Find out how GLP-1 receptor agonists can support cardiometabolic health and contribute to a healthier lifestyle.

Abstract

In this educational post, I will explore the intricate pathophysiological link between type 2 diabetes, heart failure, and kidney disease, a constellation often called cardio-renal-metabolic syndrome. From my perspective as a clinician practicing integrative and functional medicine, I will guide you through the latest findings from leading researchers, drawing on robust, evidence-based outcome trials. We will journey through complex patient cases to illustrate modern treatment strategies, focusing on the revolutionary roles of SGLT2 inhibitors and GLP-1 receptor agonists, two classes of medications reshaping treatment paradigms for cardiometabolic disease, atherosclerosis, obesity, and stroke risk. This discussion will highlight key clinical trials, explain the mechanisms of action of these drugs, and provide a framework for integrating these evidence-based therapies into patient care.

Furthermore, I will explain our unique, multidisciplinary approach at Injury Medical Clinic PA, where we combine integrative chiropractic care, functional medicine, rehabilitation, and personal injury services with the conventional medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD. This allows us to provide comprehensive, guideline-concordant, and patient-centered treatment for complex cardiometabolic conditions, ensuring that we treat the whole person, not just isolated symptoms.

Our Integrated Care Model: A Collaborative Approach to Health

At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, we have cultivated a truly integrative and multidisciplinary environment. I am Dr. Alexander Jimenez, and my work as a Doctor of Chiropractic (DC) and a board-certified Family Nurse Practitioner (FNP-BC) is enhanced by my deep training in functional and integrative medicine (CFMP, IFMCP). This allows me to view patient health through a holistic lens, focusing on the root causes of disease by uniting integrative chiropractic, rehabilitation, neuromusculoskeletal care, and autonomic regulation strategies.

This comprehensive approach is made possible through our collaborative partnership with Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933). With over 40 years of experience as a board-certified internist, Dr. Cardenas serves as our Medical Director and Collaborative Physician. Her extensive expertise in internal medicine provides essential medical oversight and direction, ensuring our patients receive safe, effective, and evidence-based care that aligns with American College of Cardiology (ACC), American Heart Association (AHA), American Diabetes Association (ADA), and renal guidelines. This model, where a chiropractor applies mechanobiologic interventions and a medical doctor provides medical direction, is a cornerstone of modern integrative and injury care.

Together, our team offers a spectrum of services, including:

• Chiropractic Care: Focusing on musculoskeletal integrity, autonomic balance, and nervous system function, and its impact on overall systemic health.
• Medical Oversight: Guided by Dr. Cardenas, ensuring all treatments align with established medical standards and addressing complex comorbidities like cardiometabolic disease, autoimmune phenomena, and multimorbidity.
• Functional Medicine: Investigating and addressing the underlying drivers of chronic disease, such as inflammation, metabolic dysfunction, and nutrient imbalances.
• Personal Injury & Rehabilitation: Providing specialized care to restore function and mobility after an injury, coordinating safe, graded physical therapy for patients with concurrent cardiometabolic disease.
• Nutritional and Lifestyle Counseling: Empowering patients to take an active role in their health through targeted dietary and lifestyle modifications.

This integrated framework is particularly vital when managing complex, intertwined conditions such as diabetes and heart failure, enabling us to address the patient’s health from multiple angles to achieve superior outcomes.

The Inseparable Link: Understanding Diabetes and Heart Failure

As a clinician who has spent years observing the progression of chronic diseases, I can tell you that type 2 diabetes and heart failure are two conditions that are, for all practical purposes, joined at the hip. To truly understand why our treatment approaches are evolving, we must first appreciate the deep physiological connections between them. When I work with patients, I find it crucial to explain the “why” behind their condition, as this empowers them to become active participants in their own healing journey.

Diabetes is a powerful and independent risk factor for the development of heart failure. This means a person can develop heart failure directly from the metabolic chaos of diabetes, even without the classic plaque buildup (atherosclerosis) we typically associate with heart disease.

The Metabolic Cascade of Type 2 Diabetes

The journey begins with hyperglycemia (high blood sugar). In type 2 diabetes, this is often driven by increasing adiposity (body fat), which leads to insulin resistance.

