Risk factors for PAD in patients with diabetes Table

The high PAD risk in patients with diabetes is due to the complex interplay between the various haemodynamic and metabolic components of the metabolic syndrome. Diabetes is no longer considered to be a disease confined to hyperglycaemia but rather part of a syndrome comprising various risk factors, all of which confer an increased risk of atherosclerosis and cardiovascular events (see also Chapter 2). Hence, although the diagnosis and symptoms of diabetes are still defined by hyperglycaemia, other features of the syndrome, especially hypertension and dyslipidaemia, are equally if not more important in the pathogenesis of diabetes-related macrovascular complications such as PAD. Thus, the development of atherothrombotic complications in larger lower limb arteries is multifactorial, reflecting interactions between high glucose, lipids and blood pressure. For example, hypercholesterolemia and hypertriglyceridaemia have been associated with the increased risk of intermittent claudication and PAD in both cross-sectional and prospective studies of type 2 diabetes (Lehto etal., 1996; Adler etal., 2002). High-density-lipoprotein (HDL)-cholesterol appears to be inversely related to PAD (Adler etal., 2002). Hypertension, both systolic and diastolic, also has a significant impact on the development and progression of PAD in the diabetic population (Murabito etal., 1997; Adler etal., 2000, 2002).

Smoking meanwhile is believed to be the most important risk factor in lower limb arteriopathy both in patients with and without diabetes, conferring nearly a threefold increased risk of PAD (Jonason and Ringqvist, 1985; Hirsch etal., 1997). Epidemiological studies have identified insulin resistance and hyperinsulinaemia, independent of glucose levels, as independent risk factors for PAD in both diabetic and non-diabetic subjects (Price etal., 1996; Matsumoto etal., 1997). An additional risk factor for PAD and amputation is renal transplantation, an effect that is more prevalent in diabetic subjects than in the non-diabetic population (Lemmers and Barry, 1991). The exact mechanism for this remains unclear.

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