The normal heart rhythm, designated sinus rhythm, is the result of coordinated action from specialised cells in the atria and the ventricles of the heart. Regular electronic activity in the atrial sinus node triggers this process and determines the rate at which the heart beats. The electronic activity of the atria reaches the ventricles following a short pause of the depolarisation wave in the atrio-ventricular node. This conduction delay allows the ventricles to fill with blood. The electronic signal is subsequently conducted through the ventricles such that the muscular contraction of the ventricles takes places in a coordinated manner.
Atrial fibrillation is characterised by uncoordinated electric activity in the atria with consequent deterioration of atrial function. This rhythm abnormality is the most common sustained cardiac arrhythmia. Because of the altered mechanics of the atria, impaired blood flow occurs and stasis of the blood may result in clots. This thrombotic material can then migrate from the atria into the arterial system (embolisation) with often dire clinical sequelae. Atrial fibrillation has negative consequences on cardiac efficiency and function. Since the normal atrial contraction (“kick”) is lacking, there is incomplete filling of the cardiac ventricles prior to contraction. In addition, the atrioventricular node is stimulated in a haphazard manner, leading to irregular and usually fast ventricular activity. Both factors may lead to further deterioration of cardiac function and thus trigger the clinical condition of heart failure.
The incidence and prevalence of atrial fibrillation increase sharply with age. The lifetime risk of developing the arrhythmia has been estimated to be as high as 25%. The prevalence of atrial fibrillation is at least 10% in elderly men and women over 80 years of age. The rhythm abnormality not only is the most common arrhythmia in clinical practice but also accounts for about a third of all hospital admissions for rhythm abnormalities. The condition results in substantial mortality and morbidity from stroke and heart failure and is associated with significant cost. The mortality rate of patients with atrial fibrillation is about two times higher than that of comparable subjects with normal sinus rhythm.
The clinical management of atrial fibrillation has been described in considerable detail in recent guidelines of American and European professional societies as well as in a clinical review update, and the interested reader is referred to these excellent documents for additional information.
In a considerable number of patients, no specific cause can be found for arrhythmia. Some morbid conditions increase the likelihood that atrial fibrillation may develop: these include hypertension, obesity, heart failure, coronary artery disease and other diseases of the heart, including valve abnormalities, specifically disease of the mitral valve resulting from rheumatic heart disease or endocarditis (see Table 1). The increase of the rhythm abnormality with age is also indicative of a degenerative component in the disease process, such as fibrosis of the cardiac conductance system and loss of atrial muscle mass. Atrial fibrillation may also occur as a result of concomitant hyperthyroidism, infection and fever, diverse metabolic disorders as well as in postoperative settings. In such circumstances, sinus rhythm usually re-establishes quickly when the external trigger is removed.
When atrial fibrillation occurs in attacks and the episodes of rhythm abnormality are shorter than one week, it is called paroxysmal – including periods of normal rhythm. Atrial fibrillation is defined as persistent when the arrhythmia does not disappear, and the term permanent or chronic atrial fibrillation is employed when the arrhythmia is continuous. This can occur either when attempts to convert the irregular rhythm to sinus rhythm using pharmacologic or electrical means are unsuccessful, or when such attempts are deemed not useful or inappropriate. In the latter instance, the presence of atrial fibrillation is accepted and therapeutic measures are aimed at preventing long-term complications.
Clinical evaluation and diagnosis
Physical examination findings of irregular pulse and heart rate are suggestive of the presence of atrial fibrillation. Further examination may also show evidence of associated comorbid conditions such as fever, hypertension, valvular heart disease or heart failure.
Establishment of a final diagnosis of atrial fibrillation is relatively simple and can be made by standard 12-lead electrocardiography. The presence of irregular fibrillatory waves in combination with irregular ventricular response (QRS complex) is pathognomic. Even in asymptomatic subjects, the diagnosis can thus be established without major problems.
Echocardiography is the technique of choice to investigate possible causes for the rhythm abnormality, to determine its consequences on cardiac function and to plan therapeutic measures. The most relevant echocardiographic parameters are those reflecting left ventricular and valvular function, the presence (or absence) of other structural cardiac abnormalities as well as the dimension of the left atrium. If the left atrium is dilated – for example, >50 mm – restoration of sinus rhythm is usually not an option.
