The intersection of type 2 diabetes mellitus (T2DM) and established atherosclerotic cardiovascular disease (ASCVD) is the clinical context most powerfully supported by large-scale cardiovascular outcome trial (CVOT) data. Both glucagon-like peptide-1 receptor (GLP-1R) agonists and sodium-glucose cotransporter 2 (SGLT-2) inhibitors reduce cardiovascular events in this population, but through different mechanisms and with different dominant benefit signals, making the selection between and combination of these agents a decision grounded in the specific cardiovascular phenotype of the individual patient.
Established ASCVD for CVOT purposes is defined as a history of myocardial infarction, unstable angina requiring hospitalization, coronary revascularization, ischemic stroke or transient ischemic attack, or peripheral arterial disease (PAD) with hemodynamic significance. Patients with only multiple cardiovascular risk factors but no prior event fall into the high-risk but not established-ASCVD category, and the CVOT data for atherosclerotic event reduction is substantially weaker in this primary-prevention population. The American Diabetes Association (ADA) 2024 Standards of Care therefore specifically reserves GLP-1R agonists and SGLT-2 inhibitors with proven ASCVD benefit for patients with established ASCVD or very high risk, not merely for all patients with multiple risk factors.1
For the dominant atherosclerotic endpoint of non-fatal myocardial infarction (MI), non-fatal stroke, and cardiovascular death, GLP-1R agonists have the strongest trial evidence. Liraglutide (Leaders in Cardiovascular Outcomes (LEADER) trial: 13% major adverse cardiovascular event (MACE) reduction) demonstrated the clearest superiority signal for atherosclerotic endpoints, including a significant reduction in cardiovascular death. Semaglutide subcutaneous similarly reduced MACE and produced the largest reduction in non-fatal stroke seen across the diabetes CVOT program, while semaglutide oral demonstrated cardiovascular safety. All three reduce atherosclerotic events with a mechanism consistent with anti-atherosclerotic effects on plaque stability, endothelial function, and inflammation.2
SGLT-2 inhibitors in the established ASCVD context provide a different and complementary benefit: reduction in cardiovascular death and heart failure hospitalizations rather than reduction in non-fatal MI or stroke. the Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG OUTCOME) demonstrated a 38% reduction in cardiovascular death and a 35% reduction in heart failure hospitalization, with no significant effect on non-fatal MI or stroke. The same pattern held in the Canagliflozin Cardiovascular Assessment Study (CANVAS): MACE was reduced numerically but the dominant signal was heart failure hospitalization. This hemodynamic benefit, operating through volume unloading and natriuresis, is complementary to the anti-atherosclerotic benefit of GLP-1R agonists, supporting simultaneous use of both drug classes in patients with established ASCVD who also have heart failure or who are at high risk for heart failure progression.3
Practical drug sequencing in T2DM with established ASCVD typically begins with metformin as the glycemic backbone if tolerated and renal function permits (estimated glomerular filtration rate (eGFR) ≥30 mL per minute per 1.73 m²), followed by a GLP-1R agonist as the second agent for ASCVD risk reduction. An SGLT-2 inhibitor is added as the third agent, or substituted as second agent when heart failure is the more pressing complication. When both ASCVD and heart failure coexist, the combination of a GLP-1R agonist plus an SGLT-2 inhibitor provides dual-pathway protection and is explicitly recommended by the ADA. Glycemic targets in this population should be individualized, with less stringent hemoglobin A1c (HbA1c) goals (7.5 to 8.0%) acceptable in patients with established cardiovascular disease and comorbidities that limit life expectancy or raise hypoglycemia risk, while tighter targets (6.5 to 7.0%) may be appropriate in younger patients with long duration of therapy benefit ahead of them.1
Dominant atherosclerotic protection (MI, stroke): GLP-1R agonists — prefer semaglutide or liraglutide with proven MACE benefit. Dominant heart failure and CV death protection: SGLT-2 inhibitors — prefer empagliflozin or dapagliflozin with proven non-glycemic indications. Both ASCVD + HF: combine both classes. Always maintain background metformin, renin-angiotensin-aldosterone system (RAAS) blockade, statin, and antiplatelet therapy as indicated per guideline-directed cardiovascular management.
