Researchers find that increases in arterial stiffness may occur in hypertensive patients other than those with T2DM….
Diabetes mellitus and abnormal glucose metabolism are known to be associated with increased cardiovascular risk. Though the mechanisms behind this relationship are complicated and multifactorial, arterial stiffness is thought to be a possible contributor to this relationship. Several studies regarding the relationship between arterial stiffness and abnormal glucose metabolism already exist. Most of the studies have found an association between arterial stiffness and T2DM. There is a lack of data, however, as to whether a relationship exists between arterial stiffness and impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). There is also no data on how pulse wave velocity (an indicator of arterial stiffness) differs among patients with normal glucose regulation. Researchers therefore conducted a study to find to what extent, and from what stage, abnormal glucose metabolism may affect arterial stiffness in hypertensive patients.
The participants of this study included 1375 subjects with never-treated arterial hypertension in Athens, Greece. Arterial stiffness, assessed by carotid-femoral pulse wave velocity (PWV), was measured in four different groups of patients. These four groups were as follows: patients with normal glucose regulation (70-99mg/dl), patients with impaired fasting glucose (fasting glucose 100-125mg/dl and normal 2-h postload glucose <140mg/dl), patients with impaired glucose tolerance (2-h postload glucose 140-199mg/dl), and patients with T2DM, defined as a FBG ≥126mg/dl in two different measurements, use of antidiabetic drugs, or a 2-h postload glucose of ≥200mg/dl. The patients with normal glucose were further divided into three groups according to their glucose levels. These three groups were: glucose concentration <80mg/dl, 80-89mg/dl, or 90-99mg/dl.
Measurements of PWV showed a significant increase from patients with normal glucose regulation to those with T2DM. Furthermore, among the patients with normal glucose regulation, there was an increase in PWV from the low normal group (<80mg/dl) to the high normal values of glucose (90-99mg/dl). Analyses showed PWV to be independently related to all glucose metabolic parameters, with an increase in arterial stiffness occurring as glucose metabolism deteriorates. This is the first study known to show that arterial stiffness may increase even in hypertensive patients with normal glucose regulation, as participants with glucose concentration 90-99mg/dl had higher PWV values that those with glucose concentration <80mg/dl.
Though this study and several others have shown arterial stiffness to increase as glucose metabolism becomes more abnormal, some studies have had different results, making the data on this relationship inconsistent. In this study, patients with T2DM showed the highest values of PWV, but no statistical difference was seen in arterial stiffness between those subjects with IFG and IGT after adjustment for confounders. Other factors may contribute to arterial stiffness in these two groups, such as advanced age. Future research is needed to determine the mechanism by which abnormal glucose metabolism increases arterial stiffness, though inflammation and increased insulin concentrations in conditions of abnormal glucose metabolism are thought to be possible causes. Though there is no target glucose level at which to aim in order to prevent CV events, providers should monitor glucose levels more closely in this population.
- Differences in carotid-femoral pulse wave velocity occurred even in hypertensive patients with normal glucose metabolism, showing that various stages of glucose intolerance can affect arterial stiffness.
- As arterial stiffness is a strong predictor of CV disease in many populations, providers should closely monitor and treat hypertensive patients with abnormal glucose metabolism.
Vyssoulis, G. et al. "Early adverse effect of abnormal glucose metabolism on arterial stiffness in drug naïve hypertensive patients" Diabetes and Vascular Disease Research. 2014; 9(1):18-24.