Differential changes of left ventricular myocardial deformation in diabetic patients with controlled and uncontrolled blood glucose: A three-dimensional speckle-tracking echocardiography-based study

摘要

Background: Preclinical left ventricular (LV) systolic dysfunction has been documented in patients with diabetes mellitus (DM) with preserved LV ejection fractions (LVEFs). The aims of this study were to investigate whether there is any difference in myocardial deformation between patients with DM with controlled (defined as glycosylated hemoglobin [HbA1c] 7%) and uncontrolled (HbA1c ≥ 7%) blood glucose using three-dimensional speckle-tracking echocardiography and to explore whether the level of HbA 1c is associated with preclinical LV systolic dysfunction. Methods: Thirty-one patients with DM with controlled blood glucose, 37 patients with DM with uncontrolled blood glucose, and 63 matched controls were studied. All subjects had normal LVEFs (≥55%). Global longitudinal strain (GLS), global circumferential strain, global area strain, and global radial strain were assessed using three-dimensional speckle-tracking echocardiography. Results: Despite similar LVEFs, patients with uncontrolled DM had decreased peak systolic strain in all directions compared with the other two groups, as evidenced by GLS, global circumferential strain, global area strain, and global radial strain (all P values .001). However, the difference between patients with controlled DM and controls was observed only for GLS (P =.038). By multivariate liner regression analysis, the level of HbA1c was independently associated with the values of GLS (β = -0.274, P =.024), global circumferential strain (β = -0.245, P =.042), and global area strain (β = -0.272, P =.024). Conclusions: GLS may be a sensitive indicator of early LV systolic dysfunction in patients with DM despite normal LVEF. Poor blood glucose control, as defined by HbA1c ≥ 7%, leads to reductions of LV systolic strain in all directions that are independently associated with preclinical LV dysfunction.