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More on AF

AF and its Management

1. Overview
2. Epidemiology and risk factors for AF
3. Symptoms of AF
4. Consequences of AF
5. Management of AF
6. Future of AF Management

1. Overview

Atrial fibrillation (AF)i, the most common cardiac arrhythmiai (abnormal heart rhythm) seen in clinical practice1, is a condition in which the atria, the upper chambers of the heart, beat in an uncoordinated and disorganised fashion, resulting in an irregular and often rapid heart rhythm leading to deterioration of the heart’s mechanical function1.
In AF, control of heart rhythm is taken away from the sinoatrial node (the heart’s natural pacemaker), and replaced by abnormal electrical activity coming from other areas of the atria. As a result, the atria beat rapidly and irregularly at rates of 400-600 beats per minute (bpm)2. As the atrioventricular node – the area that controls the passage of electrical impulses from the atria to the ventricles – filters some of these signals, the increase in ventricular rate can be in the order of 110-180 bpm.


AF can be classified into three groups:
• Paroxysmal - Recurrent episodes that terminate within seven days.
• Persistent - AF sustained beyond seven days.
• Permanent - Long standing AF in which cardioversioni is either ineffective or has not been attempted.
These categories are not mutually exclusive – a patient may have several episodes of paroxysmal AF and occasional persistent AF, or vice versa1. A paroxysmal or persistent AF patient may become permanent over time.

 
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2. Epidemiology and risk factors for AF

AF is one of the growing cardiovascular conditions of the 21st century, along with congestive heart failurei, type-2 diabetes, and metabolic syndrome14. In 2001, AF affected about 2.3 million people in North America and 4.5 million people in the European Union1,3. These figures will rise as our populations age, as AF incidence increases with age4.

The estimated prevalence of AF is less than one percent in the general population3, less than 0.1 percent per year in people younger than 40 years, more than 1.5 percent per year among women, and two percent among men older than 80 years4. Approximately 30-45 percent of cases of paroxysmal AF and 20-25 percent of cases of persistent AF occur in young patients without demonstrable underlying disease, so-called “lone AF” 4.

However, the incidence of AF increases with age to eight percent in people 80 years and older5, and given the ageing population AF, is emerging as a growing public health concern1.

A Danish study shows that, for the past 20 years, hospital admissions for AF have increased by 60 percent due to the ageing population, a rising prevalence of chronic heart disease and other factors6,7. In the US, hospitalisations for AF have increased two to three-fold in recent years8. The bulk of medical costs, 70 percent, are driven by inpatient care and interventional procedures9.

There are several risk factors for developing AF beyond simply age; these include obesity, hypertension, myocardial infarction (MI)i, congestive heart failure (CHF), and valvular heart diseases.

Although AF may occur in the elderly without underlying heart disease, the changes in cardiac structure and function that accompany ageing, such as reduced contractility of the heart muscle, may be associated with AF1.

According to the Framingham Heart Study, the lifetime risks for the development of AF are one in four for men and women aged 40 years and older. These lifetime risks remain high even in the absence of previous CHF or MI (one in six)10.

 
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3. Symptoms of AF

Common symptoms include palpitations, chest pain, breathlessness, fatigue or light-headedness. However, AF may be asymptomatic and is only diagnosed because of investigations for other conditions, such as an embolici complication or exacerbation of heart failure1.

Individuals may experience periods of both symptomatic and asymptomatic AF. Over time, symptomatic palpitations may disappear and patients who are in permanent AF may become asymptomatic; this is particularly common among the elderly. Some patients experience symptoms only during paroxysmal AF, or only intermittently during sustained AF1. Unfortunately AF may often go undetected and untreated because it can be asymptomatic in 15-35 percent of cases11.

 
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4. Consequences of AF

AF is a complex, progressive cardiovascular disease with serious consequences, including CHF, strokei and doubling the risk of death12,13,14.


Table 1 : AF Worsens the Prognosis of Patients with Co-morbidities


AF impairs quality of life because of patients are unable to perform normal daily activities due to the risk of exacerbating symptoms15.

AF is one of the most important risk factors for stroke16. People who have AF have a five-fold increase in their risk of stroke16. Strokes in patients with AF are in general severe, associated with higher risk of fatality and prone to early and long-term recurrence17. AF increases the risk of stroke because the irregular heart beat causes slower blood flow, which promotes pooling of blood in the atria and formation of clots that may travel to the cerebral vessels and cause a stroke18. Beyond stroke, AF is an independent risk factor for sudden cardiac death with a risk ratio of 1.3119.

