Table 2.
Study | N | FU (yrs) | bCVD(%) | Comparators | GLP-1RA | CV Composite Endpoint * | MACE | CV Death | All-Cause Death | Stroke | ACS/MI | PAD | HF |
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
§ Patorno, et al., 2021 | 45,047 | 0.5 | 45.2 | SGLT-2i (76.9%Cana, 13.1%Dapa, 11.1%Empa) | 58.7% Lira, 23.5% Exe, 14.8% Dula, 3.0% Albi | - | 0.98 (0.87–1.10) | 0.83 (0.64–1.07) | 0.95 (0.81–1.11) | 1.04 (0.86–1.27) | 0.98 (0.84–1.16) | - | 0.68 (0.57–0.80) |
§ DeRemer, et al., 2021 | 4829 vs. 7082 | n.a. | Subgroup 1: 0 Subgroup 2: 100 |
SGLT-2i (Empa, Cana) | Exe, Lira, Albi, Dula | Subgroup 1: 1.06 (0.72–1.49) Subgroup 2: 0.67 (0.47–0.96) | - | - | - | Subgroup 1: 1.08 (0.67–1.75) Subgroup 2: 0.85 (0.50–1.70) | Subgroup 1: 1.35 (0.67–2.71) Subgroup 2: 1.14 (0.58–2.15) |
- | Subgroup 1: 0.87 (0.47–1.61) Subgroup 2: 0.46 (0.27–0.79) |
# Nørgaard, et al., 2021 | 8913 vs. 5275 | n.a. | n.a. | SGLT-2i | - | - | 5.6% (5.2–6.1) vs. 5.6% (4.8–6.3) | - | - | 2.5% (2.2–2.9) 2.6% (2.2–3.1) | 2.1% (1.8–2.4) vs. 2.1% (1.8–2.4) |
- | 1.7% (1.5–2.0) vs. 1.8% (1.2–2.5) |
§ Patorno, et al., 2021 | Cohort 1: 133,139 Cohort 2: 52,901 |
0.6 | Cohort 1: 0 Cohort 2: 100 |
SGLT-2i (Cana, Dapa, Empa) | Albi, Dula, Exe, Lira | Cohort 1: 1.07 (0.97–1.18) Cohort 2: 0.90 (0.82–0.98) |
- | - | Cohort 1: 1.01 (0.87–1.17) Cohort 2: 0.88 (0.79–0.99) | Cohort 1: 0.96 (0.82–1.13) Cohort 2: 1.00 (0.87–1.15) |
Cohort 1: 1.13 (1.00–1.28) Cohort 2: 0.83 (0.74–0.93) |
- | Cohort 1: 0.69 (0.56–0.85) Cohort 2: 0.71 (0.64–0.79) |
§ Thomsen, et al., 2021 | 12,706 vs. 14,498 | 1.1 | 30 | SGLT-2i (Empa) | Lira | 1.02 (0.91–1.14) | - | - | 0.93 (0.89–0.98) | - | - | - | 0.77 (0.49–1.20) |
§ Lugner, et al., 2021 | 9648 vs. 12,097 | 1.7–1.1 | 15.8–17.0 | SGLT-2i (56.6%Empa, 43.2% Dapa, 0.2% Cana) | 75.1% Lira, 16.3% Dula, 6.4% ExeQW | - | 1.03 (0.89–1.21) | 1.00 (0.47–2.13) | 0.78 (0.61–1.01) | 1.44 (0.99–2.08) | 0.94 (0.68–1.3) | 1.68 (1.04–2.72) | 0.83 (0.65–1.07) |
§ Longato, et al., 2020 | 8596 | 1.08 | 18 | SGLT-2i (50% Empa, 40% Dapa, 10% Cana) | 48% Dula, 34% Lira, 14% Exe, 4% Lixi | - | 0.78 (0.61–0.99) | - | 0.74 (0.43–1.29) | 0.91 (0.56–1.48) | 0.72 (0.53–0.98) | - | 0.59 (0.35–0.99) |
§ Pineda, et al., 2020 | 947 | 1 | 12.8–12.0 | SGLT-2i | - | 1.00 (0.69–1.44) | - | - | - | 0.87 (0.38–1.97) | 1.12 (0.34–3.68) | - | 0.83 (0.53–1.30) |
N, number of pairs or number of patients treated with GLP-1RA vs. comparators; FU, follow-up; bCVD, baseline cardiovascular disease (in GLP-1RA vs. comparator cohorts); CV, cardiovascular; MACE, major adverse cardiovascular events; ACS, acute coronary syndrome; MI, myocardial infarction; PAD, peripheral arterial disease; HHF, hospitalization for heart failure; MET, metformin, SU, sulphonylureas; TZD, thiazolidinediones; DPP-4i, dipeptidyl peptidase-4 inhibitors; SGLT-2i, sodium-glucose transporter-2 inhibitors; Cana, canagliflozin; Dapa, dapagliflozin; Empa, empagliflozin; GLP-1RA, glucagon-like peptide-1 receptor agonists; Exe, exenatide; Lira, liraglutide; Lixi, lixisenatide; Dula, dulaglutide; Albi, albiglutide; BID, bis in die; QW, once weekly; GLD, glucose lowering drugs; n.a., not available. GLP-1RA vs. SGLT2i statistically significant results are in bold; SGLT-2i vs. GLP-1RA statistically significant results are underscored (p < 0.05). Follow-up is reported as mean or median. * The CV composite endpoint varied between studies. Pineda et al.: MI, stroke, unstable angina, or coronary revascularization; DeRemer et al.: stroke, MI, or HF; Patorno et al., 2021: hospitalization for ischemic or hemorrhagic stroke or MI; Thomsen et al.: stroke, MI, unstable angina, coronary revascularization, HHF, or all-cause death. § Results are presented as SGLT-2i vs. GLP-1RA as in the source manuscript. # Results are expressed as % of risk (95% CI) in GLP-1RA vs. SGLT-2i users as in the source manuscript.