In this arrhythmia, irregular atrial impulses occur at rates over 300/minute, uniform excitation of the atria is no longer possible, and the atria no longer contract synchronously. The ventricular rhythm is irregular but not as rapid as the atrial rhythm because the atrioventricular node blocks many of the atrial impulses. It may occur in otherwise normal hearts, particularly in the elderly: 5% of persons over 65 years of age have atrial fibrillation. However, it also occurs in a variety of pathological conditions, such as rheumatic mitral valve disease, ischemic heart disease, hyperactivity of the thyroid gland, acute infections, particularly when these affect the lungs, high blood pressure, cardiopulmonary surgery. Because the atria no longer contract synchronously, there is stasis of blood in the atria, which facilitates thrombus formation and embolism. The emboli may obstruct blood vessels in lungs and brain, and in the latter case stroke may occur.
The first reference to what may have been atrial fibrillation is about 4000 years old, in the Yellow Emperor’s Classic of Internal Medicine: “When the pulse is irregular and tremulous and the beats occur at intervals, then the impulse of life fades”. According to Luederitz, Shakespeare may have described atrial fibrillation in The Winter’s Tale: “ I have tremor cordis on me: my heart dances; But not for joy, not joy”. The first electrocardiograms of atrial fibrillation were made by Einthoven in 1906. Many studies in the last 60 years tried to unravel the mechanisms. A key observation was made by Haissaguerre et al in 1998, who showed that foci in the pulmonary veins served as triggers for atrial fibrillation.
There are several mechanisms that could underlie atrial fibrillation. In the multiple wavelet hypothesis formulated by Moe and Abildskov in 1959, many independent re-entrant wavelets change their position, shape, size and number with each successive excitation. Single reentrant circuits, or rotors, revolving at such a high rate that it cannot be followed in a 1:1 fashion by all parts of the atria have also been proposed. In most studies the atria are perceived as a two-dimensional structure. Recent experiments on long standing atrial fibrillation in humans by the group of Allessie have shown that complete reentrant circuits in the epicardium are extremely rare and that the substrate for atrial fibrillation is three-dimensional with fibrillation waves frequently crossing over from the endocardial to the epicardial layers. At the epicardium, sites of such epicardial breakthrough appear as foci.
Treatment is directed at 4 aspects: 1) control of the ventricular rate by digitalis or beta-adrenergic blockers; 2) restoration of sinus rhythm by electrical cardioversion, amiodarone or flecainide (not in patients with organic heart disease); 3) maintenance of sinus rate by amiodarone or flecainide; 4) prevention of emboli by anticoagulants.
Since the 1990s, catheter ablation of the tissue around the orifices of the pulmonary veins is a curative therapy directed against the trigger.
Ventricular fibrillation and sudden death
Within minutes following occlusion of a coronary artery, functional reentry occurs in the ischemic myocardium, with activation patterns resembling the multiple wavelet theory of atrial fibrillation. The resulting ventricular fibrillation is always fatal, unless immediate cardiopulmonary resuscitation and electrical defibrillation is applied.
Ventricular tachycardia in the healed myocardial infarct
In human hearts, monomorphic ventricular tachycardia is due to anatomical reentry within the complex network of surviving myocardial fibers within the infarct. Surgical or catheter ablation of crucial parts of the reentrant circuit is an effective mode of treatment. The suppression of ventricular premature beats, that act as triggers for reentry, by antiarrhythmic agents, especially class III agents, is harmful and should be avoided.
Michiel J Janse MD, Amsterdam The Netherlands