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2022 Canadian Cardiovascular Society Guideline for Use of GLP-1 Receptor Agonists and SGLT2 Inhibitors for
G B John Mancini1, Eileen O'Meara2, Shelley Zieroth3
1Division of Cardiology, Centre for Cardiovascular Innovation, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Abstract:
This guideline synthesizes clinical trial data supporting the role of glucagon-like peptide-1 receptor agonists and sodium-glucose co-transporter 2 inhibitors (SGLT2i) for treatment of heart failure (HF), chronic kidney disease, and for optimizing prevention of cardiorenal morbidity and mortality in patients with type 2 diabetes. It is on the basis of a companion systematic review and meta-analysis guided by a focused set of population, intervention, control, and outcomes (PICO) questions that address priority cardiorenal end points. The Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system and a modified Delphi process were used. We encourage comprehensive assessment of cardiovascular (CV) patients with routine measurement of estimated glomerular filtration rate, urinary albumin-creatinine ratio, glycosylated hemoglobin (A1c), and documentation of left ventricular ejection fraction (LVEF) when evaluating symptoms of HF. For patients with HF, we recommend integration of SGLT2i with other guideline-directed pharmacotherapy for the reduction of hospitalization for HF when LVEF is > 40% and for the reduction of all-cause and CV mortality, hospitalization for HF, and renal protection when LVEF is ≤ 40%. In patients with albuminuric chronic kidney disease, we recommend integration of SGLT2i with other guideline-directed pharmacotherapy to reduce all-cause and CV mortality, nonfatal myocardial infarction, and hospitalization for HF. We provide recommendations and algorithms for the selection of glucagon-like peptide-1 receptor agonists and SGLT2i for patients with type 2 diabetes and either established atherosclerotic CV disease or risk factors for atherosclerotic CV disease to reduce all-cause and CV mortality, nonfatal stroke, and for the prevention of hospitalization for HF and decline in renal function. We offer practical advice for safe use of these diabetes-associated agents with profound cardiorenal benefits.
Insights
Glucagon-like peptide-1 receptor agonists and sodium-glucose co-transporter 2 inhibitors (SGLT2i) significantly reduce cardiorenal morbidity and mortality in type 2 diabetes patients with heart failure or chronic kidney disease.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Type 2 diabetes is associated with significant cardiorenal morbidity and mortality.
- Effective management strategies are crucial for preventing adverse cardiovascular and renal outcomes.
Purpose of the Study:
- To synthesize clinical trial data on glucagon-like peptide-1 receptor agonists and SGLT2 inhibitors for cardiorenal protection.
- To provide evidence-based recommendations for managing heart failure, chronic kidney disease, and type 2 diabetes.
Main Methods:
- Systematic review and meta-analysis guided by PICO questions.
- Utilized the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system and a modified Delphi process.
- Focused on priority cardiorenal endpoints.
Main Results:
- Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are recommended for heart failure patients (LVEF > 40% and ≤ 40%) to reduce hospitalizations and mortality.
- SGLT2i integration is recommended for albuminuric chronic kidney disease to reduce mortality, myocardial infarction, and HF hospitalizations.
- Recommendations and algorithms provided for selecting GLP-1 RAs and SGLT2i in type 2 diabetes patients with established or at-risk atherosclerotic cardiovascular disease.
Conclusions:
- GLP-1 RAs and SGLT2i offer profound cardiorenal benefits in patients with type 2 diabetes.
- Comprehensive assessment including eGFR, UACR, A1c, and LVEF is encouraged for cardiovascular patients.
- Practical advice is offered for the safe and effective use of these agents.
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