AF is an independent predictor of heart failure in men. In women AF increases the risk of heart failure by 3.420. People with AF and heart failure find the conditions exacerbate one another.
 

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5. Management of AF

Maintenance of normal sinus rhythmi is often seen as the ultimate goal of therapy for patients with AF but the management of patients with AF is a major challenge1 because no single therapeutic approach can be recommended21. The American College of Cardiology (ACC), American Heart Association (AHA) and European Society of Cardiology (ESC) (American Heart Association Taskforce/European Society of Cardiology) produces recommendations on how to manage AF based on patients’ AF classification and co-morbidities1.


Initial management primarily involves oral anticoagulation (where warranted) and a rate controli or rhythm controli strategy. Current AF therapies focus on restoring and maintaining the heart's normal sinus rhythm and controlling heart ratei. The primary aim of this approach is to manage the arrhythmia itself, as well as preventing stroke1. None of the current anti-arrhythmic drugs have proven any reduction of morbidity or mortality.

The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) study compaired rhythm versus rate control. It found no difference in mortality or stroke rate between patients assigned to one strategy or the other, but there was a lower risk of adverse events with the rate control strategy22,23.

A follow up investigation concluded that maintaining normal sinus rhythm is an important strategy for survival; however, this benefit may be masked by the adverse events associated with the currently available anti-arrhythmic agents24.

Regardless of whether a rate control or rhythm control strategy is pursued, therapy preventing thromboembolismi is essential1.

AF treatment objectives can be achieved with pharmacological and non-pharmacological treatment options:

Pharmaceuticals
Drug therapy is the first line treatment choice in AF management. Antiarrhythmic drugs (AADs) are widely used, despite the fact that current agents may have limited efficacy, poor tolerability, and potential for serious ventricular proarrhythmia and / or organ toxicity25. Severe side effects have been observed in previous AAD clinical trials and, as such, safety is a key consideration in the choice of antiarrhythmic medications26.

The majority of AADs come from four broad categories, defined by their dominant electrophysiological effect1; sodium channeli blockers, beta blockers, potassium channel blockersi, and nondihydropyridine calcium channel blockers. Sodium channel blockers are further divided into three types: 1A with an increased duration of action potentiali, 1B, with a decreased duration of action potential, and 1C, which have no effect on duration of action potential. Other AADs not included in this classification that work by other mechanisms, such as digoxin and adenosine.

 

Table 2 : Four main groups of AADs

 

Cardioversion
Cardioversion resets and restores sinus rhythm in patients with persistent AF. It can be achieved with drugs or electric shocks. The need for cardioversion may be immediate when the arrhythmia is the main factor responsible for acute heart failure, hypotension, or worsening of angina pectoris in a patient with coronary artery disease. Cardioversion carries a risk of thromboembolism unless anticoagulation prophylaxis is initiated prior to the treatment. There is no evidence that the risk of thromboembolism or stroke differs between pharmacological and electrical methods1.

Ablation
Catheter ablation involves the insertion of catheters into the heart through which radiofrequency waves are transmitted to destroy areas of tissue that are the source of the abnormal electrical signals. This interventional procedure is complex and can only be successfully performed in highly specialised centres.

Ablation can be used for rate control. Atrioventricular nodal ablation in conjunction with permanent pacemaker implantation provides highly effective control of the heart rate and improves symptoms in selected patients with AF. In general, patients most likely to benefit from this strategy are those with rapid ventricular rate during AF that cannot be controlled efficiently with rate or rhythm control27.
 

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6. Future of AF management

Although pacemakers, defibrillators, radiofrequency ablation, and surgery have a place in the treatment of atrial fibrillation, drug therapy remains first-line therapy. Because of these drugs’ serious side effects, the management of AF is a prescribing challenge, involving trade-offs in risks and benefits. Furthermore, current therapies focus on symptomatic relief and prevention of recurrences but not outcomes, so there remains a substantial requirement for improved antiarrhythmic agents to manage the overall burden of the disease including both symptoms and long term cardiovascular outcomes28.