• Insulin Resistance: Your cells become less responsive to insulin, the hormone that helps move glucose from the bloodstream into cells for energy.
• Hyperinsulinemia: To compensate for this resistance, the pancreas’s beta cells work overtime, pumping out increasing amounts of insulin. This state of high insulin levels is known as hyperinsulinemia.

This metabolic environment—high sugar and high insulin—creates a perfect storm that drives several damaging processes simultaneously:

• Chronic Inflammation: Excess body fat (adiposity) is a source of chronic, low-grade inflammation. Furthermore, hyperinsulinemia itself is an independent driver of inflammation. This systemic inflammatory state is a key villain in the story.
• Dyslipidemia: By definition, if you have diabetes, you have dyslipidemia (abnormally high or low blood lipid levels). The inflammatory environment disrupts normal fat metabolism.
• Endothelial Dysfunction: The endothelium is the thin inner lining of your blood vessels. Chronic inflammation damages this delicate layer, making it “sticky” and prone to the formation of atherosclerotic plaques.

From Metabolic Dysfunction to Heart Damage

While these systemic issues are brewing, the heart itself is under direct assault. The same metabolic milieu leads to:

• Left Ventricular Hypertrophy (LVH): The heart muscle, particularly the left ventricle, begins to thicken and “beef up” in response to the increased workload and inflammatory signals.
• RAAS Activation: The Renin-Angiotensin-Aldosterone System (RAAS), a hormonal cascade that regulates blood pressure and fluid balance, becomes overactive. This drives up blood pressure, promotes fluid retention, and contributes to fibrosis (scarring) in the heart and blood vessels.
• Autonomic Dysfunction: The autonomic nervous system, which regulates involuntary functions such as heart rate, becomes imbalanced.
• Fibrosis: The heart muscle and arteries become stiff and scarred, impairing their ability to function properly.

This cascade culminates in what we call diabetic cardiomyopathy, a form of heart muscle disease that develops independently of coronary artery blockages. For patients who already have coronary artery disease, diabetes dramatically accelerates the progression to a more severe heart failure state. This is why addressing the metabolic roots of the problem is a central tenet of both my functional medicine practice and our integrated clinical approach.

Differentiating Heart Failure: HFpEF vs HFrEF

When a patient develops heart failure, we classify it by ejection fraction (EF), which measures how much blood the left ventricle pumps with each contraction. This distinction is critical because it dictates our treatment strategy.

Heart Failure with Preserved Ejection Fraction (HFpEF)

• Definition: EF is 50% or greater.
• The Problem: This is primarily a diastolic dysfunction. The heart muscle is stiff and cannot relax properly to fill with blood between beats. This leads to a “back-up” of pressure in the lungs and body. The heart’s pumping ability is preserved, but its filling capacity is compromised.
• Characteristics: The heart often exhibits concentric remodeling, in which the ventricular walls thicken inward, reducing the chamber’s volume.
• Patient Profile: More common in older adults, particularly women. It’s strongly associated with obesity, diabetes, hypertension, atrial fibrillation, and chronic kidney disease.
• Underlying Drivers: The primary culprits are systemic inflammation, endothelial dysfunction, and fibrosis within the heart muscle and small blood vessels.
• Treatment Focus: Historically, treatment has been challenging. The focus is on decongestion (managing fluid overload), controlling risk factors such as hypertension and diabetes, and, now, using newer agents like SGLT2 inhibitors.

Heart Failure with Reduced Ejection Fraction (HFrEF)

• Definition: EF is less than 40%.
• The Problem: This is primarily a systolic dysfunction. The heart muscle is weakened and cannot contract effectively.
• Characteristics: The heart often shows eccentric remodeling and dilation (enlargement). The left ventricular end-diastolic dimension (LVEDD) is often greater than 5 cm.
• Patient Profile: More common in men and often a result of ischemic heart disease (e.g., a prior heart attack). Some HFpEF patients can progress to HFrEF over time.
• Underlying Drivers: Primarily neurohormonal activation, specifically overstimulation of the RAAS and the sympathetic nervous system.
• Treatment Focus: The goal is to block this harmful neurohormonal activation using quadruple medical therapy: an ARNI (angiotensin receptor-neprilysin inhibitor), a beta-blocker, an MRA (mineralocorticoid receptor antagonist), and an SGLT2 inhibitor.

