Association between glycemic control and morning blood pressure surge with vascular endothelial dysfunction in type 2 diabetic patients

Abstract

OBJECTIVE Morning blood pressure surge (MBPS) is an independent predictor of cardiovascular events. However, little is known about the association between glycemic control and MBPS, and its effect on vascular injury in patients with type 2 diabetes mellitus (T2DM). The current study examined the association between glycemic control and MBPS, and the involvement of MBPS in the development of vascular dysfunction in T2DM patients. RESEARCH DESIGN AND METHODS Weexamined MBPS in T2DMpatients (25male patients/25 female patients;mean age, 60.1 6 13.2 years; n = 50) using 24-h ambulatory blood pressure monitoring, and assessed vascular function by brachial artery flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD). RESULTS HbA1c (r = 0.373, P = 0.009) and triglyceride (TG) (r = 0.375, P = 0.009) levels correlated significantly and positively with MBPS. In multiple regression analysis, including TG and HbA1c levels in addition to age and 24-h systolic blood pressure (SBP) as independent variables, HbA1c (b = 0.328, P = 0.016) and TG (b = 0.358, P = 0.014) were associated significantly in a positive manner with MBPS. In a noninsulin user,when homeostasismodel assessment ratio (HOMA-R) was included in place of TG, HOMA-R emerged as a significant factor.MBPS (r =20.289, P = 0.043) and HbA1c (r = 20.301, P = 0.035) correlated significantly and negatively with FMD, whereas 24-h SBP correlated with both FMD (r = 20.359, P = 0.012) and NMD (r = 20.478, P = 0.004). In multiple regression analysis, including age, gender, 24-h SBP, MBPS, LDL cholesterol, and HbA1c, MBPS (b = 20.284, P = 0.044) alone associated significantly in a negative manner with FMD, but not with NMD. CONCLUSIONS The current study demonstrated that poor glycemic control and insulin resistance are independently associated with the occurrence of MBPS in T2DM patients, which might be significantly associated with endothelial dysfunction. © 2014 by the American Diabetes Association.