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Try out PMC Labs and tell us what you think. Learn More. The last three decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation AF. It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported seventeen independent signals for AF at fourteen genomic regions. Casual dating websites in cape coral.

The incidence rates per person-years for SEE and stroke were 0. The mechanisms underlying thromboembolism with SEE are similar to that of AF-related strokes. In patients with normal baseline cognitive function and no history of stroke, meta-analysis of eight studies found a significantly increased risk of incident dementia in those with AF HR, 1. Multiple mechanisms may explain the association of AF and dementia. Nearly one third of patients with AF have been observed to have silent brain infarcts on brain magnetic resonance imaging and micro thromboembolisms with covert infarction have been implicated as one possible mechanism.

The FHS showed that over the last three decades, the incidence of dementia including dementia associated with AF has decreased. This supposition is supported by a retrospective study of patients receiving long-term warfarin showing that incident dementia was 2. A second possible mechanism may involve cerebral hypoperfusion associated with AF. HF is both a RF and an adverse clinical cardiovascular outcome associated with AF.

The association was first recognized in the s and it is now established that HF and AF often co-exist, 2 predispose to the other, and share common RFs including hypertension, diabetes, coronary disease, and valvular disease.

The FHS uniquely reported the joint incidence of AF and HF and their temporal relationship. One fifth of participants had AF and HF detected on the same day, demonstrating the closely interlinked pathophysiology.

The incidence of first HF in FHS participants with AF is 33 per person years, which is comparable to that observed in the Danish nationwide cohort study. The association of AF on HF subtype has also been reported. AF precedes HF with preserved ejection fraction HFpEF more commonly than HF with reduced ejection fraction HFrEF. Among patients with prevalent AF, the adjusted HRs of incident HFpEF and HFrEF were 2.

In the FHS, the combination of AF and HF was associated with reduced survival. The strong association of HF and AF has been attributed to shared mechanisms that lead to neurohormonal and proinflammatory activation, which induces myocardial inflammation and fibrosis. It is distinct from the electrophysiologic changes associated with AF-induced atrial remodeling.

Histologic studies in HF dogs revealed structural changes including interstitial fibrosis with cellular hypertrophy, degeneration, and loss. These changes were associated with regions of delayed conduction and AF susceptibility. In human, extensive atrial fibrosis has been observed at autopsy in patients with dilated cardiomyopathy and areas of low voltage or electrical silence scar and fractionated or delayed potentials slow conduction have been identified during electrophysiology studies in patients with HF but no AF.

Increased trigger activity also is associated with HF and may increase risk of AF in the vulnerable substrate by generating a rapid burst of ectopic firing or maintaining a focal driver. In dogs, HF prolongs the APD and increases the phosphorylation of key regulatory kinases and phosphatases including calmodulin-dependent protein kinase II. Finally, tachycardia and shortening of diastolic filling time associated with irregular ventricular activation with AF further impair diastolic relaxation and promote clinical HF, which further induces atrial remodeling leading to the perpetuation of AF.

As with HF there is a bidirectional relationship between AF and myocardial infarction MI. Coronary heart disease is associated with an increased risk of AF, but AF also is associated with increased risk of MI.

The Olmsted study reported similar unadjusted risk of coronary ischemic event, but after adjusting for age the incidence was higher in men than woman. Interestingly, as observed with strokes and SEEs, the event rate of coronary ischemic events was highest within the first year of incident AF 4. The mechanisms linking AF to MI are not completely understood.

First, both AF and MI have overlapping RFs that may lead to the development of AF and MI in parallel. For instance, both AF and coronary heart disease are associated with proinflammatory and prothombotic states. Second, MI in AF may be attributed to coronary artery thromboembolism. Third, myocardial ischemia may arise from supply-demand mismatch in the setting of tachycardia associated with AF.

Fourth, MI may lead to left ventricular remodeling that may predispose to AF. Increased BMI, obesity, and smoking are associated with venous thromboembolism VTE - as well as AF. Potential direct causal relationship between AF and VTE has been proposed, but needs to be studied further.

A few studies have reported increased risk of VTE in AF and vice versa. In a retrospective cohort study based on the national administrative database in Taiwan, the risks of VTE adjusted HR, 1. In the Norwegian study, the mean age and BMI were 64 years and The mechanisms underlying the AF-VTE association are inexplicable. Several studies have shown that AF is associated with a hypercoagulable state attributed to elevated hemostatic factors including fibrinogen, D-dimer, prothombin fragment, factor VIII, and von Willebrand factor;- however, many of these studies were not adjusted for co-existing cardiovascular RF.

