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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
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Chapter Summary
This chapter discusses the development, prevention, and management of cardiovascular disease in patients with diabetes mellitus. The number of patients with diabetes is rapidly increasing, and the condition is a major risk factor for the development of cardiovascular disease (see Fuster and Hurst’s Central Illustration). Microvascular complications of diabetes include nephropathy, neuropathy, and retinopathy. Macrovascular and cardiovascular complications of diabetes include coronary heart disease—the leading cause of death in patients with type 2 diabetes (T2D)—diabetes-related cardiomyopathy and heart failure, atrial fibrillation, ventricular arrhythmia, cerebrovascular disease, and peripheral artery disease. Mechanisms of development of cardiovascular disease in patients with diabetes and insulin resistance include β-cell dysfunction and hyperglycemia, dyslipidemia, M1 macrophage activation, inflammation, endothelial dysfunction, and atherosclerosis. A major focus in the management of patients with type 1 or T2D is the prevention of cardiovascular disease. Strategies known to reduce cardiovascular events in patients with diabetes include diet and lifestyle modification, targeted glycemic and weight control, cardio-protective glucose-lowering medications, and effective management of dyslipidemia and hypertension.
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Diabetes mellitus refers to a group of diseases, with different etiologies and pathophysiological mechanisms, which result in blood glucose (BG) levels that are sufficiently high to cause specific clinical complications. Historically, diabetes was first an uncommon condition exclusively found in children, in whom there was a defect in insulin production, tendency toward diabetic ketoacidosis (DKA), and rapid natural progression of a catabolic state with classic symptoms of polyuria, polydipsia, polyphagia, weight loss, dehydration, and then death. Prior to the discovery and ability to harness insulin as a therapy in 1921, patients with diabetes could have their life extended with semi-starvation, although at the expense of severe cachexia and malnutrition. However, with insulin, patients with diabetes lived longer, though diabetes-related complications were still inevitable. It was only with the description of another form of hyperglycemia, referred to as type 2 diabetes (T2D) that the previously regarded form was referred to as type 1 diabetes (T1D), and the two types were distinguished separately in 1936. Classically, T2D was characterized by a tendency toward adult onset, overweight/obesity, insulin resistance, and elevated insulin levels, with treatment with insulin or, once available, oral agents or noninsulin injectable agents. Over the years, the prevalence rate of T2D far exceeded that of T1D.
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Glycemic status can be described as normo-, dys-, hypo-, and hyperglycemia, which are defined by statistical-based classifiers correlating clinical metrics to stipulated risk levels for prediabetes, diabetes, and/or diabetes-related complications (Table 7–1).1 The salient differences among T1D, T2D, and atypical types with distinct management approaches are provided in Table 7–2.2,3
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