D., Inzucchi, S. E., Køber, L., Kosiborod, M. N., Martinez, F. A., … & DAPA-HF Trial Committees and Investigators. (2019). Dapagliflozin in patients with heart failure and reduced ejection fraction. New England Journal of Medicine, 381(21), 1995–2008.
• Perkovic, V., Jardine, M. J., Neal, B., Bompoint, S., Heerspink, H. J. L., Charytan, D. M., Edwards, R., Agarwal, R., Bakris, G., Bull, S., Cannon, C. P., Capuano, G., Chu, P.-L., de Zeeuw, D., Greene, T., Levin, A., Pollock, C., Wheeler, D. C., Yavin, Y., & Zhang, H. (2019). Canagliflozin and renal outcomes in type 2 diabetes and nephropathy. The New England Journal of Medicine, 380(24), 2295–2306.
• Ryan, D. H., Lingvay, I., Colhoun, H. M., Deanfield, J., Emerson, S. S., Frias, J. P., … & SELECT Step Study Group. (2024). Semaglutide effects on cardiovascular outcomes in people with overweight or obesity and people with prediabetes. Nature Medicine, 30(5), 1438-1447.
• Voors, A. A., Angermann, C. E., Teerlink, J. R., Collins, S. P., Kosiborod, M., BL, … & EMPULSE Trial Committees and Investigators. (2022). The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial. Nature Medicine, 28(3), 568–574.
• Zinman, B., Wanner, C., Lachin, J. M., Fitchett, D., Bluhmki, E., Hantel, S., … & EMPA-REG OUTCOME Investigators. (2015). Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. New England Journal of Medicine, 373(22), 2117–2128.

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