BLOOD PRESSURE VARIABILITY AND TARGET ORGAN DAMAGE INDICES IN PATIENTS WITH TYPE 2 DIABETES MELLITUS

Objective: Blood pressure (BP) variability (BPV) has been identified as an independent predictor of cardiovascular risk and morbidity. Scarce information regarding the BPV in patients with diabetes mellitus (DM) exists, especially on short-term average real variability (ARV). In our study, we compared ARV indices and surrogate target organ damage markers in patients with Type 2 DM (T2DM) and in control individual. Design and method: In this cross sectional study, we identified individuals with T2DM and adequate controls. Patients were matched to controls on a 1:1 ratio using propensity score matching. Matching was based on age, gender, BMI, previous diagnosis of hypertension and office Systolic and Diastolic BP values. Office BP values were measured and Ambulatory BP Monitoring was performed, and central BP and Pulse Wave Velocity were calculated with validated devices. The BPV parameters of ARV and weighted Standard deviation (wSD) were calculated using standardized formulas based on the ABPM data. Results: A total of 190 individuals (95 with DM and 95 controls) were studied (mean age was 55.0±10.0 and 63% were males. Notably, the DM group had only slightly elevated HbA1c and preserved eGFR, indicating a cohort with adequate DM control. 24-hour SBP ARV correlated with age, Aortic SBP and PWV (r = 0.295, 0.287 &0.253 respectively, p for all<0.001). DM patients had significantly increased 24-hour SBP ARV (10.00±2.40 vs 9.40±1.76, p = 0.049) and significantly elevated PWV (8.93±1.89 vs. 8.30±1.69, p =0.017) compared to the control group. Conclusions: In a cohort of T2DM patients with adequate glycemic control, BPV indices are significantly increased compared to euglycemic controls. The correlation of BPV parameters with indices of TOD, could partly explain its prognostic significance regarding CV risk prediction. Diabetes triggers the dysregulation of the homeostasis of BP even in the early stages of the disease, possibly through impaired endothelial function. Further studies are necessary to confirm our findings and shed light on the pathophysiology of this effect.