Atrial Fibrillation - Update

Summarized by Robert W. Griffith, MD
June 4, 2002 (Reviewed: June 29, 2004)

Introduction

Atrial fibrillation (AF) is the commonest cardiac arrhythmia, and is increasing in frequency. It's more prevalent as people get older, but it's also more common after adjustment for age and structural heart disease. Professor Peters and his colleagues at St Mary's Hospital, London, UK have summarized the progress made in understanding AF over the last decade, and the main points are recapped here.

Epidemiology

Today, more than 5% of those over 65 have AF. And most of these cases have underlying structural heart disease, which may be hypertensive, ischemic, or valvular in nature. The risk factors for AF include: male sex, hypertension (seen in 14% of cases), diabetes, thyrotoxicosis, heart failure, valvular disease, and excess alcohol intake. Myocardial infarction is a risk factor in men only. Rarely, AF occurs in a familial pattern; it's probable that more than one gene is involved.

The chief consequence of AF is an increased likelihood of stroke; this occurs in 1.5% of persons with AF in their 50s, to a 23.5% risk for those in their 80s. Mortality rates are doubled, in both sexes, due to stroke, heart failure, or myocardial infarction.

Classification

AF can be termed Acute (a first attack), or Recurrent. If episodes stop spontaneously, it's called Paroxysmal AF, if electrical or pharmacological cardioversion is needed it's Persistent AF. If episodes cannot be stopped by cardioversion, or if they have lasted a year without attempts at cardioversion, the AF is regarded as Permanent.

One type of AF, called Focal, is characterized by fibrillation initiated at one or more focal ectopic sources, often in a structurally normal heart. This type (which may be paroxysmal or permanent) is commoner in patients in their 50s and 60s, and is three times more frequent in men.

Pathology

Shortening of the electrical refractory period (the unexcitable period) is fundamental to the physiological change of AF. Younger patients with healthy hearts and paroxysmal AF tend to have a 'trigger-predominant' mechanism, i.e. something sets off abnormal excitation that spreads around the atrial myocardium, while older patients with structural heart disease and permanent AF have a 'substrate-predominant' mechanism, due to an abnormal atrial tissue substrate. The atria adapt to fibrillation by progressively shortening their refractory periods, leading to the adage "atrial fibrillation begets atrial fibrillation".

The responsible excitatory foci are often to be found in the sleeves of myocardium that extend into the proximal pulmonary veins. Less common sites are the proximal superior vena cava, and other parts of either atrium. How a focus is triggered, and what triggers it, is still an open question.

With fibrillation, the atria fail to contract adequately, and stasis occurs. This is most marked in the left atrium, the usual site for thrombus formation in these patients. Anticoagulation is therefore an important step in keeping morbidity and mortality low.

Diagnosis

AF is diagnosed from the history, clinical exam, and a 12-lead ECG. Holter monitoring can help detect paroxysmal AF in the absence of symptoms. An echocardiogram is helpful in estimating the size and functioning of the heart chambers.

Management

Early restoration of sinus rhythm is the first step to consider. This conversion can be achieved pharmacologically or electrically. If AF has existed for 48 hours, patients need to be adequately anticoagulated before cardioversion is attempted. (Trans-esophageal echocardiography can detect the presence of atrial thrombi.)

Medicinal cardioversion: Flecainide, given intravenously, is very effective if given within 24 hours of the onset of AF. Dofetilide may be used with fair results if AF has been present for a longer period, but it may provoke ventricular arrhythmias, so its use requires hospitalization. Amiodarone is probably the best drug for more persistent AF, combining effectiveness (up to 68%) and comparative safety.

Electrical cardioversion: External cardioversion (i.e. using paddles applied to the chest wall) under general anesthesia is a safe and effective procedure in cases of persistent AF. If it isn't successful, pretreatment with class III anti-arrhythmic agents (sotalol, amiodarone, ibutilide) can help to reduce the threshold for atrial defibrillation. Class I-C agents ((e.g. flecainide) can also be used as pretreatment for direct cardioversion.

Internal electrical cardioversion involves percutaneous electrode catheters placed in the heart under sedation that deliver shocks at specific sites (the right atrium and coronary sinus). Sinus rhythm is restored in 90% of cases where external cardioversion has failed. The same approach can be used for implantable atrial defibrillators. Early, repeated defibrillation should, theoretically, produce 'remodelling' so that the refractory period is gradually restored, but this technique is not used widely.

Maintaining sinus rhythm: Sotalol, flecainide, propafenone, and amiodarone are all effective in suppressing paroxysms of AF. Atrial pacing is also effective, by suppressing focal ectopic beats, and reducing delays in conduction and the spread of refractoriness. Pacemakers with complex algorithms are particularly successful.

Ablation of foci: Mapping to detect arrythmogenic foci in the pulmonary veins is done using percutaneous catheters. Radiofrequency energy is then delivered to cause localized necrosis. Alternatively, the sleeves of myocardium extending into the veins can be ablated. In patients with only one focus, success rates are near 90%, but this falls to about 50% in those with multiple (three or more) foci.

In a surgical approach, called the Maze operation, the atria are dissected into segments, which are then rejoined by sutures; this reduces the amount of tissue in which waves of fibrillation can iterate. Mortality is about 3%, but success rates are as high as 95%.

Controlling ventricular rate: The calcium-channel blockers diltiazem and verapamil are superior to digoxin for controlling the ventricular rate in patients with AF and ventricular tachycardia. Chronic amiodarone treatment also slows ventricular rates. As a last resort, the atrioventricular node can be ablated and a permanent pacemaker implanted.

Preventing thromboembolism

As stated already, antithrombotic treatment is necessary for patients within 48 hours of onset of AF and in those undergoing cardioversion. The need for long-term anticoagulation is a risk-benefit evaluation. In this case, the benefit is avoidance of ischemic stroke, while the risk is that of the side effects of anticoagulation -- chiefly hemorrhage.

To evaluate the potential benefit, consider the risk factors for stroke in people with AF:

• Previous transient ischemic attack (TIA) or stroke
• Age over 65
• Hypertension
• Diabetes
• Heart failure
• Structural heart disease (including rheumatic valvular disease)
• Left ventricular systolic dysfunction

Results from pooled studies show that correctly dosed warfarin therapy reduces the risk of ischemic stroke in AF patients by 68%, and cuts mortality by 33%. Aspirin is clearly less effective, and should only be used in those who have no additional risk factors for stroke, or who cannot tolerate warfarin.

Conclusion

This summary has only been able to hit a few of the highlights in Professor Peters' excellent review. For instance, he includes an algorithm for the management of AF, based on the latest results from clinical trials. The overall picture is one of optimism, with the future focus likely to be on curing AF, rather than on cardioversion followed by suppression of future episodes.

Source

• Atrial fibrillation: strategies to control, combat, and cure. NS. Peters, RJ. Schilling, P. Kanagaratnam,  et al., Lancet, 2002, vol. 359, pp. 593--603

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