In an adjusted model, the FHS showed no significant difference in levels of fibrinogen, von Willebrand factor, or tissue plasminogen activator suggesting that co-existing RFs rather than AF may explain elevated thrombotic risk. The FHS was one of the first studies to report that AF had a multivariable-adjusted association with increased risk of death.

At year follow up, A similar trend was found in women with The increased risk was consistent across all decades of age from years. Even in individuals without clinical evidence of cardiovascular or valvular disease at baseline, AF was associated with a 2-fold increased risk of death. It is noteworthy that there is growing evidence that AF is associated with an increased risk of sudden cardiac death SCD. Pooled-analysis of the ARIC and Cardiovascular Health Study cohorts showed that AF was associated with more than a doubling of the risk of SCD SCD compared to participants without AF HR, 2.

A meta-analysis of anti-thrombotic studies has shown that oral anticoagulation reduced risk of all-cause mortality with an absolute risk reduction of 1. In the ROCKET-AF trial cardiovascular deaths occurred over two times more often than strokes. Thus further advances in anticoagulation strategies may have little effect on improving overall mortality in AF.

Over the last 50 years, the FHS and other epidemiological studies have yielded a breadth of data associating various RFs with risk of AF and providing insight into their mechanistic link to AF genesis. However, many questions remain. Will genetic studies improve AF risk assessment, identify novel therapeutic targets, and help guide treatment strategies for both primary and secondary prevention of AF? By what degree does RF modification alter the atrial substrate, AF burden, and clinical outcomes?

What are the target goals for RF modification and how will genetics alter these targets? Ongoing and future epidemiological, translational, and clinical studies may provide insight into these unanswered questions and improve clinical outcomes in patients with AF. AF risk factors induce structural and histopathological changes to the atrium that are characterized by fibrosis, inflammation, and cellular and molecular changes. Such changes increase susceptibility to AF.

Persistent AF further induces electrical and structural remodeling that promotes perpetuation of AF. AF also may lead to the development of additional AF risk factors that further alters the atrial substrate. Finally, AF is associated with several clinical outcomes. National Center for Biotechnology InformationU.

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Journal List HHS Author Manuscripts PMC Circ Res. Author manuscript; available in PMC Apr PMCID: PMC NIHMSID: NIHMS Laila StaerkMD, 1, 2, 3 Jason A. ShererMD, MPH, 4 Darae KoMD, 2, 5, 6 Emelia J. BenjaminMD, ScM, 2, 3, 5, 6, 7 and Robert H. HelmMD 6.

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Jason A. Sherer 4 Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States Find articles by Jason A. Darae Ko 2 Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, United States 5 Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States 6 Section of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States Find articles by Darae Ko.

Emelia J. Robert H. Helm 6 Section of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States Find articles by Robert H. Author information Copyright and License information Disclaimer. Correspondence to: Laila Staerk, MD moc. liamg kreatsaliaL ; Robert H. Helm, MD gro.

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cmb mleH. Copyright notice. The publisher's final edited version of this article is available at Circ Res. See other articles in PMC that cite the published article. Abstract The last three decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation AF.

Keywords: atrial fibrillation, epidemiology, risk factors, prognosis, pathophysiology.

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Introduction The association of an irregular pulse and mitral stenosis was first described by Robert Adams inbut it was not until the turn of the 20 th century when William Einthoven invented electrocardiography that atrial fibrillation AF was first recorded on the electrocardiogram.

Pathophysiology and Natural History AF AF is characterized by high frequency excitation of the atrium that results in both dyssynchronous atrial contraction and irregularity of ventricular excitation.

Open in a separate window. Figure 1. Pathophysiology Sedentary lifestyle is known to increase risk of AF RFs including hypertension, 86 obesity, 86 and diabetes Pathophysiology Smoking is thought to increase AF susceptibility through indirect and direct mechanisms. Pathophysiology Excess AF risk associated with obesity has been attributed to left atrial enlargement, increased left ventricular mass, and diastolic dysfunction.

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Pathophysiology Glucose intolerance and insulin resistance appear to mediate the development of the AF substrate. Pathophysiology Electroanatomic mapping in patients undergoing AF ablation has been used to characterize the AF substrate associated with OSA. Pathophysiology Increased left atrial size is a well-established, independent predictor of AF,but other pathologic features of chronic hypertension including left ventricular hypertrophy, and impaired diastolic dysfunction are also associated with AF.

Pathophysiology Thrombogenesis in AF is not fully elucidated. Pathophysiology The mechanisms underlying thromboembolism with SEE are similar to that of AF-related strokes.

