Impact of Race and Risk Factors on AF Incidence
Despite some common risk factors for atrial fibrillation (AF) being more prevalent among blacks, African Americans are increasingly being reported with lower prevalence and incidence of AF compared with whites. Contemporary studies have not provided a complete explanation for this apparent AF paradox in African Americans. Although many traditional and novel risk factors for AF have been identified, the role of ethnic-specific risk factors has not been examined. Whereas hypertension has been the most common risk factor associated with AF, coronary artery disease also plays an important role in AF pathophysiology in whites. Thereby, elucidating the role of ethnic-specific risk factors for AF may provide important insight into why African Americans are protected from AF or why whites are more prone to develop the arrhythmia. The link between AF susceptibility and genetic processes has only been recently uncovered. Polymorphisms in renin-angiotensin system genes have been characterized as predisposing to AF under certain environmental conditions. Several ion channel genes, signaling molecules, and several genetic loci have been linked with AF. Thereby, studies investigating genetic variants contributing to the differential AF risk in individuals of African American versus European ancestry may also provide important insight into the etiology of the AF paradox in blacks.
Atrial fibrillation (AF) is the most commonly encountered sustained arrhythmia among ambulatory and hospitalized patients. It is a significant cause of morbidity and mortality that consumes a substantial amount of health care spending and with increasing prevalence projected to more than double by 2050. Atrial fibrillation is often a progressive and self-perpetuating disease with complex mechanisms. It has been determined that abnormally rapid impulses from within the pulmonary veins can trigger initiation and maintenance of AF where there is a conducive and vulnerable substrate. The substrate for AF typically result from the effects of both electrical and structural remodeling that can arise from chronic hypertension; cardiac ischemia or infarction; autonomic disorder; and genetic mutations, among many others. Atrial fibrillation induces further electrophysiologic changes in the atria by affecting calcium homeostasis, leading to shortening of atrial effective refractory period as well as structural remodeling with atrial fibrosis, stretch, and dilatation. The ultimate consequence of these changes is a perpetuation of the arrhythmia described by the dictum "AF begets AF" (Figure 1).
(Enlarge Image)
Figure 1.
Conceptual model of AF pathophysiology and pathogenesis. (Adapted from Benjamin et al.)
The Framingham Heart Study (FHS) identified demographic and clinical risk factors for AF in a population-based cohort of predominantly whites. Congestive heart failure (CHF) and rheumatic heart disease were reported as the most powerful predictors and precursors of AF. Subsequently, risk factors were updated to include age, sex, diabetes, hypertension, and myocardial infarction in addition to CHF and rheumatic heart disease. The epidemiology of AF has changed during the past half century, with rheumatic valvular heart disease becoming almost extinct in the Western world while new risk factors such as sleep apnea, obesity, and metabolic syndrome have emerged. Recently, chronic kidney disease has been associated with increased risk of AF and doubles the risk of mortality among hemodialysis patients.
The disproportionate rates of AF between blacks and whites are increasingly being recognized. Some risk factors for AF particularly constituents of metabolic syndrome such as hypertension, diabetes, body mass index, waist circumference, and obesity have been reported as more prevalent in blacks. Recent approaches have incorporated these risk factors into the metabolic syndrome and have shown this to increase the risk for AF and by equally comparable measures in both blacks and whites. Nevertheless, there remains a strong body of evidence in support of overall lower rates in the incidence and prevalence of AF among blacks and, hence, a perceived paradox. Although several recent publications continue to raise doubts, the terms blacks or African Americans, whites, race, and ethnicity will be used in this manuscript by historical standards but understood to be broad generalizations being applied to a heterogenous group of persons based chiefly on the dominant phenotypic expression. In this review, we use these terms interchangeably but with keen awareness and understanding of the complexities inherent in the definitions. The role of race and genetic background on AF remains largely underappreciated. Here, we will discuss available data that support the existence of an AF paradox in African Americans and highlight areas where further investigation is warranted for improved understanding of this phenomenon.