A New Pillar of Treatment: SGLT2 Inhibitors

For years, the management of type 2 diabetes and heart failure followed separate paths. That has changed dramatically with the rise of Sodium-Glucose Cotransporter-2 (SGLT2) inhibitors. These medications—such as dapagliflozin and empagliflozin—have become a cornerstone of therapy not just for diabetes, but for heart failure and chronic kidney disease as well, fundamentally changing how we approach cardiometabolic health.

When canagliflozin (Invokana), one of the first SGLT2 inhibitors, hit the market around 2014, the initial reaction was one of cautious curiosity. The idea of lowering blood sugar by causing the kidneys to excrete excess glucose in the urine was novel. Little did we know that this class of drugs would become one of the most significant breakthroughs in cardiovascular medicine in decades.

Groundbreaking Clinical Trials

Our confidence in these medications is built on a mountain of robust, evidence-based research. Several major outcome trials have demonstrated their profound benefits, transforming them from”diabetes drugs” to “cardio-renal-metabolic” drugs recommended for patients with heart failure regardless of their diabetes status.

• EMPEROR-Reduced and DAPA-HF: These landmark trials studied empagliflozin and dapagliflozin, respectively, in patients with HFrEF (with and without diabetes). Both trials showed a remarkable reduction in cardiovascular death and hospitalizations for heart failure (around a 25-26% relative risk reduction), cementing SGLT2 inhibitors as a core pillar of HFrEF therapy.
• EMPEROR-Preserved: This was the first trial to show a clear, positive benefit for any drug in patients with HFpEF. For a field that had seen countless failed trials, this was a monumental achievement. Empagliflozin reduced the risk of cardiovascular death or hospitalization for heart failure in this difficult-to-treat population.
• EMPULSE: This trial demonstrated that initiating empagliflozin safely during hospitalization for acute heart failure provided consistent benefits, guiding clinicians to start SGLT2 inhibitors when patients are compensated or decompensated and across all NYHA classes.
• EMPA-KIDNEY and CREDENCE: These trials looked at empagliflozin and canagliflozin in patients with chronic kidney disease (CKD). They demonstrated that SGLT2 inhibitors significantly slow the progression of kidney disease and reduce the risk of kidney failure or death by approximately 30%. This is game-changing, as CKD is a common and deadly complication of both diabetes and heart failure.
• SCORED: This trial, using sotagliflozin (which has both SGLT1 and SGLT2 inhibitory effects), further confirmed the benefits, showing significant reductions in cardiovascular death, heart failure hospitalizations, and the burden of CKD.

The Multifaceted Mechanism of SGLT2 Inhibitors

How do these drugs achieve such impressive results? Their mechanism is far more complex than simply making you excrete sugar. They work on the proximal convoluted tubule in the kidney, blocking the SGLT2 protein that reabsorbs glucose and sodium back into the blood. This leads to a cascade of beneficial effects:

What SGLT2 Inhibitors Give Us (The “More” ):

• Natriuresis: Excretion of sodium, which helps reduce fluid volume, interstitial fluid, and blood pressure (decreased ventricular wall stress).
• Plaque Stability: They appear to help stabilize atherosclerotic plaques, reducing the likelihood of rupture and heart attack.
• Endothelial Stability: They improve the health of the blood vessel lining.
• Increased Ketosis: This is one of the most fascinating aspects. Sick hearts are inefficient at using glucose for energy. However, they are very good at using ketone bodies as fuel. SGLT2 inhibitors promote a mild state of ketosis, essentially providing the struggling heart with a more efficient “super-fuel” and improving ATP yield per oxygen consumed.

What SGLT2 Inhibitors Reduce (The “Less” ):

• Metabolic Demand on the Heart: By improving efficiency, they reduce theheart’ss workload.
• Oxidative Stress & Inflammation: They have powerful anti-inflammatory and antioxidant effects, tackling the root drivers of cardiometabolic disease.
• Glomerular Pressure: By reducing pressure within the kidney’s filtering units (via tubuloglomerular feedback), this mechanism protects the kidneys from damage and slows the progression of CKD.
• Myocardial Fibrosis: They help reduce scarring and stiffening of the heart muscle, which are key factors in both HFrEF and HFpEF.
• Epicardial Adipose Tissue (EAT): The fat layer that lies directly on the heart muscle. EAT is highly pro-inflammatory. SGLT2 inhibitors have been shown to reduce this specific, harmful fat depot, directly blunting inflammation where it matters most.