1. Prevention of thromboembolic complications
Prevention of thromboembolism and associated clinical sequelae is a major therapeutic objective. To this end, administration of antithrombotic agents is almost invariably necessary, usually by subcutaneous or intravenous administration of heparin in in-hospital settings, and using oral anticoagulants (vitamin K antagonists) in ambulant patients. The recommended target of anticoagulation is that of international normalised ratio (INR) between two and three. Since the risk of the most feared complication, ischaemic stroke, is particularly high in people over 75 years of age, elderly subjects are the main targets for antithrombotic treatment, even more so in the presence of structural heart disease, hypertension, diabetes mellitus and previous stroke or TIA (see Box 2).
Long-term anticoagulation is usually recommended in all patients with atrial fibrillation, with the exception of the (sub)group of patients characterised by young (<65 years) age without previous stroke and without cardiac abnormalities. In such subjects, aspirin may be an alternative treatment option. In a recent meta-analysis, aspirin proved to be better than placebo (or no drug) in preventing stroke, vascular death or myocardial infarction. The efficacy of aspirin may be derived from the drug's general effects on platelet aggregation – preventing the development of new atherosclerotic complications – and less from its influence on thromboembolism associated with the rhythm abnormality itself.
2. Rhythm restoration and rhythm control
Normalisation of rhythm is often possible when atrial fibrillation has developed acutely. Under such circumstances, pharmacologic and electrical cardioversion are both appropriate and often successful. Because thrombus formation is usually not an issue when the arrhythmia has just commenced, anticoagulant therapy is not mandatory when rhythm restoration takes place within two days following its onset. Still, even then, many cardiologists prefer to perform oesophageal echocardiographic examination prior to attempted cardioversion to exclude the presence of a small thrombus.
Direct-current electrical cardioversion is recommended when atrial fibrillation is accompanied by a rapid ventricular response not reactive to pharmacologic measures, or when the arrhythmia is accompanied by myocardial ischaemia or angina, severe hypotension or heart failure. It is customary to start with energy levels of at least 100 joules, although some prefer 200 joules. If unsuccessful, energy levels should be increased by 100 joules until the maximum level of 40 joules has been reached. Pretreatment with beta-blockers or antiarrhythmic drugs may increase the success rate of electrical cardioversion.
Some trials have compared outcomes of rhythm- versus rate-control strategies. A trend towards lower mortality in the rate-control strategy has been observed. It is therefore reasonable to conclude that rate control is a sensible approach in elderly subjects without major symptoms.
Drugs and (invasive) ablative procedures are effective for both rate and rhythm control. Beta-blockers are effective for control of ventricular response, in particular in states of elevated adrenergic tone such as in postoperative atrial fibrillation. The calcium antagonists verapamil and diltiazem are also commonly used. However, all of these drugs should be used with considerable caution in patients with cardiac abnormalities because they may decrease cardiac function or exert other unwanted effects on the heart.
Digoxin used to be the drug of choice in atrial fibrillation, but its position is being overtaken by beta-blockers. Combination therapy of digoxin and a beta-blocker is often necessary in many patients with permanent atrial fibrillation. There is usually no role for digoxin in subjects with paroxysmal atrial fibrillation because recurrence is not modified by this drug. The same is true for such older antiarrhythmic drugs as procainamide and quinidine.
Amiodarone is an alternative agent for heart rate control when other, more conventional measures are ineffective. However, the drug has serious side-effects, and its long-term employment for this indication is better left to cardiac specialists. Amiodarone is effective in controlling rate in subjects with atrial fibrillation and heart failure. Electrical cardioversion is an alternative therapeutic approach in such patients.
Antiarrhythmic drugs may be useful to restore sinus rhythm. Different drugs can be used, including propafenon, ibutilide and dofetilide, flecainide and disopyramide. These drugs can also be used in paroxysmal atrial fibrillation.
Ablation procedures for atrial fibrillation have become more popular but are technically difficult and require significant experience. Such procedures are not without risk, and although favourable short-term results have been reported, long-term data are needed to establish the true efficacy of these procedures in “real-life” clinical practice.
- Lip GY, Tse HF. Management of atrial fibrillation. Lancet 2007;370:604-18.
- ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Europace 2006;8(9):651-745.