Atrial fibrillation is a highly prevalent arrhythmia, common in the elderly, and often but not always associated with cardiovascular risk. The arrhythmia predominantly emerges against 2 often intermingled backgrounds: increasing age and cardiovascular disease. However, many factors may play an aetiological and/or mechanistic role in the development of this rhythm disturbance, ranging from genetic factors to the consequences of long-term wear and tear associated with underlying cardiovascular and cardiopulmonary disease. The arrhythmia is associated with a substantial risk of all-cause mortality, cardiovascular mortality, and sudden cardiac death, stroke, systemic thromboembolism, heart failure, and acute coronary syndrome. Patients with atrial fibrillation are at high risk of cardiovascular hospitalizations related to these complications and for the management of atrial fibrillation itself. It is far from clear whether and how atrial fibrillation itself is mechanistically linked to these events, but it seems likely that the arrhythmia is central to the development of most of these complications.
The prediction of the occurrence of atrial fibrillation and the recognition of the precise aetiology and mechanism of the arrhythmia would allow the development and introduction of interventions to eliminate or reduce the causative factors, or to stabilize the atria and ward off the development of the arrhythmia. We have substantial information relating to the association of atrial fibrillation, but the details of the interactions between them are largely missing. It is possible to weigh the predictive value of underlying factors and combine them into scoring systems that will predict the long-term development of the arrhythmia. As yet, we do not have any validated methods of foretelling the time of onset of the arrhythmia, although extensive electrocardiograph monitoring, perhaps with implantable devices, might provide such a tool. If we knew when atrial fibrillation would occur, anticoagulant therapy could be introduced prior to the development of the full blown arrhythmia in a timely fashion to prevent the cardio-thrombotic strokes that are associated with the arrhythmia.
Atrial fibrillation generally starts with asymptomatic self-terminating episodes of atrial tachyarrhythmia, which may then progress to more sustained episodes that are more symptomatic and need to be terminated by an intervention such as an antiarrhythmic drug or electrical cardioversion. Eventually, the atrial fibrillation becomes more difficult to terminate, or it recurs so frequently that the patient or the physician decides that the arrhythmia is best left alone, and it is then permanent in nature. This progression may be very brief, prolonged, or in some it may never occur. On average, paroxysmal atrial fibrillation progresses to persistent and/or permanent atrial fibrillation at a rate of about 5% per year. The factors that underlie this progression are poorly understood, but cardiac or pulmonary pathologies have been identified as being important. Only with a better understanding of this process will it be possible to delay or reduce the progression of the arrhythmia, although some headway has been made empirically with the use of antiarrhythmic drugs, upstream therapies such as angiotensin-converting enzyme inhibitors, and left atrial ablation therapy.
Stroke is the most dramatic complication of atrial fibrillation. Not everyone with the arrhythmia develops this complication, but many do. We have effective anticoagulant treatments to greatly reduce the likelihood of stroke in patients with atrial fibrillation, but all anticoagulants carry the inherent risk of hemorrhagic complications. Doctors and patients are therefore wary of such treatment, and would like to be sure that there is a need for anticoagulation in an individual, and the net benefit of prescribing anticoagulant therapy would be positive. A simple assessment of atrial pathophysiology should be a straightforward approach to this problem, but it does not seem to be as good as a comprehensive evaluation of the overall cardiovascular disease status. Scoring systems are currently in vogue to help define thromboembolic risk. The CHA2DS2VASc score is more helpful than the CHADS2 score in predicting those at little or no risk and is being taken up in favor of the CHADS2 schema at present. In parallel with the endeavor to identify patients at risk from thromboembolic stroke, those at risk of bleeding complications must also be recognized to gauge the prospect of achieving a net benefit from recommending anticoagulation therapy. A number of scoring systems have been developed to help the physician accomplish this.
Although stroke is a very obvious untoward outcome in patients with atrial fibrillation, other adverse events are also strongly associated with the arrhythmia. In clinical trial populations and in epidemiological cohorts, mortality is clearly increased, and the excess mortality is cardiovascular in nature, and much of it is sudden. Ventricular arrhythmias may also be increased in patients with atrial fibrillation, but this has not been convincingly demonstrated. Heart failure is aggravated by atrial fibrillation largely because of irregular and uncontrolled ventricular rates and the loss of atrial contraction. Heart failure, whether due to systolic or diastolic dysfunction, leads to the development of atrial fibrillation, and patients with atrial fibrillation are often admitted to the hospital with cardiac decompensation. There is an increased incidence of acute coronary syndrome in patients with atrial fibrillation, probably because patients with coronary disease are more likely to have coronary disease, and the high heart rates seen with the arrhythmia may trigger ischemia. It is important to recognize that a variety of serious cardiovascular outcomes are associated with this arrhythmia.
It is now recognized that atrial fibrillation often occurs within the context of widespread vascular disease, and that the risks associated with atrial fibrillation are multiplied by the association of aortic, peripheral, coronary, or carotid disease. This is particularly obvious with regard to the risk of stroke, but also relates to the increased likelihood of acute coronary syndrome. In the latter context, the management of acute coronary syndrome in patients with atrial fibrillation is a particular problem, especially when acute angioplasty and coronary stenting has been part of the management strategy. The combined use of antiplatelet and anticoagulant therapy is particularly risky with regard to hemorrhagic complications, and the situation must be very carefully managed by careful reassessment of the risks at each time point in the evolution of the coronary event.
The direct management of atrial fibrillation would be best if atrial fibrillation can be suppressed or delayed. Clinical trials have not supported this clinical conviction, and rate control seems to be at least as good. However, our antiarrhythmic armamentarium has been weak and ineffective, and associated with significant cardiac or extracardiac adverse effects. Several new antiarrhythmic drugs have recently been approved, and their preapproval development suggested that they might be superior to our conventional antiarrhythmic therapy. However, recent trial data have cast some doubt on this.
All of the above-mentioned subject matter are discussed in detail in this ClinicalCardiology supplement dealing with atrial fibrillation.