This 2019 update to the American Diabetes Association/European Association for the Study of Diabetes consensus report on managing hyperglycaemia in type 2 diabetes should be read alongside the original 2018 report (Davies et al, 2018). It incorporates new data from a number of large studies on dulaglutide, dapagliflozin and metformin/vildagliptin.
The update includes three key changes. First, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) or sodium–glucose cotransporter-2 (SGLT2) inhibitors with proven cardiovascular benefit are recommended in appropriate patients to reduce the risk of major adverse cardiovascular events (MACE), chronic kidney disease (CKD) progression or hospitalisation for heart failure, irrespective of whether HbA1c is at target levels for the individual. Secondly, GLP-1 RAs should be used in preference to SGLT2 inhibitors if atherosclerotic cardiovascular disease (ASCVD) predominates, and should be considered also in those with risk factors for, but not established, ASCVD. Thirdly, SGLT2 inhibitors are recommended preferentially in those with or without ASCVD who have heart failure (particularly with reduced ejection fraction, <45%), and in those with CKD (estimated glomerular filtration rate [eGFR] 30–60 mL/min/1.73 m2, or albuminuria).
For people with type 2 diabetes and established ASCVD, in whom MACE is the most serious threat, GLP-1 RAs with cardiovascular benefit (dulaglutide, liraglutide and semaglutide) are now the drugs of choice. This drug class should also be considered in those with type 2 diabetes at high risk of CVD (defined as age ≥55 years with >50% stenosis of the coronary, carotid or peripheral arteries, left ventricular hypertrophy, eGFR <60 mL/min/1.73 m2 or albuminuria).
As we review glycaemic control in people with type 2 diabetes who have established CVD, high CVD risk, CKD or heart failure, we can opportunistically offer drugs with proven benefits in reducing cardiovascular events and CKD and heart failure progression. We can also take a proactive approach and search for each group and ensure we optimise treatment. We need to interpret the evidence carefully and individualise drug choice depending on the predominant comorbidity.
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