Abstract and Introduction
Abstract
Despite some common risk factors for atrial fibrillation (AF) being more prevalent among blacks, African Americans are increasingly being reported with lower prevalence and incidence of AF compared with whites. Contemporary studies have not provided a complete explanation for this apparent AF paradox in African Americans. Although many traditional and novel risk factors for AF have been identified, the role of ethnic-specific risk factors has not been examined. Whereas hypertension has been the most common risk factor associated with AF, coronary artery disease also plays an important role in AF pathophysiology in whites. Thereby, elucidating the role of ethnic-specific risk factors for AF may provide important insight into why African Americans are protected from AF or why whites are more prone to develop the arrhythmia. The link between AF susceptibility and genetic processes has only been recently uncovered. Polymorphisms in renin-angiotensin system genes have been characterized as predisposing to AF under certain environmental conditions. Several ion channel genes, signaling molecules, and several genetic loci have been linked with AF. Thereby, studies investigating genetic variants contributing to the differential AF risk in individuals of African American versus European ancestry may also provide important insight into the etiology of the AF paradox in blacks.
Introduction
Atrial fibrillation (AF) is the most commonly encountered sustained arrhythmia among ambulatory and hospitalized patients. It is a significant cause of morbidity and mortality that consumes a substantial amount of health care spending and with increasing prevalence projected to more than double by 2050. Atrial fibrillation is often a progressive and self-perpetuating disease with complex mechanisms. It has been determined that abnormally rapid impulses from within the pulmonary veins can trigger initiation and maintenance of AF where there is a conducive and vulnerable substrate. The substrate for AF typically result from the effects of both electrical and structural remodeling that can arise from chronic hypertension; cardiac ischemia or infarction; autonomic disorder; and genetic mutations, among many others. Atrial fibrillation induces further electrophysiologic changes in the atria by affecting calcium homeostasis, leading to shortening of atrial effective refractory period as well as structural remodeling with atrial fibrosis, stretch, and dilatation. The ultimate consequence of these changes is a perpetuation of the arrhythmia described by the dictum "AF begets AF" (Figure 1).
(Enlarge Image)
Figure 1.
Conceptual model of AF pathophysiology and pathogenesis. (Adapted from Benjamin et al.)
The Framingham Heart Study (FHS) identified demographic and clinical risk factors for AF in a population-based cohort of predominantly whites. Congestive heart failure (CHF) and rheumatic heart disease were reported as the most powerful predictors and precursors of AF. Subsequently, risk factors were updated to include age, sex, diabetes, hypertension, and myocardial infarction in addition to CHF and rheumatic heart disease. The epidemiology of AF has changed during the past half century, with rheumatic valvular heart disease becoming almost extinct in the Western world while new risk factors such as sleep apnea, obesity, and metabolic syndrome have emerged. Recently, chronic kidney disease has been associated with increased risk of AF and doubles the risk of mortality among hemodialysis patients.
The disproportionate rates of AF between blacks and whites are increasingly being recognized. Some risk factors for AF particularly constituents of metabolic syndrome such as hypertension, diabetes, body mass index, waist circumference, and obesity have been reported as more prevalent in blacks. Recent approaches have incorporated these risk factors into the metabolic syndrome and have shown this to increase the risk for AF and by equally comparable measures in both blacks and whites. Nevertheless, there remains a strong body of evidence in support of overall lower rates in the incidence and prevalence of AF among blacks and, hence, a perceived paradox. Although several recent publications continue to raise doubts, the terms blacks or African Americans, whites, race, and ethnicity will be used in this manuscript by historical standards but understood to be broad generalizations being applied to a heterogenous group of persons based chiefly on the dominant phenotypic expression. In this review, we use these terms interchangeably but with keen awareness and understanding of the complexities inherent in the definitions. The role of race and genetic background on AF remains largely underappreciated. Here, we will discuss available data that support the existence of an AF paradox in African Americans and highlight areas where further investigation is warranted for improved understanding of this phenomenon.
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