Atrial Fibrillation | UMCG | Atrial Fibrillation
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Atrial Fibrillation

What is atrial fibrillation?

Atrial fibrillation – a growing epidemic

Atrial fibrillation is the most common cardiac arrhythmia, affecting 1 in 4 persons over the age of 55 years. The prevalence of atrial fibrillation increases with age; from 2-3% in individuals >60 years to 8-10% in those >80 years. Atrial fibrillation affects 33.5 million people worldwide, 8.8 million in the European Union.1,2 With the increased survival of individuals with chronic cardiovascular disease, the prevalence and numbers of individuals with atrial fibrillation will grow exponentially.

Consequences of atrial fibrillation

Atrial fibrillation is accompanied by increased stroke, heart failure, dementia and death risk.3-5 Symptoms associated with atrial fibrillation include palpitations, shortness of breath, and chest pain. Individuals with atrial fibrillation also have decreased exercise tolerance and reduced quality of life. Approximately, two-thirds of all emergency department visits with primary diagnosis of atrial fibrillation result in hospital admissions and one-third of all hospital admissions for arrhythmia are attributable to atrial fibrillation.6 As a consequence, atrial fibrillation is associated with high healthcare costs. Atrial fibrillation places a large burden on both individuals and public health systems, therefore prevention of atrial fibrillation should be the ultimate goal.

Risk factors of atrial fibrillation

Atrial fibrillation affects individuals with a variety of risk factor patterns and underlying heart diseases. Traditional risk factors for atrial fibrillation are advancing age, male sex, diabetes, hypertension, valve disease, myocardial infarction, and heart failure.7 Recently, the list has expanded with obesity, inactivity, elevated blood pressure within normal ranges, and the list keeps growing.8 It has been estimated that ~60% of atrial fibrillation can be explained by the presence of 1 or more borderline or elevated risk factor(s). Assuming that these associated risk factors are directly causal to atrial fibrillation, it implies that more than half of the atrial fibrillation burden is potentially avoidable through the optimization of cardiovascular risk factors treatment.9 Lifestyle-related atrial fibrillation risk factors are in theory modifiable, and therefore potential treatment targets.

Genetics of atrial fibrillation

Before genome wide association studies (GWAS), candidate-gene studies screened genes for causative mutations based on assumptions regarding their pathophysiological role, in relatively small patient samples, and found several genetic variants in ion channels, gap junction proteins, atrial natriuretic peptide, inflammatory mediators, renin-angiotensin-aldosterone system and hypercoagulability genes that may relate to atrial fibrillation.10 Within the last years, there is increasing evidence for familial clustering and heritability of atrial fibrillation, and a genetic component to atrial fibrillation in general population.11 In the last 10 years, we and others published genome wide association studies (GWAS) discovering >12 genetic variants associated with atrial fibrillation.12 These novel atrial-fibrillation loci implicating transcription factors related to cardiac development, ion channels, and cellular signaling molecules. Genetic information can be used to infer causal relations between atrial fibrillation and its risk factors, and points towards novel pathways not previously known to be involved in atrial fibrillation.

Management of atrial fibrillation

The acute and chronic management of atrial fibrillation consists of 5 treatment domains, with different desired outcomes and benefit for the patient.13

After acute rate or rhythm treatment in the setting of hemodynamic instability (1st domain), the 2nd domain consists of manage potential underlying causes of atrial fibrillation. This can reduce the cardiovascular risk and improve prognosis and symptoms. In the Routine versus Aggressive upstream rhythm Control for prevention of Early atrial fibrillation in heart failure (RACE 3) study we tests the hypothesis that aggressive upstream rhythm control aiming at optimal management of associated disorders and triggers increases persistence of sinus rhythm compared with conventional rhythm control in patients with short-lasting (i.e., early) atrial fibrillation and mild to moderate early heart failure undergoing electrical cardioversion. Results are expected to presented at the European Society of Cardiology congress in Barcelona September 2017.14

The 3th domain consists of assessing the stroke risk, and treat with anticoagulation. Only for anticoagulation it has been proven that it can improve prognosis by reducing the atrial fibrillation-associated stroke risk. However, the association between atrial fibrillation and stroke is still unclear.15, 16 There seems to be a disconnect between the occurrence of stroke and atrial fibrillation questioning whether atrial fibrillation is causal or just another associated risk marker.17 In the the Reappraisal of Atrial Fibrillation: Interaction between hyperCoagulability, Electrical remodeling, and Vascular Destabilisation in the Progression of atrial fibrillation (RACE V) study we try to elucidate the role of hypercoagulability in atrial fibrillation progression. The 4th domain consists of assessing the heart rate and provide adequate rate control (RACE II study18). We are the leading world opinion leaders on rate control.19 The 5th domain consists of assessing symptoms, and consider a rhythm control treatment strategy (anti-arrhythmic drugs or pulmonary vein isolation, or a combination). Rate and rhythm control treatment strategies are non-inferior to each other regarding cardiovascular morbidity and mortality, as was proven by among others the RACE study20, so treatment decisions are aiming to reduce the symptom burden.

References

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  2. Krijthe BP, et al. Eur Heart J 2013;34:2746-51.
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  8. Kirchhof P, et al. Europace 2012;14:8-27.
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  12. Ellinor PT, et al. Nat Genet 2012; 44:670-675.
  13. Kirchhof P, et al. Eur Heart J 2016: [epublished ahead of print] doi:10.1093/eurheartj/ehw210.
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  17. Van Gelder IC, et al. Eur Heart J 2016; accepted.
  18. Van Gelder et al. N Engl J Med 2010; 362;1363-1373.
  19. Van Gelder, et al. Lancet 2016;388(10046):818-28.
  20. Van Gelder et al. N Engl J Med 2002; 347;1834-1840.