Optimal Management of Glucose in Patients with Diabetes and Heart Failure

Abstract

Type 2 diabetes confers a two-fold excess risk of heart failure. Established risk factors for developing heart failure in people with type 2 diabetes include old age, obesity, poor glycemic control, impaired kidney function and pre-existing coronary heart disease. Prognosis of people with comorbid type 2 diabetes and heart failure is poor with up to one quarter of them dying at 1 year and half not surviving at 5 years. Glucose-lowering drugs have divergent effects on the progression of heart failure. Thiazolidinediones and dipeptidyl-peptidase 4 inhibitors may induce or worsen symptoms of heart failure, although these risks do not appear to extend to other incretin-based therapy, namely glucagon-like peptide-1 receptor agonists, whereas metformin has been shown to improve prognosis in people with comorbid type 2 diabetes and heart failure in observational studies. Recent cardiovascular outcome trials provided robust evidence for sodium-glucose co-transporter-2 (SGLT-2) inhibitors in preventing death and/or hospitalization for heart failure. Current guideline recommends initiation of SGLT-2 inhibitors in people with type 2 diabetes and heart failure, independent of the need of additional glucose lowering. However, consideration must be given to risks of hypoglycemia, dehydration and euglycemic ketoacidosis upon initiation of SGLT-2 inhibitors, as the majority of people in the treatment group are old, have kidney dysfunction, on diuretics, or have long diabetes duration with high likelihood of insulin deficiency. Type 2 diabetes confers a two-fold excess risk of heart failure. Established risk factors for developing heart failure in people with type 2 diabetes include old age, obesity, poor glycemic control, impaired kidney function and pre-existing coronary heart disease. Prognosis of people with comorbid type 2 diabetes and heart failure is poor with up to one quarter of them dying at 1 year and half not surviving at 5 years. Glucose-lowering drugs have divergent effects on the progression of heart failure. Thiazolidinediones and dipeptidyl-peptidase 4 inhibitors may induce or worsen symptoms of heart failure, although these risks do not appear to extend to other incretin-based therapy, namely glucagon-like peptide-1 receptor agonists, whereas metformin has been shown to improve prognosis in people with comorbid type 2 diabetes and heart failure in observational studies. Recent cardiovascular outcome trials provided robust evidence for sodium-glucose co-transporter-2 (SGLT-2) inhibitors in preventing death and/or hospitalization for heart failure. Current guideline recommends initiation of SGLT-2 inhibitors in people with type 2 diabetes and heart failure, independent of the need of additional glucose lowering. However, consideration must be given to risks of hypoglycemia, dehydration and euglycemic ketoacidosis upon initiation of SGLT-2 inhibitors, as the majority of people in the treatment group are old, have kidney dysfunction, on diuretics, or have long diabetes duration with high likelihood of insulin deficiency.