ReviewArterial stiffness in diabetes mellitus
Section snippets
Background
Arterial stiffness is an age-related progressive process that is a shared consequence of numerous diseases including diabetes mellitus (DM), hypertension, the metabolic syndrome (METS) and chronic kidney disease (CKD), among others. DM is as an increasingly prevalent disease with well-recognized short and long-term cardiovascular consequences. In this paper, we discuss recent findings from clinical and population-based studies assessing arterial stiffness in diabetic cohorts. There is a
Methods
We searched Medline (from 1946 to 2013) and Embase (from 1947 to 2013) databases, using detailed search strategies, as detailed in the online supplement. We developed search methods to capture publications related to arterial stiffness and DM, AGEs, and microvascular complications of DM. This search generated 1700 articles and abstracts which were reviewed in their entirety and discussed by the authors to establish their relevance to this review. When appropriate, we discuss major contributions
Human studies of DM and arterial stiffness
Arterial stiffness represents a subclinical marker of cardiovascular risk. Arterial stiffness has been shown to be an independent risk factor for adverse cardiovascular events and all-cause mortality in the general population [1]. Markers of large artery stiffness such as pulse pressure (PP), pulse wave velocity (PWV), and aortic characteristic impedance (Zc), have been widely studied over the past two decades. With improvements in techniques to non-invasively measure these hemodynamic
Arterial stiffness and microvascular/macrovascular changes in DM
This section reviews current studies examining the relationship between arterial stiffness and target organ dysfunction in DM, specifically: nephropathy, retinopathy, and neuropathy/autonomic dysfunction. Additionally, association between stiffness and cognitive dysfunction and stroke are discussed as well. Studies assessing the relationship between arterial stiffness and/or related hemodynamic indices and target organ dysfunction in type 2 DM are summarized in Table 3.
Advanced glycation end-products, nitric oxide dysregulation, and arterial stiffness
The remainder of the paper will focus on potential mechanisms of arterial stiffness in DM, with particular emphasis on the role of advanced glycation endproducts (AGEs) and nitric oxide (NO) dysregulation.
Several studies have implicated AGEs in the acceleration of age-related vascular changes and development of cardiovascular events in both diabetic and non-diabetic populations [68]. AGE formation consists of several reversible and irreversible steps that culminate in the detrimental
Conclusions
Accumulating evidence suggests that arterial stiffness is a key component in the pathogenesis of DM, and importantly, that endothelial dysfunction may even occur with early insulin resistance and impaired fasting glucose, before the development of overt DM. Both AGEs and endothelial NO dysregulation play critical roles in the pathogenesis of arterial stiffness. Arterial stiffness is an independent predictor of mortality both in the diabetic population and in the population as a whole, and
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