From my perspective in functional and chiropractic care, this holistic mechanism is exciting. It’s not just treating a symptom (high blood sugar); it’s rebalancing multiple physiological systems—metabolic, inflammatory, hemodynamic—which aligns perfectly with our philosophy of treating the whole person.

---

Optimizing Your Wellness- Video

---

GLP-1 Receptor Agonists for ASCVD, Weight Loss, and Stroke Risk

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), including liraglutide and semaglutide, offer powerful cardiometabolic improvements in patients with and without type 2 diabetes, including meaningful reductions in major adverse cardiovascular events (MACE)—CV death, non-fatal MI, and non-fatal stroke.

• LEADER (liraglutide) demonstrated a 13 percent reduction in MACE over nearly 4 years in more than 9,000 patients.
• REWIND (dulaglutide) showed about a 12 percent reduction in MACE, remarkable for broad, long-term prevention.
• SUSTAIN-6 (semaglutide) and PIONEER-6 (oral semaglutide) reported substantial MACE reduction and signals for stroke benefit.
• SELECT extended semaglutide’s benefits to patients with overweight or obesity without diabetes, delivering a 20 percent reduction in composite CV events.
• STEP trials showed an average 15–16 percent weight loss over 68 weeks with semaglutide 2.4 mg weekly, along with improvements in blood pressure, lipids, and inflammatory markers.

Physiologically, GLP-1 RAs slow gastric emptying and enhance satiety, leading to reduced postprandial glucose excursions, lower insulin exposure, and decreased visceral adiposity. They also reduce low-grade inflammation, endothelial activation, and foam cell formation, stabilize atherosclerotic plaque, and improve nitric oxide bioavailability.

ADA Guideline Orientation: When to Use SGLT2 vs GLP-1

The American Diabetes Association (ADA) guidelines emphasize a tailored approach based on comorbidities:

• For established ASCVD, prioritize GLP-1 RAs given strong evidence of MACE reduction, including stroke.
• For heart failure and CKD, prioritize SGLT2 inhibitors due to potent reductions in heart failure hospitalization and renal protection.
• In high-risk patients, consider using both agents concurrently if coverage allows, as they act via ddistinct pathwaysand confer additive benefit

The Challenge of Type 1 Diabetes A: Case Study

My heart truly goes out to my patients with type 1 diabetes. While we’ve seen incredible advancements for type 2 diabetes, many of these drugs are not officially approved for type 1. This is a concern because they can develop aggressive forms of kidney disease (nephropathy) and heart disease.

Let’s consider “James,” a 57-year-old man with latent autoimmune diabetes in adults (LADA), a form of type 1 diabetes.

• Clinical Profile: A1c 7.9%, BMI 38 (obese), Stage 3A CKD (eGFR 48), CAD with stents, and heart failure with moderately reduced ejection fraction (HFmrEF) with an EF of 48%. His current medications include Losartan 25mg and Pravastatin 20mg.
• Immediate Needs: First, his lipid management is inadequate. Pravastatin 20mg is not a high-intensity statin. For a patient with established heart disease, high-intensity therapy is non-negotiable. I often prefer rosuvastatin due to its tolerability in my clinical experience.
• Off-Label Use of SGLT-2 Inhibitors: Would we add an SGLT-2 inhibitor? Although not FDA-approved for type 1 diabetes in the U.S., the potential benefits for James are immense. The primary risk is euglycemic diabetic ketoacidosis (DKA). If we proceed with this off-label use, we do so with extreme caution, providing thorough education and ketone test strips.
• Role of GLP-1 Receptor Agonists: A GLP-1 receptor agonist is also highly appropriate to address his weight, A1c, and cardiovascular risk.
• Navigating Barriers: Insurance may deny these drugs for type 1 diabetes. However, we can leverage other approved indications. SGLT-2 inhibitors like dapagliflozin (Farxiga) and empagliflozin (Jardiance) are approved for heart failure, with or without diabetes, providing a legitimate on-label reason. For GLP-1s, an obstructive sleep apnea (OSA) diagnosis related to his obesity can sometimes secure approval for weight management.

