Effect of SGLT2 inhibitor therapy on left ventricular longitudinal and circumferential strain in patients with type 2 diabetes mellitus and normal left ventricular ejection fraction

Background Type 2 diabetes mellitus (T2DM) is a major cardiovascular risk factor associated with coronary artery disease (CAD), heart failure, and hypertension. Subtle structural and functional changes may precede the onset of left ventricular (LV) dysfunction in T2DM. Early detection of LV dysfunction is important for early interventions and prevention of heart failure. In T2DM patients 2D speckle tracking echocardiography (2DSTE) detects LV dysfunction by measuring LV strain. The duration of T2DM and level of glycemic control has effect on progression of LV dysfunction. Most of hypoglycemic drugs lower the plasma glucose level with no effect on LV dysfunction. Sodium-Glucose Cotransporter 2 inhibitors (SGLT2i) have shown benefits in reducing cardiovascular death in addition to lowering plasma glucose levels. Purpose We aimed to study the effect of SGLT2 inhibitors on LV strain as compared to other oral hypoglycemic agents and insulin in asymptomatic T2DM patients with normal ejection fraction. Methods Conventional echocardiography, diastolic parameters along with LV strain were measured in 121 asymptomatic diabetics (age- 53.68±11.40 years, mean HBA1c 8.22 ± 2.08 g%). The LV strain in patients on SGLT2 inhibitors was compared with patients on other hypoglycemic agents [(SGLT2 group: Mean duration of treatment-14.13±3.98 years; Mean HbA1c-7.95±2.26; Non SGLT2 group: Mean duration of treatment-13.26±4.27 years; Mean HbA1c-8.22±2.08); P value-0.33]. Similarly LV strain in patients on SGLT2 inhibitors was compared with patients on insulin [(SGLT2 group: Mean duration of treatment-14.13±3.98 years; Mean HbA1c-7.95±2.26; Insulin group: Mean duration of treatment-15.48 ± 4.65 years; Mean HbA1c-7.65 ± 3.52); P value-0.478]. Results Longitudinal strain (LS) was significantly lower in diabetic patients on other hypoglycemic agents as compared with those on SGLT2 inhibitors [-14.34 ± 3.71 vs -15.57±2.95 (P value- 0.04) {Table 1 and Figure 1}]. Longitudinal strain (LS) [-12.96 ± 3.79 vs -14.99 ± 3.79 (P value < 0.01)] and Circumferential strain [-17.25 ± 5.94 vs -20.56 ± 5.93 (P value < 0.006)] was significantly lower in diabetic patients on insulin as compared with those on SGLT2 inhibitors {Table 2 and Figure 2}. No difference was noted in GCS in asymptomatic T2DM patients on SGLT2 inhibitors and other hypoglycemic agents [-19.63 ± 5.36 vs -21.81 ± 6.20 (P value-0.05)]. Conclusion T2DM patients treated with SGLT2 inhibitors were found to be associated with normal LV longitudinal myocardial function. Thus SGLT2 inhibitors helps attenuating subclinical LV systolic dysfunction in patients with asymptomatic T2DM as compared to other hypoglycemic agents. 2D speckle tracking echocardiography guided management and use of SGLT2 inhibitors may thus lead to improved outcome in T2DM patients. Further studies on larger populations and with follow-up are warranted to confirm findings in our study.