Effect of glycemic control on progression of left ventricular hypertrophy and diastolic dysfunction in patients with type 2 diabetes mellitus

AIM To investigate the effect of glycemic control on the progress of left ventricular hypertrophy and diastolic dysfunction in patients with type 2 diabetes mellitus (T2DM). METHODS A total of 40 T2DM patients (observation group) and 40 age-matched healthy controls (control group) were recruited. Patients in the observation group received standard treatment for glycemic control (including diabetes education, self-blood glucose monitoring and daily exercise). All patients were followed-up after 24 months and were evaluated by echocardiography to compare the left ventricular structural and functional parameters. At the end of our study, patients in the observation group were stratified into three subgroups according to glycemic level: well-controlled group (HbA1c<7.6%, n=17), mildy controlled group (7.6%≤HbA1c≤ 9%, n=14), and poorly controlled group (HbA1c>9%, n=9) respectively. Echocardiographic parameters were compared among the three groups before and after follow-up. RESULTS IVSd, LVPW, LVEDd and cardiac systolic function were similar between groups. IVRT was elevated but E/A decreased in the observation group compared with those in the control group at baseline (P<0.05). No significant differences were found in the echocardiographic parameters of left ventricular structure and function in well-controlled patients. The mildly controlled group and poorly controlled group demonstrated increased IVSd, LVPWd and LVMI, and exacerbated left ventricular diastolic function with prolonged IVRT and decreased E/A. In addition, patients receiving metformin therapy demonstrated a significant reduction in IVRT and E/A compared with patients receiving insulin therapy. CONCLUSION ST2DM patients tend to develop left ventricular diastolic dysfunction. Improved glycemic control can delay the progress of LVH, but cannot ameliorate the decreased diastolic dysfunction. Poor glycemic control can accelerate left ventricular remodeling and exacerbate diastolic dysfunction in patients with T2DM.