The metabolic abnormalities associated with DM are well recognized and include insulin resistance (or, more appropriately, dysinsulinemia), hyperglycemia, hypertension, and dyslipidemia. These factors are associated with a panoply of biological perturbations that result in endothelial dysfunction with impaired coronary flow reserve, increased platelet activity, increased thromboxane A2 secretion, |
higher fibrinogen and factor VII levels, lower antithrombin III and plasma fi- S
brinolytic activity, and higher concentrations of plasminogen activator inhibitor (PAI-1). It is thus axiomatic that the dysinsulinemia of type 2 DM as well as <j other traditional risk factors be treated aggressively to delay or impede the genesis of cardiovascular and cerebrovascular events. What remains uncertain, at present, J
is whether treating aggressively the insulin resistance (or metabolic) syndrome in
& u the years leading up to frank type 2 DM will decrease the likelihood of subsequent clinical events. The metabolic syndrome, first described by Reaven, has been proposed as a ''disease'' that includes many of the clinical, biological, and vascular abnormalities observed in non-insulin-requiring DM patients.
The metabolic syndrome includes hyperinsulinemia (impaired glucose tolerance) an abnormal lipid profile characterized by elevated triglycerides, low levels of high-density-lipoprotein (HDL) cholesterol, and increased low-density-li-poprotein (LDL) cholesterol, hypertension, and central obesity with an increased waist-to-hip ratio. Many cross-sectional studies have indicated that insulin resistance is associated with ultrasonographically or angiographically demonstrable atherosclerosis, even in the absence of other risk factors for CAD. However, controversy still exists about the mechanisms by which the metabolic syndrome induces or accelerates atherogenesis. Some have proposed that ''traditional'' cardiac risk factors are enhanced by hyperinsulinemia and may account for accelerated atherogenesis. Reaven hypothesized that insulin resistance and compensatory hyperinsulinemia might be the primary, or inciting, event causing hypertension and leading in turn to an increased risk of CAD. The exact role of insulin remains to be defined.
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