Chronic kidney disease (CKD) is the most common serious complication of longstanding type 2 diabetes mellitus (T2DM), and the interaction between diabetes pharmacology and renal function is bidirectional: declining kidney function alters drug pharmacokinetics, clearance, and safety thresholds, while the choice of anti-diabetic agent has a direct impact on the rate of kidney disease progression. Integrating estimated glomerular filtration rate (eGFR) staging and albuminuria quantification into prescribing decisions is mandatory in this population.
The pharmacokinetic consequences of declining eGFR are agent-specific and clinically significant. Metformin accumulates in advanced renal impairment and raises the risk of lactic acidosis through impaired lactate clearance. The current consensus threshold for metformin continuation is eGFR ≥30 mL per minute per 1.73 m², with dose reduction recommended below 45 mL per minute per 1.73 m². Sulfonylureas with active renally cleared metabolites, particularly glibenclamide (glyburide) and, to a lesser extent, glipizide and glimepiride , accumulate in CKD, prolonging insulin secretory stimulus and raising hypoglycemia risk substantially; these agents should generally be avoided below eGFR 45 mL per minute per 1.73 m² and all should be used with extreme caution as eGFR declines further. Insulin requirements fall unpredictably in advanced CKD because the kidney contributes to insulin clearance (approximately 30 to 40% of circulating insulin is degraded renally); patients with eGFR below 30 mL per minute per 1.73 m² on insulin require frequent dose reductions to avoid hypoglycemia, often by 25 to 50% from their pre-CKD requirement.4
Among agents with direct renoprotective effects, sodium-glucose cotransporter 2 (SGLT-2) inhibitors and renin-angiotensin-aldosterone system (RAAS) blockade (angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB)) are the two pharmacological pillars of diabetic kidney disease (DKD) management supported by outcome trial data. RAAS blockade reduces intraglomerular pressure by dilating the efferent arteriole, slowing albuminuria progression and protecting residual nephron mass. SGLT-2 inhibition reduces intraglomerular pressure by constricting the afferent arteriole through tubuloglomerular feedback, operating at a different hemodynamic node of the same glomerular pressure circuit. The Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation trial (CREDENCE) (canagliflozin 100 mg, eGFR 30 to 90, urinary albumin-to-creatinine ratio (UACR) >300 mg per gram, all on maximum tolerated RAAS blockade) demonstrated a 30% reduction in the primary renal composite on top of background RAAS blockade, confirming additive nephroprotection from dual-pathway pressure reduction.5 SGLT-2 inhibitors should be initiated as early as possible in DKD and continued as long as the eGFR remains above the agent-specific and indication-specific floor; for canagliflozin in the DKD indication, continued use is supported down to eGFR 30 mL per minute per 1.73 m².1
Dipeptidyl peptidase-4 (DPP-4) inhibitors are generally well-tolerated in CKD and do not require dose adjustment for saxagliptin and linagliptin; sitagliptin and alogliptin require dose reduction as eGFR falls. Among glucagon-like peptide-1 receptor (GLP-1R) agonists, semaglutide and liraglutide are not renally cleared and do not require dose adjustment for renal impairment, though nausea-driven volume depletion is a practical concern in patients with CKD stage G3 (eGFR 30–59 mL per minute per 1.73 m²) or lower who are already fluid-sensitive; both agents are used cautiously in patients with eGFR below 15 mL per minute per 1.73 m² due to limited data. Finerenone, a non-steroidal mineralocorticoid receptor antagonist (MRA), received regulatory approval for DKD based on the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease (FIDELIO-DKD) trial, which demonstrated significant reductions in renal composite endpoints in T2DM with DKD on background RAAS blockade, with a more favorable hyperkalemia profile than steroidal MRAs such as spironolactone. The potential for triple nephroprotective therapy combining RAAS blockade, an SGLT-2 inhibitor, and finerenone is supported by FIDELIO-DKD outcome data and is gaining traction in guidelines for patients with high-risk DKD and persistent albuminuria despite dual blockade.6
eGFR ≥60: All agents generally safe; full doses. eGFR 45–59: Reduce metformin dose; avoid glibenclamide; SGLT-2i glycemic indication acceptable; monitor volume status on GLP-1RAs. eGFR 30–44: Stop metformin at eGFR <30 threshold approaching; SGLT-2i for DKD/CV indication (canagliflozin, dapagliflozin, empagliflozin) still usable; avoid most sulfonylureas; insulin dose reduction required. eGFR 15–29: SGLT-2i for HF (dapagliflozin, empagliflozin) still usable down to eGFR 20–25; DPP-4i (linagliptin) safe; insulin with close hypoglycemia monitoring. eGFR <15 / dialysis: Insulin primary agent; linagliptin safe; avoid most other oral agents.
