Diabetes is being called a cardiovascular disease.1 Clearly, it is an independent risk factor for cardiovascular disease in both men and women. Two thirds of people with diabetes die of some form of heart or blood vessel disease.1 For adults with diabetes, death from heart disease and the risk of stroke are about two to four times higher than in individuals without diabetes.2
Of serious concern is that diabetes mellitus has moved from a chronic disease to a public health threat of epidemic proportions. The number of persons in the US with diagnosed diabetes has significantly increased in the past four decades (fig. 1).3 Diabetes and obesity continue to be twin epidemics. A recent Centers for Disease Control and Prevention Study reported that from 1991 to 2000, there was a 49% increase in diabetes and a 61% increase in obesity in Americans.4 Increases in diabetes were observed in every category examined: all ages, both sexes, all races, all education levels, and almost every US state.5-6 While the statistics of diabetes in the United States are alarming, the global picture is even worse. Worldwide it is estimated that more than 100 million people have diabetes, and this figure is projected to double over the next 20 years as Third World people increasingly adopt a Western lifestyle with its accompanying increase in obesity and decrease in physical activity.7
Diabetes mellitus is not a single disease but a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin actions, or both. Prior classification and diagnosis of diabetes was developed by the National Diabetes Data Group (NDDG) and published in 1979 and later endorsed by the World Health Organization (WHO) in 1980. In 1997, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus changed the NDDG/WHO classification scheme.8 For the purposes of this journal issue, we will focus primarily on type 2 diabetes (T2DM). This accounts for about 90% to 95% of all diagnosed diabetes and is characterized by insulin resistance and usually relative insulin deficiency.8 Insulin secretion is defective in these individuals and insufficient to compensate for the insulin resistance. Although the specific etiologies are unknown, autoimmune destruction of beta-cells does not occur and individuals do not have any secondary cause of diabetes. However, it is noteworthy that most patients are obese, and obesity itself further increases insulin resistance.
The health consequences of diabetes are overwhelming, with the direct and indirect costs of diabetes accounting for 15% of health care expenditures in the United States or at least $100 billion annually.2 These costs primarily relate to the microvascular and macrovascular complications of T2DM. While there is general consensus that the degree of glycemia in diabetic patients is associated with its microvascular complications (such as renal disease and retinopathy), the relationship of glycemia to macrovascular disease is less clearly understood. However, the disease implications are staggering. Both type 1 and type 2 diabetes are associated with accelerated macrovascular disease (coronary heart disease, stroke, and amputations), accounting for 65% to 75% of the deaths in diabetic individuals and much of the disability and costs.2
The etiology of this increase in risk is multifactorial, with hyperglycemia likely playing a significant role. Most patients with T2DM have the insulin resistance syndrome, which involves a clustering of cardiovascular risk factors. In addition, diabetes is associated with reduced antioxidant defenses, coagulopathy and endothelial dysfunction with impaired nitric oxide production, creating an environment of oxidative stress that promotes further atherogenesis.9 Of note, the incidence of macrovascular disease increases even before glucose levels reach the diagnostic threshold for diabetes. Nearly 25% of newly diagnosed type 2 diabetics have evidence of cardiovascular disease, sparking the debate over the role of glycemia per se and macrovascular disease.10
New evidence demonstrates that T2DM can be prevented or significantly delayed in onset by modification of traditional risk factors. Obesity and physical activity seem to play the most important roles. Research indicates that obesity is highly correlated with type 2 diabetes (r = .64, p < .001)5 and physical activity is important for the prevention of T2DM.11 It is important to note that exercise does not have to be strenuous; regular, moderate physical activity can be beneficial. Regular walking has been demonstrated to have positive effects on cardiovascular risk factors and body composition in women who are normoglycemic as well as those with type 2 diabetes.12 Recently, a landmark clinical trial, the Diabetes Prevention Program (DPP)13-14 showed that lifestyle prevention strategies were successful across a broad spectrum of racial and ethnic groups. It demonstrated conclusively that T2DM is not inevitable for those at risk of developing it. Persons with impaired glucose tolerance who were overweight (average body mass index of 34) were randomly assigned to intensive lifestyle changes (exercising for 150 minutes per week with walking or other moderate intensity exercise and a low-fat diet), treatment with metformin (850 mg, twice daily), and a control group taking placebo pills in place of metformin. The last two groups also received general diet and exercise information. Results showed that those randomized to intensive lifestyle intervention were more successful in reducing their risk of getting diabetes. While those randomized to metformin had reduced their risk of getting diabetes by 31%, those in the intensive lifestyle changes had a reduction of 51%. Researchers will analyze the data to identify whether the interventions will reduce cardiovascular disease.13-14
As the table of contents clearly shows, this issue is replete with articles that cover the depth and breadth of the diabetes epidemic and its major complications of cardiovascular disease. Quinn sets the stage by tackling the complex underlying pathophysiology of diabetes. She clearly maps out the problems of glucose metabolism and insulin resistance and graphically presents a three-stage process for the development of T2DM. Though many of the mechanisms involved in the genesis of diabetes-related cardiovascular disease remain to be elucidated, Quinn presents an intriguing discussion of the biochemical pathways known to be involved in hyperglycemia, insulin resistance, and cardiovascular disease. She also discusses the effect of exercise on diabetes and insulin resistance.
