Late Cardiovascular Consequences of Gestational Diabetes Mellitus
Late Cardiovascular Consequences of Gestational Diabetes Mellitus
Gestational diabetes mellitus (GDM), defined as carbohydrate intolerance of any degree first recognized during pregnancy, complicates ~4% of all pregnancies in the United States. Several factors can increase one's risk of developing GDM, including obesity, family history of type 2 diabetes mellitus (T2DM), and race/ethnicity. Conversely, a history of GDM can increase the risk of developing not only T2DM but also cardiovascular disease (CVD) independent of a diagnosis of T2DM. Several investigations have explored GDM relationships with CVD risk factors, CVD surrogate markers, and clinically evident CVD. These studies have included evaluations of biochemical parameters, such as inflammatory and endothelial biomarkers; endothelial dysfunction, such as that seen in impaired brachial artery flow-mediated vasodilation; and vascular dysfunction, manifest as cardiac dysfunction or in diseases such as hypertension. This article will review these studies and examine factors considered to be responsible for promoting CVD in women with a history of GDM, such as T2DM and metabolic syndrome and its components. In addition, studies evidencing CVD in women with a history of GDM will be explored.
Gestational diabetes mellitus (GDM), defined as carbohydrate intolerance of any degree first recognized during pregnancy, complicates ~4% of all pregnancies in the United States with a prevalence of 1 to 14% and an annual incidence of more than 135,000 cases. Prevalence estimates of GDM vary depending on the population under examination, and several studies report that the prevalence of GDM is higher among racial/ethnic minorities compared with that among non-Hispanic white populations. One population study reported that the age-adjusted prevalence of GDM per 100 births in 2005 was 4.9% among non-Hispanic whites and 5.2% among non-Hispanic blacks. Additionally, the increasing prevalence among ethnic minorities of risk factors associated with the development of GDM, such as obesity, suggests that the racial disparity in GDM prevalence will persist.
There are several factors that can increase the risk of developing GDM, including obesity, family history of type 2 diabetes mellitus (T2DM), and race/ethnicity. Notably, features that increase the risk of developing GDM, including obesity and the metabolic syndrome components, are also associated with an increased risk of developing cardiovascular disease (CVD). Normoglycemic pregnancy presents a metabolic stress characterized by insulin resistance with postprandial hyperglycemia; dyslipidemia with increased triglycerides and low-density lipoprotein (LDL); and increased inflammation including elevated C-reactive protein (CRP) and plasminogen activator inhibitor-1 (PAI-1). Therefore, the stress imposed by GDM on an already compromised metabolic state can potentially convert a usually transient metabolic derangement into a more permanent abnormality that will increase the likelihood of CVD development. This review will examine investigations of GDM with respect to CVD risk factors, such as T2DM; CVD surrogate measures, such as endothelial dysfunction; and diagnosed CVD, such as coronary artery disease (Table 1).
Abstract and Introduction
Abstract
Gestational diabetes mellitus (GDM), defined as carbohydrate intolerance of any degree first recognized during pregnancy, complicates ~4% of all pregnancies in the United States. Several factors can increase one's risk of developing GDM, including obesity, family history of type 2 diabetes mellitus (T2DM), and race/ethnicity. Conversely, a history of GDM can increase the risk of developing not only T2DM but also cardiovascular disease (CVD) independent of a diagnosis of T2DM. Several investigations have explored GDM relationships with CVD risk factors, CVD surrogate markers, and clinically evident CVD. These studies have included evaluations of biochemical parameters, such as inflammatory and endothelial biomarkers; endothelial dysfunction, such as that seen in impaired brachial artery flow-mediated vasodilation; and vascular dysfunction, manifest as cardiac dysfunction or in diseases such as hypertension. This article will review these studies and examine factors considered to be responsible for promoting CVD in women with a history of GDM, such as T2DM and metabolic syndrome and its components. In addition, studies evidencing CVD in women with a history of GDM will be explored.
Introduction
Gestational diabetes mellitus (GDM), defined as carbohydrate intolerance of any degree first recognized during pregnancy, complicates ~4% of all pregnancies in the United States with a prevalence of 1 to 14% and an annual incidence of more than 135,000 cases. Prevalence estimates of GDM vary depending on the population under examination, and several studies report that the prevalence of GDM is higher among racial/ethnic minorities compared with that among non-Hispanic white populations. One population study reported that the age-adjusted prevalence of GDM per 100 births in 2005 was 4.9% among non-Hispanic whites and 5.2% among non-Hispanic blacks. Additionally, the increasing prevalence among ethnic minorities of risk factors associated with the development of GDM, such as obesity, suggests that the racial disparity in GDM prevalence will persist.
There are several factors that can increase the risk of developing GDM, including obesity, family history of type 2 diabetes mellitus (T2DM), and race/ethnicity. Notably, features that increase the risk of developing GDM, including obesity and the metabolic syndrome components, are also associated with an increased risk of developing cardiovascular disease (CVD). Normoglycemic pregnancy presents a metabolic stress characterized by insulin resistance with postprandial hyperglycemia; dyslipidemia with increased triglycerides and low-density lipoprotein (LDL); and increased inflammation including elevated C-reactive protein (CRP) and plasminogen activator inhibitor-1 (PAI-1). Therefore, the stress imposed by GDM on an already compromised metabolic state can potentially convert a usually transient metabolic derangement into a more permanent abnormality that will increase the likelihood of CVD development. This review will examine investigations of GDM with respect to CVD risk factors, such as T2DM; CVD surrogate measures, such as endothelial dysfunction; and diagnosed CVD, such as coronary artery disease (Table 1).
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