Heart failure is both a consequence of longstanding type 2 diabetes mellitus (T2DM) and an independent driver of mortality in the diabetic population, with T2DM patients having a two- to fourfold higher risk of heart failure than age-matched non-diabetic individuals. The intersection requires attention not only to which anti-diabetic agents benefit heart failure outcomes, but also to which agents are contraindicated or harmful in patients with reduced cardiac output and volume overload.
The most consequential pharmacological advance for T2DM with heart failure is the establishment of sodium-glucose cotransporter 2 (SGLT-2) inhibitors as disease-modifying therapy across the full ejection fraction spectrum. For heart failure with reduced ejection fraction (HFrEF), defined as left ventricular ejection fraction (LVEF) at or below 40%, both dapagliflozin (Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF) trial) and empagliflozin (Empagliflozin Outcome Trial in Patients with Chronic Heart Failure and a Reduced Ejection Fraction (EMPEROR-Reduced) trial) demonstrated significant 25 to 26% reductions in the primary composite of cardiovascular death or heart failure hospitalization, consistent in patients with and without T2DM. For heart failure with preserved ejection fraction (HFpEF), defined as LVEF above 40%, empagliflozin (Empagliflozin Outcome Trial in Patients with Chronic Heart Failure with Preserved Ejection Fraction (EMPEROR-Preserved)) and dapagliflozin (Dapagliflozin Evaluation to Improve the Lives of Patients with Preserved Ejection Fraction Heart Failure (DELIVER)) have both demonstrated significant reductions in the primary heart failure hospitalization composite, making SGLT-2 inhibitors the first pharmacological class with broad benefit across ejection fraction categories. No T2DM status is required for these heart failure indications.7
Several anti-diabetic agents carry specific concerns or contraindications in heart failure. Thiazolidinediones (TZDs), pioglitazone and rosiglitazone, are contraindicated in New York Heart Association (NYHA) class III or IV heart failure and should be used with great caution in class II, because thiazolidinedione-mediated sodium and water retention through peroxisome proliferator-activated receptor-gamma (PPAR-γ) activation in the collecting duct exacerbates fluid overload and has been associated with increased rates of heart failure hospitalization in clinical trials. Saxagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, was associated with a 27% increase in heart failure hospitalization compared with placebo in the Saxagliptin Assessment of Vascular Outcomes Recorded in Patients with Diabetes Mellitus (SAVOR-TIMI 53) trial, a finding not replicated with other DPP-4 inhibitors; saxagliptin should be avoided in patients with established heart failure or high heart failure risk. Alogliptin showed a numerical but non-significant heart failure hospitalization excess in the Examination of Cardiovascular Outcomes with Alogliptin versus Standard of Care (EXAMINE) trial. Sitagliptin (Saxagliptin Assessment of Vascular Outcomes Recorded in Patients with Diabetes Mellitus (TECOS) trial) and linagliptin (Cardiovascular and Renal Microvascular Outcome Study with Linagliptin (CARMELINA) trial) demonstrated neutral heart failure outcomes in their respective CVOTs.8
Glucagon-like peptide-1 receptor (GLP-1R) agonists occupy an intermediate position in heart failure: they are not contraindicated in stable heart failure, have shown neutral to favorable effects on heart failure hospitalizations in patients with established atherosclerotic cardiovascular disease (ASCVD), but have not consistently demonstrated superiority over placebo for heart failure-specific endpoints in HFrEF trials. The Functional Impact of Glucagon-Like Peptide-1 (GLP-1) for Heart Failure Treatment (FIGHT) trial of liraglutide in hospitalized HFrEF patients raised concerns about potential increase in heart failure events in the decompensated setting, though subsequent analyses suggested confounding by baseline characteristics. Current guidance positions GLP-1R agonists as appropriate to continue in T2DM patients with stable heart failure who have them for ASCVD indication, but they are not initiated primarily for heart failure benefit and are used with caution during acute decompensated heart failure hospitalizations.9