A cardiologist would also strongly consider a mineralocorticoid receptor antagonist (MRA), such as spironolactone or the newer agent finerenone, which has demonstrated heart and kidney benefits in diabetes. A critical point is sick-day management: patients must be instructed to “If you can’t eat, don’t take your SGLT-2 inhibitor” to reduce the risk of DKA.

Managing Complex Comorbidities: Advanced CKD and Heart Failure. Let’s look at another common scenario: “Karen,” a 70-year-old female with HFrEF (EF 30%), Stage 4 CKD (eGFR 24), type 2 diabetes, CAD, and COPD. Her labs show high potassium (5.2) and creatinine (2.3), and her blood pressure is low-normal at 90/70.

For many clinicians, these labs are alarming. However, we must resist the urge to stop her guideline-directed medical therapy.

• Add an SGLT-2 inhibitor? She has HFrEF and type 2 diabetes, and her eGFR is above the 20 mL/min cutoff.
• What about the transient drop in kidney function? We anticipate a temporary dip in eGFR when starting an SGLT-2 inhibitor. This is the medication working, not kidney damage. We must ride it out.
• What about high potassium? I would not stop her MRA. SGLT-2 inhibitors promote potassium excretion, blunting the potassium-elevating effect of MRAs and allowing us to keep patients on these life-saving drugs.
• What medication should we stop? She is on a diuretic but not congested. A good rule is to reduce the dose of the standing diuretic by 50% when starting an SGLT-2 inhibitor to prevent dehydration.

Integrative Chiropractic and Functional Medicine in Cardiometabolic Care

While these pharmacological interventions are powerful, they are only one piece of the puzzle. At our clinic, integrative chiropractic care and functional medicine are essential pillars of the treatment plan, complementing pharmacotherapy through mechanobiologic and autonomic regulation. As I share in my clinical observations and educational resources, we align these approaches to reduce systemic stressors driving cardiometabolic burden.

• Autonomic Balance and Inflammation: Cardiometabolic disease is an inflammatory state driven by sympathetic overdrive. Using gentle spinal and rib cage mobilization and soft-tissue release, we aim to promote parasympathetic tone and modulate the autonomic nervous system. Improved vagal activity supports endothelial function and baroreflex sensitivity, helping downregulate the chronic stress response that fuels inflammation and insulin resistance.
• Improving Musculoskeletal Function for Exercise: For patients like James and Karen, exercise is medicine. However, obesity or chronic pain often creates barriers. As a chiropractor, I address these musculoskeletal issues to improve mobility and reduce pain, empowering patients to engage in the physical activity necessary to improve insulin sensitivity, lose weight, and strengthen their cardiovascular system.
• Movement Prescription and Biomechanics: We prescribe targeted low-impact exercise (walking, tempo breathing) to increase skeletal muscle glucose uptake via AMPK activation. By correcting postural distortions and improving thoracic mechanics, we can enhance respiratory efficiency and reduce accessory muscle strain, a subtle but important factor for patients with dyspnea.
• Anti-inflammatory Nutrition and Lifestyle: Our functional medicine approach involves a deep dive into diet, stress, and sleep. We work with patients to adopt an anti-inflammatory, low-glycemic diet. With GLP-1 RAs, we leverage their satiety mechanisms to help patients adhere to meal plans. Sleep optimization and stress-reduction practices, such as paced breathing, lower cortisol and catecholamine surges that worsen blood pressure.

For more on my approach and clinical observations, see:

• https://chiropracticscientist.com/
• https://www.linkedin.com/in/dralexjimenez/

These integrative methods are carefully coordinated with Dr. Cardenas to ensure safety, appropriate monitoring, and synergistic benefit with guideline-directed medical therapy.

