TABLE 1.
Clinical application of hypoglycemic drugs in patients with HF and T2DM.
| Drug | Clinical application | References | |||||
|---|---|---|---|---|---|---|---|
| Clinic types of experiments | Patients | Number of examinees (n) | Drug usage and dosage | Usage time | Main results and conclusion | ||
| Metformin | Prospective study | HF patients with DM (mean age is 71.7 ± 7.8 years) | n = 1,519; metformin therapy group (n = 592) | / | / | Metformin therapy is associated with reduced mortality of HF patients with new-onset DM, mainly due to decreased cardiovascular mortality, and with a lower hospitalization rate. | Romero et al. (2013) |
| A randomized, double-blind, placebo-controlled, crossover study | Treatment naive diabetic patients with chronic HF | n = 45 | p.o., 2 g/day | 3 months | Compared to placebo, metformin significantly reduced HbA1c and improved insulin sensibility. It confirms that metformin improves blood glucose control in patients with T2DM and chronic HF. | Stolarikova et al. (2018) | |
| A multicenter prospective study | Propensity score–matched patients with stable angina | n = 258 | / | 6 months | The patients with pre-DM had a higher percentage of endothelial LAD dysfunction as compared to patients with pre-DM treated with metformin. At the 24th month of follow-up, in pre-DM metformin patients, MACE was lower than that of pre-DM patients. | Sardu et al. (2019) | |
| A retrospective observational study | Patients with left ventricular hypertrophy (LVH) | n = 212 | / | / | There is significant reduction in the incidence of HF in the metformin group compared to the non-metformin group (risk reduction 54%). And the metformin group did not develop any symptoms of HF. Metformin may delay the progression of early stages of HF to the advanced stage. | David and Droogan (2013) | |
| Sitagliptin | A population-based study | Patients with diabetes (age ≥45 years) | n = 8,288 | / | / | There were 935 events of hospitalization for HF (HHF), in which the association between the number of HHF events and the adherence to sitagliptin was linear. The use of sitagliptin was associated with a higher risk of HHF, but no excessive risk for mortality was observed. | Wang et al. (2014) |
| A population-based, retrospective cohort study | Patients with diabetes and incident HF | n = 7,620; sitagliptin therapy group (n = 887) | / | / | Sitagliptin use was not associated with an increased risk of all-cause hospitalizations or death but was associated with an increased risk of HF-related hospitalizations among patients with T2DM with pre-existing HF. | Weir et al. (2014) | |
| A randomized controlled clinical trial | Patients with T2DM and HF | n = 36; experimental group (n = 18), control group (n = 18) | p.o., 100 mg/day | 24 weeks | The blood glucose indicators FPG, 2hPG, HbAlc, and BMI in the experimental group were significantly lower than those in the control group. LVEF was higher than that in the control group, and the cardiac function and blood glucose were both improved. | Jin et al. (2014) | |
| Exenatide | A double-blind, randomized controlled clinical trial | Patients with T2DM with congestive HF (CHF) | n = 20 | i.v.gtt., 0.12 pmol/kg/min | 6 h | Exenatide has rapid hemodynamic effects in male patients with type 2 diabetic CHF. Infusion of exenatide to patients will increase the cardiac index (CIP) due to time. | Nathanson et al. (2012) |
| A randomized controlled trial | Patients with T2DM with HF | n = 2,389; exenatide therapy group (n = 1,161), placebo group (n = 1,228) | 2 mg, once a week | / | The reduction in all-cause death or HHF was seen with exenatide in patients. And HHF was reduced in the exenatide group versus placebo. | Fudim et al. (2019) | |
| A randomized, double-blind, placebo-controlled, crossover study | Patients with ST-segment elevation myocardial infarction | n = 334; exenatide therapy group (n = 175), placebo group (n = 159) | / | / | Admission for HF was lower in the exenatide group (11%) compared to the placebo group (20%). All-cause mortality occurred in 14% in the exenatide group versus 9% in the placebo group. | Kyhl et al. (2016) | |
| Liraglutide | A single-center, open-label, randomized, parallel-group, pilot study | T2DM patients with history of post-ischemic chronic HF | n = 32; liraglutide therapy group (n = 10), sitagliptin therapy group (n = 10), insulin glargine therapy group (n = 12) | i.h., establish tolerance to 1.8 mg/day | 52 weeks | Only in liraglutide-treated patients, left ventricular end-systolic volume index (LVESVI) reduced and cardiac output and cardiac index increased significantly. | Arturi et al. (2017) |
| A randomized, double-blinded, placebo-controlled multicenter trial | Patients with reduced LVEF ≤45% | n = 241; liraglutide therapy group (n = 122), placebo group (n = 119) | i.h., establish tolerance to 1.8 mg/day | 24 weeks | Liraglutide did not affect left ventricular systolic function compared with placebo in stable chronic HF patients with and without diabetes. And liraglutide was associated with an increase in heart rate and more serious cardiac adverse events. | Jorsal et al. (2017) | |
| A multicenter, double-blind, randomized, placebo-controlled clinical trial | Stable chronic HF patients with and without DM | n = 541 | i.h., establish tolerance to 1.8 mg/day | / | In LIVE, liraglutide significantly decreased hemoglobin A1c and increased heart rate and serious cardiac adverse events. | Liang and Gu (2020) | |
“/” means unclear; “q.d.” means once a day; “b.i.d.” means twice a day; “t.i.d.” means three times a day; “p.o.” means oral administration; “i.m.” means intramuscular injection; “i.v.” means intravenous injection; “i.v.gtt.” means intravenous infusion; “i.h.” means hypodermic injection.