Learning Objective 1: compare the AI in type 2 diabetic normotensive patients and mild hypertensive patients
Learning Objective 2: examine the association among AI, diurnal blood pressure variation and HRV in patients with cardiovascular risk
Previous studies have been supported the role of hypertension in the increased arterial stiffness in type 2 diabetes. However, the changing of arterial stiffness indicated by augmentation index (AI) in type 2 diabetics in the absence of hypertension has not been measured. The comparison of AI in type 2 diabetic normotensive patients and mild hypertension has also not been investigated. In addition, whether AI is correlated with other subclinical cardiovascular risk factors including blunted blood pressure (BP) variation and reduced heart rate variability (HRV) in these populations has yet to be examined.
This study was conducted to compare the AI in type 2 diabetic normotensive patients and mild hypertensive patients. The association among AI, diurnal BP variation and HRV was also examined.
53 type 2 diabetic individuals and 23 hypertensive individuals enrolled in this study. All participants were tested for anthropometric, hemodynamic measurements and 5-min HRV. Radial applanation tonometry was used to acquire the aortic pressure waveform noninvasively using the generalized transfer function. AI (%) was then calculated as the ratio of augmented pressure to pulse pressure. Ambulatory BP measurements were performed over a 24-hour period.
There was no difference between the mean value of AI in type 2 diabetics and mild hypertensives after controlled for age and body height (28.0±7.0% vs. 21.5±13.2 %, p=0.413). AI did not significantly correlate to the parameters of diurnal BP variation and four indices of HRV.
Although the increased AI has been demonstrated in type 2 diabetic normotensive patients with less nocturnal SBP decline and reduced HRV, there was no difference between AI in type 2 normotensive diabetics and mild hypertensives. There was also no association among AI, diurnal BP variation and HRV. The plausible mechanism that linking the ANS deregulation to the higher AI was not supported.