Review: Type 2 diabetes — implications for macrovascular mechanics and disease

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Abstract
Before macrovascular disease is established, type 2 diabetes is associated with structural and functional changes in large arteries that lead to increased stiffness, abnormal pulse wave travel and systolic hypertension. Structural changes result mainly from glycation of wall components. Functional changes originate in endothelial dysfunction. Increased arterial stiffness, or decreased arterial distensibility, increases pulse wave velocity and the amplitude of reflected waves, so that reflected waves arrive early and augment central systolic pressure. This promotes the development of left ventricular hypertrophy, an independent risk factor for cardiovascular mortality. One of the major mechanisms of arterial stiffening is endothelial dysfunction with reduced nitric oxide (NO)-mediated vasodilatation, the initial lesion in pre-atherosclerotic diabetes. To understand better the mechanisms of endothelial dysfunction will be vital if future therapeutic interventions are targeted to disease prevention. Protein glycation in poorly controlled diabetes is also damaging to blood vessels and must be limited by good diabetic control over the longer term.