Table 2 Clinical studies on the effects of the therapy with SGLT-2i on left ventricular function and structure in patients with T2D

Systolic parameters

[44]

Retr, vs. aCTR

SGLT-2i, 6–24 m

LVEF (%), US

HFp/rEF, SGLT-2i, 74

36.1 (26–48)

+ 8.9 (24%)

< 0.0001

HFrEF, 45

NA

+ 8.8 (NA)

0.022

HFmr/pEF, 29

NA

0

ns

HFp/rEF, NoSGLT-2i, 76

38.8 (28–55)

+ 5.0 (12%)

0.014

NoHF, SGLT-2i, 78

59.4 (49–64)

+ 2.6 (4%)

< 0.001

NoHF, NoSGLT-2i, 76

60.4 (52–64)

0

ns

[42]

Retr, vs. DPP4i

SGLT-2i, 2 yrs

CAD, SGLT-2i, 41

46.2 ± 13.5

+ 2.4 (4%)

ns

HFrEF, 13

29.0 ± 6.2

+ 9.6 (33%)

0.03

HFmrEF, 7

45.7 ± 3.2

+ 4.3 (9%)

ns

HFpEF, 21

57.0 ± 4.6

− 1.9 (3%)

ns

CAD, DDP4i, 40

56.7 ± 16.1

 + 0.4

[59]

Prosp, vs. aCTR

TOFO 20 mg, 6 m

Outp, SGLT-2i, 21

55 ± 14

+ 5.0 (9%)

0.006

Outp, NoSGLT-2i, 21

57 ± 18

− 0.6

ns

[60]

Prosp, single arm

CANA 100 mg, 12 m

HFpEF, 35

60.9 ± 1.6

+ 3.7 (6%)

0.023

[61]

1 centre, EMPA-REG

EMPA 10 mg, 3 m

CVD, 10

63 ± 8.0

+ 3.0 (5%)

ns

[62]

Prosp, single arm

CANA 100/300, 3 m

± CVD, 37

65.7 ± 5.0

− 0.4 (1%)

ns

[41]

Prosp, single arm

DAPA 5 mg, 6 m

HFpEF, 53

62.3 (49–68)

+ 1.3 (2%)

0.011

[46]

1 centre, EMPA-REG

EMPA 10 mg, 6 m

LVEF (%), CMRI

CVD, SGLT-2i, 44

58.0 ± 7.5

+ 0.7 (1%)

ns

CVD, NoSGLT-2i, 46

55.5 ± 8.7

+ 1.0 (2%)

ns

[47]

Prosp, R, vs. aCTR

EMPA 10 mg, 6 m

Outp, SGLT-2i, 20

63.4 ± 1.7

+ 0.2

ns

Outp., NoSGLT-2i, 8

62.7 ± 2.1

 + 4.2 (7%)

ns

[44]

Retr, vs. aCTR

HF, SGLT-2i, 74

GLS (%)

HFp/rEF, SGLT-2i, 74

− 10.3 (7.3–12.5)

− 1.1 (11%)

0.0001

HFrEF, 45

NA

− 1.7 (NA)

< 0.001

HFmr/pEF, 29

NA

− 0.3 (NA)

ns

HFp/rEF, NoSGLT-2i, 76

− 10.9 (8.4–12.3)

− 0.2 (2%)

ns*

NoHF, SGLT-2i, 78

− 14.6 (12.1–17.0)

− 0.6 (4%)

0.012

NoHF, NoSGLT-2i, 76

− 15.2 (12.5–16.9)

0

ns

[41]

Prosp, single arm

DAPA 5 mg, 6 m

HFpEF, 53

15.4 ± 3.4

− 1.4 (9%)

< 0.001

Diastolic parameters

[10]

[44]

Retr, vs. aCTR

SGLT-2i, 6–24 m

E/e′, US/TD

HF, SGLT-2i, 74

15.6 (11.9–24.3)

− 2.2 (14%)

< 0.001

HFrEF, 45

NA

− 4.0 (NA)

0.034

HFmr/pEF, 29

NA

− 1.5 (NA)

ns

HF, NoSGLT-2i, 76

13.2 (9.8–17.8)

0.0

ns

NoHF, SGLT-2i, 78

10.6 (9.0–13.5)

0.0

ns

NoHF, NoSGLT-2i, 76

10.8 (8.9–14.0)

0.0

0.03

[43]

Prosp, single arm

DAPA 5 mg, 6 m

HFpEF, 58

9.3

− 0.8 (9%)

0.02

[42]

Retr, vs. DPP4is

SGLT-2i, 2 yrs

CAD, SGLT-2i, 38

11.4 ± 4.8

− 0.6 (5%)

ns

CAD, DDP4i, 21

12.9 ± 5.4

− 2.3 (18%)

ns

[41]

Prosp, single arm

DAPA 5 mg, 6 m

HFpEF, 53

9.3 (7.7–11.8)

− 0.8 (9%)

0.020

[59]

Prosp, vs. aCTR

TOFO 20 mg, 6 m

Outp, SGLT-2i, 21

13.0 ± 4.8

− 2.4 (18%)

0.024

Outp, NoSGLT-2i, 21

13.9 ± 4.6

+ 0.8 (5%)

ns

[60]

Prosp, single arm

CANA 100 mg, 12 m

HFpEF, 35

16

− 6.0 (38%)

< 0.001

[62]

Prosp, single arm

CANA 100/300, 3 m

 ± CVD, 37

13.7 ± 3.5

− 1.6 (12%)

0.001

[61]

1 centre, EMPA-REG

EMPA 10 mg, 3 m

lateral e′, TD

CVD, 10

8.5 ± 1.6

+ 1.1 (13%)

0.002

Left ventricular remodeling

[44]

Retr, vs. aCTR

SGLT-2i, 6–24 m

LVMi (g/m²), US

HFp/rEF, 74

126.3

− 11.1 (9%)

0.026

LVEDD (mm), US

57.4

− 4.4 (8%)

< 0.01

LVMi (g/m²), US

NoHF, 78

96.6

0.0

ns

LVEDD (mm), US

49

− 2.0 (4%)

0.036

[43]

Prosp, single arm

DAPA 5 mg, 6 m

LVMi (g/m²), US

HFpEF, 58

75.0

− 8.0 (11%)

< 0.001

LVEDV (mL), US

74.2 (55.1–74.1)

− 5.7 (8%)

ns

[60]

Prosp, single arm

CANA 100 mg, 12 m

LVMi (g/m²), US

HFpEF, 35

166.5

− 25.9 (16%)

< 0.001

LVEDD (mm), US

47.1

− 0.8 (2%)

ns

[61]

Prosp, R, vs. Pl

EMPA 10 mg, 3 m

LVMi (g/m²), US

CVD, 10

88

13 (15%)

0.01

LVEDD (mm), US

47

− 1 (2%)

ns

[47]

Prosp, R, vs. aCTR

EMPA 10 mg, 6 m

LVM (g), CMRI

CVD, 17

93.1 ± 4.8

0

ns

LVEDV (ml), CMRI

155

− 10 (6%)

< 0.01

[46]

1 centre, EMPA-REG

EMPA 10 mg, 6 m

LVMi, (g/m²), CMRI

T2D, 44

59.3 ± 10.9

− 2.6 (4%)

< 0.01

LVEDV (mL), CMRI

124 ± 33

− 2.9 (2%)

ns