Key Takeaways for Patients and Clinicians

• SGLT2 inhibitors deliver robust reductions in heart failure hospitalizations and cardiorenal benefits.
• GLP-1 receptor agonists lower MACE, drive significant weight loss, and reduce stroke risk, even in non-diabetic patients with obesity.
• Transitioning away from older agents that increase hypoglycemia risk and lack cardiovascular benefit is often warranted.
• Let Go of Outdated Practices: We are moving away from strict fluid and sodium restrictions for most heart failure patients on modern medications. The new mantra is: “Let them listen to their bodies. If they’re thirsty, they should drink.”
• Do Not Stop Protective Medications: Once a patient is on an SGLT-2 inhibitor, we generally do not stop it, even if their GFR declines, as it continues to provide powerful protection.
• Integrative chiropractic and functional medicine amplify pharmacologic outcomes by reducing autonomic stress, improving movement, and changing inflammatory inputs.
• A multidisciplinary model with internal medicine oversight ensures safety, alignment with guidelines, and individualized care. By integrating our expertise, we can truly transform patient outcomes and build a healthier future.

References

1. American Diabetes Association. (2024). Standards of care in diabetes—2024. Diabetes Care.
2. Anker, S. D., Butler, J., Filippatos, G., Ferreira, J. P., Bocchi, E., Böhm, M., Brueckmann, M., Choi, D.-J., Chopra, V., Chuquiure-Valenzuela, E., Giannetti, N., Gomez-Mesa, J. E., Janssens, S., Januzzi, J. L., Gonzalez-Juanatey, J. R., Merkely, B., Nicholls, S. J., Perrone, S. V., Piña, I. L., … EMPEROR-Preserved Trial Investigators. (2021). Empagliflozin in heart failure with a preserved ejection fraction. New England Journal of Medicine, 385(16), 1451–1461.
3. Bakris, G. L., Agarwal, R., Anker, S. D., Pitt, B., Ruilope, L. M., Rossing, P., Kolkhof, P., Stefánsson, B. V., Wæver, C., & McMurray, J. J. V. (2020). Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes. New England Journal of Medicine, 383(23), 2219–2229.
4. 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., Liu, M., Kes, V., Lokhnygina, Y., Rosano, G. M. C., & Probstfield, J. L. (2021). Sotagliflozin in patients with diabetes and recent worsening heart failure. New England Journal of Medicine, 384(2), 117–128.
5. Brown, E., Heerspink, H. J. L., Cuthbertson, D. J., & Wilding, J. P. H. (2021). GLP-1 receptor agonists in type 2 diabetes, cardiovascular disease, and obesity. Circulation Research, 128(11), 1638–1655.
6. Gerstein, H. C., Colhoun, H. M., Dagenais, G. R., Diaz, R., Lakshmanan, M., Pais, P., Probstfield, J., Riesmeyer, J. S., Riddle, M. C., Rydén, 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.
7. Heidenreich, P. A., Bozkurt, B., Aguilar, D., Allen, L. A., Byun, J. J., Colvin, M. M., Deswal, A., Drazner, M. H., Dunlay, S. M., Evers, L. R., Fang, J. C., Fedson, S. E., Fonarow, G. C., Hayek, S. S., Hernandez, A. F., Khazanie, P., Kittleson, M. M., Lee, C. S., Link, M. S., … Yancy, C. W. (2022). 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation, 145(18), e895–e1032.
8. Heerspink, H. J. L., Stefánsson, B. V., Chertow, G. M., Correa-Rotter, R., Greene, T., Hou, F. F., Mann, J. F. E., McMurray, J. J. V., Lindberg, M., Rossing, P., Sjöström, C. D., Toto, R. D., & Wheeler, D. C. (2018). Rationale and protocol of the Dapagliflozin And Prevention of Adverse-outcomes in Chronic Kidney Disease (DAPA-CKD) randomized controlled trial. Nephrology Dialysis Transplantation, 33(10), 1839–1840.
9. Husain, M., Birkenfeld, A. L., Donsmark, M., Dungan, K., Eliaschewitz, F. G., Franco, D. R., Hovingh, G. K., Ikeda, F., Lingvay, I., Mosenzon, O., Pedersen, S. D., Tack, C. J., Thomsen, M., Vilsbøll, T., Warren, M. L., & Bain, S. C. (2019). Oral semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine, 381(9), 841–851.
