Every patient who presents with AF for the first time is considered a patient with first diagnosed AF, irrespective of the duration of the arrhythmia or the presence and severity of AF-related symptoms.
Paroxysmal AF is self-terminating, usually within 48 h, but may continue for up to 7 days.
Persistent AF is present when an AF episode either lasts longer than 7 days or requires termination by cardioversion, either with drugs or by direct current cardioversion.
Long-standing persistent AF has lasted for ≥1 year when it is decided to adopt a rhythm control strategy.
Permanent AF is said to exist when the presence of the arrhythmia is accepted by the patient (and physician).
Silent AF is defined as asymptomatic AF often diagnosed by an opportune ECG or rhythm strip. Any of the above mentioned types of AF may be silent (ie, asymptomatic). It is recognized that a particular patient may have AF episodes that fall into one or more of these categories.
AF is associated with increased rates of death, stroke and other thrombo-embolic events, heart failure and hospitalizations, impaired quality of life, reduced exercise capacity, and left ventricular dysfunction. Death rates are doubled by AF, independently of other known predictors of mortality. Stroke in AF is often severe and results in long-term disability or death. Approximately every fifth stroke is due to AF. Quality of life and exercise capacity are impaired in patients with AF. Patients with AF have a significantly poorer quality of life compared with healthy controls, the general population, or patients with coronary heart disease in sinus rhythm. Hospitalizations due to AF account for one-third of all admissions for cardiac arrhythmias and thus pose a significant economic burden to the healthcare system.
Structural changes as cause for atrial fibrillation
Any kind of structural heart disease may trigger a slow but progressive process of structural remodeling in both the ventricles and the atria. In the atria, proliferation and differentiation of fibroblasts into myofibroblasts and enhanced connective tissue deposition and fibrosis are the hallmarks of this process. Structural remodeling results in electrical dissociation between muscle bundles and local conduction heterogeneities facilitating the initiation and perpetuation of AF. This electro-anatomical substrate permits multiple small re-entrant circuits that can stabilize the arrhythmia.
After the onset of AF, changes of atrial electrophysiological properties, mechanical function, and atrial ultrastructure occur with different time courses and with different pathophysiological consequences. Shortening of the atrial effective refractory period within the first days of AF has been documented in humans. The electrical remodeling process contributes to the increasing stability of AF during the first days after its onset. Perturbation of atrial contractile function also occurs within days of AF. Even in patients with ‘lone’ AF, fibrosis and inflammatory changes have been documented.
The initiation and perpetuation of a tachyarrhythmia requires both triggers for its onset and a substrate for its maintenance. These mechanisms are not mutually exclusive and are likely to co-exist at various times.
Focal mechanisms potentially contributing to the initiation and perpetuation of AF have attracted much attention. Cellular mechanisms of focal activity might involve both triggered activity and re-entry. Because of shorter refractory periods as well as abrupt changes in myocyte fiber orientation, the pulmonary veins (PVs) have a stronger potential to initiate and perpetuate atrial tachyarrhythmias.
Multiple wavelet hypothesis
According to the multiple wavelet hypotheses, AF is perpetuated by continuous conduction of several independent wavelets propagating through the atrial musculature in a seemingly chaotic manner. Fibrillation wavefronts continuously undergo wavefront–waveback interactions, resulting in wavebreak and the generation of new wavefronts, while block, collision, and fusion of wavefronts tend to reduce their number. As long as the number of wavefronts does not decline below a critical level, the multiple wavelets will sustain the arrhythmia. While in most patients with paroxysmal AF localized sources of the arrhythmia can be identified, such attempts are often not successful in patients with persistent or permanent AF.
The combination of local shortening of the action potential and a stabilizing mechanism, e.g. a branching structure in the vicinity of an orifice like a PV ostium, can produce activation patterns consisting of a wavefront with high rate, surrounded by activation with hierarchically lower frequencies and less organization. Ablation of sites with a high dominant frequency, mostly located at or close to the junction between the PVs and the left atrium, results in progressive prolongation of the AF cycle length and conversion to sinus rhythm in patients with paroxysmal AF, while in persistent AF, sites with a high dominant frequency are spread throughout the entire atria, and ablation or conversion to sinus rhythm is more difficult.