Pathophysiology Multiple mechanisms may explain the association of AF and dementia. HF as an Outcome Associated with AF The FHS uniquely reported the joint incidence of AF and HF and their temporal relationship. Pathophysiology The mechanisms linking AF to MI are not completely understood. Pathophysiology The mechanisms underlying the AF-VTE association are inexplicable. Conclusion Over the last 50 years, the FHS and other epidemiological studies have yielded a breadth of data associating various RFs with risk of AF and providing insight into their mechanistic link to AF genesis.

Figure 2. Abbreviations and acronyms AA African Americans AF Atrial fibrillation APD Action potential duration ARIC Atherosclerosis Risk in Communities Study BMI Body mass index CI Confidence interval CRF Cardiorespiratory fitness EAT Epicardial adipose tissue ERP Effective refractory period FHS Framingham Heart Study GWAS Genome-wide association study HF Heart failure HFpEF Heart failure with preserved ejection fraction HFrEF Heart failure with reduced ejection fraction HR Hazard ratio LAA Left atrial appendage MESA Multi-Ethnic Study of Atherosclerosis MI Myocardial infarction OR Odds ratio OSA Obstructive sleep apnea PV Pulmonary vein RAAS Renin-angiotensin-aldosterone system RF Risk factor SCD Sudden cardiac death SEE Systemic embolism events SNP Single-nucleotide polymorphism SR Sarcoplasmic reticulum VTE Venous thromboembolism.

Footnotes Disclosures: Laila Staerk has received research funding from Boehringer Ingelheim. Sherer: none Darae Ko: none Emelia J. Benjamin: none Robert H. Helm: none. References 1. Lip GY, Beevers DG. ABC of atrial fibrillation. History, epidemiology, and importance of atrial fibrillation. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. Stroke severity in atrial fibrillation. The Framingham Study. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study.

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Shan H, Zhang Y, Lu Y, Zhang Y, Pan Z, Cai B, Wang N, Li X, Feng T, Hong Y, Yang B. Downregulation of miR and miR contributes to nicotine-induced atrial remodelling in canines. Wang H, Yang B, Zhang L, Xu D, Wang Z. Direct block of inward rectifier potassium channels by nicotine. Toxicol Appl Pharmacol. Wang H, Shi H, Zhang L, Pourrier M, Yang B, Nattel S, Wang Z. Effects on cloned Kv4. Stamler R, Stamler J, Riedlinger WF, Algera G, Roberts RH. Weight and blood pressure.

Findings in hypertension screening of 1 million Americans. Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS. Prevalence of obesity, diabetes, and obesity-related health risk factors, Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P, Jr, Razak F, Sharma AM, Anand SS, Investigators IS Obesity and the risk of myocardial infarction in 27, participants from 52 countries: a case-control study.

Lauer MS, Anderson KM, Kannel WB, Levy D. The impact of obesity on left ventricular mass and geometry. Gottdiener JS, Reda DJ, Williams DW, Materson BJ. Left atrial size in hypertensive men: influence of obesity, race and age.

Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.

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J Am Coll Cardiol. Powell BD, Redfield MM, Bybee KA, Freeman WK, Rihal CS. Association of obesity with left ventricular remodeling and diastolic dysfunction in patients without coronary artery disease. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, Larson MG, Kannel WB, Vasan RS. Obesity and the risk of heart failure. Obesity and the risk of new-onset atrial fibrillation.

Frost L, Hune LJ, Vestergaard P. Overweight and obesity as risk factors for atrial fibrillation or flutter: the Danish Diet, Cancer, and Health Study.

Murphy NF, MacIntyre K, Stewart S, Hart CL, Hole D, McMurray JJ. Long-term cardiovascular consequences of obesity: year follow-up of more than 15 middle-aged men and women the Renfrew-Paisley study Eur Heart J. Wanahita N, Messerli FH, Bangalore S, Gami AS, Somers VK, Steinberg JS. Atrial fibrillation and obesity-results of a meta-analysis.

American heart journal. Tedrow UB, Conen D, Ridker PM, Cook NR, Koplan BA, Manson JE, Buring JE, Albert CM. Gami AS, Hodge DO, Herges RM, Olson EJ, Nykodym J, Kara T, Somers VK. Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. Aronis KN, Wang N, Phillips CL, Benjamin EJ, Marcus GM, Newman AB, Rodondi N, Satterfield S, Harris TB, Magnani JW, Health ABCs Associations of obesity and body fat distribution with incident atrial fibrillation in the biracial health aging and body composition cohort of older adults.

Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden.

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