References :

1. Fuster V et al.ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. European Heart Journal (2006) 27, 1979-2030.
2. Johan E.P. Waktare. Atrial Fibrillation. Circulation 2002;106;14-16. Available at: http://www.wilmingtoncardiology.com/articles/atrialfibrillation.pdf. Last accessed 25th August 2008.
3. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001; 285:2370–5.
4. Psaty BM, Manolio TA, Kuller LH, et al. Incidence of and risk factors for atrial fibrillation in older adults. Circulation 1997; 96:2455–61.
5. Furberg CD, Psaty BM, Manolio TA, et al. Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study). Am J Cardiol 1994;74:236-41.
6. Revised ACC/AHA/ESC Guidelines on atrial fibrillation recommend new approach. Stroke risk should determine anti-clotting treatment for people with irregular heartbeat. Available at: http://www.acc.org/qualityandscience/clinical/guidelines/atrial_fib/pdfs.... Last accessed: 05 November 2008.
7. Friberg J, Buch P, Scharling H, et al. Rising rates of hospital admissions for atrial fibrillation. Epidemiology 2003;14:666–72.
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9. Ringborg A, Nieuwlaat R, Lindgren P, Jönsson B, Fidan D, Maggioni AP, Lopez-Sendon J, Stepinska J, Cokkinos DV, Crijns HJ. Costs of atrial fibrillation in five European countries: results from the Euro Heart Survey on atrial fibrillation. Europace. 2008 Apr;10(4):403-11. Epub 2008 Mar 7.
10. Lloyd-Jones et al. Lifetime Risk for Development of Atrial Fibrillation: The Framingham Heart Study. Circulation. 2004; 110:1042-1046.
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12. Stewart S, Hart CL, Hole DJ, et al. A population-based study of the long-term risks associated with atrial fibrillation: 20-year follow-up of the Renfrew/Paisley study. Am J Med. 2002; 113:359–64.
13. Benjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB, Levy D.  Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998; 98: 946-52.
14. Wolf PA, Dawber TR, Thomas HE Jr, Kannel WB.  Epidemiologic assessment of chronic atrial fibrillation and risk of stroke: the Framingham study. Neurology. 1978; 28: 973-77.
15. Hamer ME, Blumenthal JA, McCarthy EA, et al. Quality-of-life assessment in patients with paroxysmal atrial fibrillationi or paroxysmal supraventricular tachycardia. Am J Cardiol. 1994;74:826–9.
16. PA Wolf, RD Abbott and WB Kannel. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991;22;983-988
17. Ferro JM. Atrial fibrillation and cardioembolic stroke. Minerva Cardioangiologica. 2004, 52, 111-124.
18. Medline Plus medical encylopedia. Stroke secondary to cardiogenic embolism. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000735.htm. Last accessed on August 5, 2008.
19. Pedersen OD, Abildstrom SZ, Ottesen MM, et al, on behalf of the TRACE study investigators. Increased risk of sudden and non-sudden cardiovascular death in patients with atrial fibrillation/flutter following acute myocardial infarction. Eur Heart J 2006;27:290-5.
20. Stewart S; Hart CL; Hole DJ; McMurray JJ. A population-based study of the long-term risks associated with atrial fibrillation: 20-year follow-up of the Renfrew/Paisley study. American Journal of Medicine. 113(5):359-64, 2002 Oct 1.
21. Stanley Nattel. Rhythm versus rate control for atrial fibrillation management: what recent randomized clinical trials allow us to affirm. JAMC. 4 MARS 2003; 168 (5). Available at: http://www.cmaj.ca/cgi/reprint/168/5/572. Last accessed: 8 April 2005.
22. Sherman DG, Kim SG, Boop BS, et al. Occurrence and characteristics of stroke events in the Atrial Fibrillation Follow-up Investigation of Sinus Rhythm Management (AFFIRM) study. Arch Intern Med 2005; 165:1185–91.
23. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators.  A Comparison of Rate Control and Rhythm Control in Patients with Atrial Fibrillation. NEJM. 2002, 347 (23):1825-1833.
24. AFFIRM Investigators. Relationships between sinus rhythm, treatment and survival in the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) Study. Circulation. 2004 Mar 30;109(12):1509-13. Epub 2004 Mar 8.
25. Doggrell SA, Hancox JC. Dronedarone: an amiodarone analogue. Expert Opin Investig Drugs. 2004; 13: 415-26.
26. Van Gelder IC et al. A comparison of rate control and rhythm control in patients with recurrent persistent atial fibrillation. Study Group: a comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillationi. New England Journal of Medicine 2002, 347: 1834-40.
27. Wood MA, Brown-Mahoney C, Kay GN, et al. Clinical outcomes after ablation and pacing therapy for atrial fibrillation: a meta-analysis. Circulation. 2000;101:1138-44.
28. Morrow et al. New antiarrhythmic drugs for establishing sinus rhythm in atrial fibrillation: What are our therapies likely to be by 2010 and beyond? American Heart Journal.Volume 154, Number 5, p824.

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