10. Lincoff, A. M., Brown-Frandsen, K., Colhoun, H. M., Deanfield, J., Dhatariya, K., Dicker, D., Eckel, R. H., Friedman, N., Hovingh, G. K., Jabbour, S., Kosiborod, M. N., Mann, J. F. E., Mosenzon, O., Palmer, M., Petrie, M. C., Rockoff, P., Rosenstock, J., Ryan, D. H., Sjöstrand, M., … SELECT Trial Investigators. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. New England Journal of Medicine.
11. Marso, S. P., Daniels, G. H., Brown-Frandsen, K., Kristensen, P., Mann, J. F. E., Nauck, M. A., Nissen, S. E., Pocock, S., Poulter, N. R., Ravn, L. S., Steinberg, W. M., Stockner, M., & Buse, J. B. (2016). Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. New England Journal of Medicine, 375(4), 311–322.
12. Marso, S. P., Bain, S. C., Consoli, A., Eliaschewitz, F. G., Jódar, E., Leiter, L. A., Lingvay, I., Rosenstock, J., Saugstrup, T., Warren, M. L., & Vilsbøll, T. (2016). Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine, 375(19), 1834–1844.
13. McMurray, J. J. V., Solomon, S. D., Inzucchi, S. E., Køber, L., Kosiborod, M. N., Martinez, F. A., Ponikowski, P., Sabatine, M. S., Anand, I. S., B?lohlávek, J., Böhm, M., Chiang, C.-E., Chopra, V. K., de Boer, R. A., Desai, A. S., Diez, M., Drozdz, J., Dukát, A., Ge, J., … 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.
14. Packer, M., Anker, S. D., Butler, J., Filippatos, G., Pocock, S. J., Carson, P., Januzzi, J., Verma, S., Tsutsui, H., Brueckmann, M., Jamal, W., Kimura, K., Schnee, J., Zeller, C., Cotton, D., Bocchi, E., Böhm, M., Choi, D.-J., Chopra, V., … EMPEROR-Reduced Trial Investigators. (2020). Cardiovascular and renal outcomes with empagliflozin in heart failure. New England Journal of Medicine, 383(15), 1413–1424.
15. Rosuvastatin Use in High-Risk Patients. (2011). Journal of the American College of Cardiology, 58(20), 2110.
16. The EMPA-KIDNEY Collaborative Group. (2023). Empagliflozin in patients with chronic kidney disease. New England Journal of Medicine, 388(2), 117–127.
17. Voors, A. A., Angermann, C. E., Teerlink, J. R., Collins, S. P., Kosiborod, M., Biegus, J., Ferreira, J. P., Nassif, M. E., Psotka, M. A., Tromp, J., Borleffs, C. J. W., Ma, C., Salsali, A., Hyland, M. H., & Ponikowski, P. (2022). The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial. JAMA, 327(13), 1252-1262.
18. Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine, 384(11), 989–1002.
19. Zinman, B., Wanner, C., Lachin, J. M., Fitchett, D., Bluhmki, E., Hantel, S., Mattheus, M., Devins, T., Johansen, O. E., Woerle, H. J., Broedl, U. C., & Inzucchi, S. E. (2015). Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. New England Journal of Medicine, 373(22), 2117–2128.

SEO Tags: SGLT2 inhibitors, GLP-1 receptor agonists, heart failure treatment, type 2 diabetes, integrative care, Dr. Alex Jimenez, Dr. Maria Cardenas, El Paso chiropractor, functional medicine, cardiovascular disease, diabetic cardiomyopathy, HFpEF, HFrEF, empagliflozin, dapagliflozin, chronic kidney disease, integrative medicine, chiropractic care, multidisciplinary clinic, evidence-based medicine, metabolic health, EMPEROR-Preserved, EMPULSE, DAPA-HF, LEADER trial, REWIND trial, SUSTAIN-6, PIONEER-6, SELECT trial, STEP trials, cardiometabolic care, atherosclerosis, stroke reduction, internal medicine oversight, El Paso Injury Medical Clinic, autonomic regulation, endothelial function, weight loss semaglutide, cardiorenal protection, Cardio-Renal-Metabolic Syndrome, Type 1 Diabetes, Off-Label Prescribing, Euglycemic DKA, Lipid Management, Rosuvastatin, Personal Injury Care, Rehabilitation