Insulin management in heart failure with T2DM requires particular care. High-dose insulin promotes sodium retention through renal tubular insulin receptor activation, which can worsen fluid overload in decompensated heart failure; patients requiring large insulin doses may benefit from transition to SGLT-2 inhibitor-containing regimens that partially offset insulin-mediated sodium retention. During hospitalization for acute decompensated heart failure (ADHF), intravenous insulin infusion protocols are frequently used for glycemic control, with glucose targets of 7.8 to 10.0 mmol/L (140 to 180 mg per deciliter) per the American Diabetes Association (ADA) inpatient guidelines, avoiding hypoglycemia which carries independent adverse outcomes in the substantially ill cardiac patient. SGLT-2 inhibitors should be held during ADHF hospitalization and restarted only after clinical stabilization due to the volume depletion and euglycemic diabetic ketoacidosis (DKA) risks in the fluid-restricted, fasting patient.1
Thiazolidinediones (pioglitazone, rosiglitazone): contraindicated in NYHA class III–IV; cause fluid retention. Saxagliptin: avoid in established HF or high HF risk (SAVOR-TIMI 53 signal). SGLT-2 inhibitors during acute decompensation: hold during hospitalization; risk of euglycemic DKA and excessive volume depletion in the fasting, fluid-restricted patient. High-dose insulin: sodium-retaining effect via renal tubular insulin receptors; consider dose reduction when adding SGLT-2 inhibitor.
Diabetes in pregnancy encompasses gestational diabetes mellitus (GDM), pre-existing type 2 diabetes mellitus (T2DM) in a pregnant patient, and type 1 diabetes mellitus (T1DM) in pregnancy. The pharmacological approach to all three is governed by the same overriding principle: insulin is the only agent with long-term safety data in pregnancy, the only agent with dose-titratable precision, and the regulatory standard of care. Most oral and injectable non-insulin agents lack adequate human pregnancy safety data, and several carry specific teratogenic or fetal safety concerns that preclude their use.
Gestational diabetes mellitus is defined as glucose intolerance first recognized during pregnancy, typically diagnosed between 24 and 28 weeks gestation by either the one-step approach (75-gram oral glucose tolerance test (OGTT) with fasting, 1-hour, and 2-hour plasma glucose measurements) or the two-step approach (50-gram glucose challenge test followed by 100-gram OGTT if the screen is positive). GDM complicates 5 to 10% of pregnancies in the United States and carries risks for both mother (pre-eclampsia, cesarean delivery, progression to T2DM postpartum) and neonate (macrosomia, neonatal hypoglycemia, shoulder dystocia, respiratory distress syndrome). Medical nutrition therapy (MNT) is the first-line intervention; pharmacological treatment is initiated when fasting glucose exceeds 5.3 mmol/L (95 mg per deciliter) or postprandial glucose exceeds 7.8 mmol/L (140 mg per deciliter) one hour post-meal or 6.7 mmol/L (120 mg per deciliter) two hours post-meal despite adequate MNT.10
Insulin is the pharmacological standard of care for GDM requiring treatment and for all pre-existing diabetes in pregnancy. The physiological basis is the progressive insulin resistance of the second and third trimesters driven by placental hormones (human placental lactogen, cortisol, progesterone, prolactin), which increases insulin requirements by 50 to 200% over pre-pregnancy doses in T2DM patients. NPH (neutral protamine Hagedorn) insulin remains the most extensively studied intermediate-acting formulation in pregnancy; insulin detemir is the preferred long-acting analog based on the most robust pregnancy safety data. Among rapid-acting analogs, insulin aspart and insulin lispro have adequate pregnancy safety data and are preferred over regular insulin for post-prandial glucose control. Target glucose levels in pregnancy are tighter than non-pregnant targets: fasting plasma glucose below 5.3 mmol/L (95 mg per deciliter), one-hour post-meal below 7.8 mmol/L (140 mg per deciliter), and two-hour post-meal below 6.7 mmol/L (120 mg per deciliter).10
Metformin crosses the placenta and achieves fetal concentrations approximating maternal concentrations. While metformin has not been associated with structural teratogenicity in human observational studies, long-term follow-up data from the Metformin in Gestational Diabetes (MiG) study raised concerns about higher rates of large-for-gestational-age neonates and increased childhood adiposity in offspring of metformin-treated mothers compared with insulin.11 The Metformin in Women with Type 2 Diabetes in Pregnancy (MiTy) trial in T2DM in pregnancy found that adding metformin to insulin reduced maternal weight gain and large-for-gestational-age rates but was associated with a higher rate of small-for-gestational-age neonates, a concerning finding. Metformin is therefore used in pregnancy only when insulin cannot be used (patient refusal, access barriers) and is not a first-line pharmacological option per the American Diabetes Association (ADA) and American College of Obstetricians and Gynecologists (ACOG) guidance.1