The next article by Fletcher, Gulanick and Lamendola provides background on diabetes prevalence and risk factors. While T2DM is strongly linked to genetics and ethnicity, it also increases with age, obesity, and a sedentary lifestyle, which highlights the paramount role lifestyle and environment play in the prevalence of this disease. Because diabetes is characterized by insulin resistance, individuals with this disease also have associated metabolic abnormalities such as hypertension, elevated triglycerides, and low HDL cholesterol that are also identified as risk factors for T2DM. This article highlights the more traditional risk factors for diabetes.
Stanciu, Peralta, Emmanuele, and Emmanuele present the latest clinical trial evidence for cardiovascular risk reduction in diabetes. They begin with an overview of the major trials that showed strong correlation between glycemic control and reduction in microvascular complications. While no prospective trial has yet shown that glycemic control can prevent the cardiovascular effects of diabetes, these authors clearly describe the groundbreaking trials that are currently examining the efficacy of controlling related risk factors such as hypertension, dyslipidemia, and platelet aggregation.
Standards of care for T2DM are presented by Kernan-Schroeder and Cunningham in an easy-to-remember ABC format. These 2001 clinical practice guidelines provide a comprehensive framework for addressing the potential problems related to glycemic control and the complications of diabetes. Nurses are challenged to aggressively assist clients in maintaining healthy behaviors such as controlling weight through nutrition and physical activity, adhering to pharmacologic therapy, and reducing identified cardiovascular risk factors.
Providing comprehensive pharmacologic care to the rapidly increasing numbers of individuals with diabetes presents many challenges. McCormick and Quinn present the current classes of oral anti-diabetic agents, along with several types of insulin and insulin analogs. Their tables will serve as useful reference tools for cardiovascular nurses who are caring for an expanding number of diabetic clients. The issues related to mono versus combination therapy are also discussed.
Penckofer, Schwertz, and Florczak examine the evidence that links oxidative stress with diabetes and cardiovascular disease. The authors define oxidative stress and diabetes and examine why cardiovascular disease is accelerated in persons with T2DM. They propose that antioxidants, pro-oxidants and other factors may contribute to oxidative stress and free radical formation in T2DM. Clinical trial data addressing the effectiveness of antioxidants (primarily vitamin E and beta carotene) in the primary and secondary prevention of cardiovascular disease are addressed. The implications from these trials as well as other research studies that have examined the effectiveness of antioxidants in diabetics are provided. The authors also present information on how pro-oxidants, primarily glucose, ferritin, and homocystine, may contribute to oxidative stress in diabetes. The impact that aging, diet, and physical activity may have on oxidative stress also is discussed. Finally, the implications for nursing, particularly regarding the use of alternative therapies such as antioxidants for persons with T2DM, are examined.
Finally, Armstrong concludes this issue with an indepth review of a broad range of clinical trials supported by the National Institute of Nursing Research at the National Institutes of Health that relate to diabetes and cardiovascular disease. She concludes with a presentation of research opportunities in the field and challenges nurses to work toward filling the gaps in our current knowledgebase.
Cardiovascular nurses are being challenged to expand their specialty to include a greater understanding of the pathophysiology of diabetes and insulin resistance, identification and treatment of risk factors for both cardiovascular disease and diabetes, medication therapy, and comprehensive management plans that include lifestyle changes. Only through aggressive identification and treatment of diabetes and its related complications can the epidemic and health burdens of these related diseases be halted. This special issue will serve nurses well in their fight against these diseases.
Recommended web sites for this issue include the following:
* http://www.diabetes.org (American Diabetes Association)
* http://www.cdc.gov/diabetes (Centers for Disease Control and Prevention)
* http://www.aadenet.org (American Association of Diabetes Educators)
* http://www.niddk.nih.gov (National Institute of Diabetes and Digestive and Kidney Disease of the National Institutes of Health)
* http://www.ndep.nih.gov (National Diabetes Education Program: A joint program of NIH & CDC)
* http://www.americanheart.org (American Heart Association)
Meg Gulanick, PhD, RN
Associate Professor
School of Nursing
Loyola University Chicago
Chicago, Illinois
Sue Penckofer, PhD, RN
Professor and Associate Dean for Research
School of Nursing
Loyola University Chicago
Chicago, Illinois
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