Glucagon-like peptide-1 receptor (GLP-1R) agonists, sodium-glucose cotransporter 2 (SGLT-2) inhibitors, dipeptidyl peptidase-4 (DPP-4) inhibitors, and thiazolidinediones are all contraindicated or not recommended in pregnancy due to absent or inadequate human safety data. GLP-1R agonists produced fetal malformations and increased fetal mortality in rodent studies at exposures approximating clinical doses; semaglutide carries a label warning requiring discontinuation at least two months before planned conception. SGLT-2 inhibitors, by inducing glucosuria, theoretically alter the fetal urinary glucose environment, and animal studies showed fetal renal abnormalities. Because SGLT-2 inhibitor exposure during second and third trimester coincides with critical periods of fetal renal development, they are contraindicated in the second and third trimesters; FDA labeling advises discontinuation when pregnancy is recognized. Postpartum, T2DM management must be re-evaluated: GDM resolves in most patients after delivery (though 50% progress to T2DM within 10 years), breastfeeding-compatible agents are restricted (metformin is considered compatible; most other oral agents have insufficient data), and insulin requirements fall sharply within hours of placental delivery and require immediate dose reduction to avoid postpartum hypoglycemia.10
Any diabetes in pregnancy: start insulin immediately — do not delay for MNT trial if glucose targets are clearly not met. Stop all GLP-1R agonists, SGLT-2 inhibitors, DPP-4 inhibitors, and TZDs before or at the time pregnancy is recognized. Metformin: second-line if insulin access is impossible. Post-partum: reduce insulin dose by 50% at delivery; reassess GDM resolution at 4–12 weeks post-partum with a 75-gram OGTT; counsel on high lifetime T2DM risk.
The management of type 2 diabetes mellitus (T2DM) in older adults is characterized by a fundamental shift in therapeutic priorities: the prevention of hypoglycemia and the maintenance of functional independence take precedence over tight glycemic control in most patients above age 75 or those with frailty, cognitive impairment, or limited life expectancy. The harms of hypoglycemia in this population, including falls, fractures, cardiac arrhythmias, accelerated cognitive decline, and emergency hospitalizations, outweigh the benefits of strict glucose lowering that accrue only over many years.
Glycemic targets in elderly patients with T2DM are explicitly stratified by functional status and comorbidity burden in the American Diabetes Association (ADA) Standards of Care. For cognitively intact, functionally independent older adults with long life expectancy, targets approaching those for younger patients (hemoglobin A1c (HbA1c) below 7.0 to 7.5%) are reasonable if achieved safely. For patients with multiple comorbidities, moderate cognitive impairment, or moderate frailty, a less stringent target of HbA1c 7.5 to 8.0% is appropriate. For patients with end-stage organ disease, limited life expectancy, profound frailty, or dementia requiring institutional care, the focus shifts entirely to symptom management: avoiding hyperglycemic symptoms (polyuria, polydipsia, dehydration) without imposing treatment burden, typically targeting HbA1c below 8.5% or even 9.0% if strict control would require regimens that risk hypoglycemia or impair quality of life. HbA1c interpretation itself can be unreliable in elderly patients with anemia, renal disease, or transfusion history; fasting plasma glucose and two-hour postprandial glucose monitoring may provide more meaningful targets in this group.12
Hypoglycemia in elderly patients carries a disproportionate risk burden compared with younger patients. The counter-regulatory response to hypoglycemia is attenuated in older adults due to impaired glucagon secretion and diminished adrenergic response, and hypoglycemia unawareness is more prevalent, meaning that many elderly patients do not experience the early warning symptoms (tremor, sweating, palpitations) that prompt self-treatment before cognitive impairment supervenes. Falls during hypoglycemic episodes are a major source of hip fracture and subdural hematoma in the elderly diabetic population. Recurrent hypoglycemia accelerates cognitive decline and has been associated with dementia progression in longitudinal studies. These risks place sulfonylureas, particularly long-acting agents such as glibenclamide (glyburide) and glimepiride, and high-dose insulin at the top of the pharmacological risk hierarchy for elderly patients. The American Geriatrics Society Beers Criteria specifically identifies glibenclamide as a potentially inappropriate medication in adults over 65, due to the prolonged duration of action and risk of severe hypoglycemia.13
For pharmacological management, agents with low or no intrinsic hypoglycemia risk are preferred in elderly patients. Metformin remains acceptable in older adults with preserved renal function (eGFR ≥30 mL per minute per 1.73 m²), requires eGFR monitoring at least annually, and provides the benefit of no hypoglycemia risk, low cost, and weight neutrality. Dipeptidyl peptidase-4 (DPP-4) inhibitors are generally well-tolerated in the elderly: they are weight neutral, have minimal hypoglycemia risk as monotherapy, require only dose adjustment (not discontinuation) for renal impairment with most agents, and are available as once-daily oral formulations with low pill burden. Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are valuable in elderly patients with specific comorbid indications (heart failure, CKD, ASCVD) but require particular attention to volume depletion risk: the osmotic diuresis produced by glycosuria exacerbates the volume-sensitive state of many older patients who are already on loop diuretics or angiotensin-converting enzyme (ACE) inhibitors and have limited compensatory reserve, and orthostatic hypotension with fall risk is an important concern. Glucagon-like peptide-1 receptor (GLP-1R) agonists are effective in older adults but injection-based delivery and nausea side effects are more burdensome in cognitively impaired or frail patients; oral semaglutide offers an alternative delivery route but also carries nausea risk and requires careful administration instructions that may be difficult for patients with cognitive decline.12
Deprescribing, defined as the intentional supervised reduction or cessation of medications that are no longer benefiting the patient or where the harm-benefit balance has shifted, is a central geriatric clinical skill in diabetes management. Common deprescribing targets include: long-acting sulfonylureas causing recurrent hypoglycemia (substitute DPP-4 inhibitor or discontinue if HbA1c allows); high-dose insulin regimens in patients with declining food intake or weight loss (reduce basal insulin first, then eliminate premixed or prandial insulin); SGLT-2 inhibitors in patients with severe volume depletion, recurrent urinary tract infections, or eGFR that has fallen below the indication-specific floor; and GLP-1R agonists in patients with significant weight loss, anorexia, or dysphagia where further appetite suppression is harmful. Polypharmacy is the norm in elderly diabetic patients, and drug-drug interactions, particularly between sulfonylureas and azole antifungals, fluoroquinolones, trimethoprim, or fibrates, can precipitate severe hypoglycemia; medication reconciliation at every clinical encounter is essential.13
Step 1: Assess functional status, cognitive status, life expectancy, and comorbidity burden before setting any glycemic target. Step 2: Identify and eliminate sulfonylureas with prolonged action in frail or cognitively impaired patients. Step 3: Set a realistic HbA1c target (7.5–8.5% for most older adults with comorbidities). Step 4: Prefer DPP-4 inhibitors or GLP-1R agonists over sulfonylureas; add SGLT-2 inhibitor only if clear comorbid indication and volume status is safe. Step 5: Review all medications for hypoglycemia-potentiating interactions at each visit. Step 6: Initiate deprescribing when functional goals shift or life expectancy shortens.
American Diabetes Association Professional Practice Committee. Standards of Care in Diabetes — 2024. Diabetes Care. 2024;47(Suppl 1):S1–S321.
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doi:10.1056/NEJMoa1307684Margulies KB, Hernandez AF, Redfield MM, et al. Effects of liraglutide on clinical stability among patients with advanced heart failure and reduced ejection fraction (FIGHT). JAMA. 2016;316(5):500–508.
doi:10.1001/jama.2016.10260American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol. 2018;131(2):e49–e64.
doi:10.1097/AOG.0000000000002501Rowan JA, Hague WM, Gao W, Battin MR, Moore MP; MiG Trial Investigators. Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med. 2008;358(19):2003–2015.
doi:10.1056/NEJMoa0707193American Diabetes Association Professional Practice Committee. Older Adults: Standards of Care in Diabetes — 2024. Diabetes Care. 2024;47(Suppl 1):S244–S257.
doi:10.2337/dc24-S013American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2023;71(7):2052–2081.
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