Atrial fibrillation and flutter â€” epidemiology and mechanisms
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940ftxt06 14/7/04 11:22 am Page 104 104 ARRHYTHMIAS Atrial ﬁbrillation and ﬂutter — epidemiology and mechanisms within the pulmonary vein oriﬁces, are commonly responsible Atrial ﬁbrillation for episodes of atrial ﬁbrillation in patients with otherwise Atrial ﬁbrillation is a supraventricular arrhythmia characterised apparently normal hearts (Fig. 3). Once initiated, the by rapid, chaotic depolarisation of the atria. The atrial rhythm arrhythmia is maintained by re-entry (pp. 98–99). Macro re- is irregular, with rate from 300–500 per minute. Although the entry occurs when a continuous loop of atrial depolarisation is AV node limits the number of these impulses that reach the set up around an anatomical or functional conduction barrier ventricles, atrial ﬁbrillation usually produces a rapid, irregular (e.g. vein oriﬁce, zone of diseased atrial tissue). During atrial ventricular rhythm (Fig. 1; Table 1). Since the AV node ﬁbrillation, multiple re-entry circuits are established in the determines heart rate, the ventricular rate tends to be slower in atria. These circuits tend to maintain themselves more readily elderly patients in whom the AV node conducts less well. in diseased or enlarged atria. Once atrial ﬁbrillation is established, the chance of spontaneous return to sinus rhythm Epidemiology diminishes because of maladaptive changes that occur in atrial Atrial ﬁbrillation is the most common arrhythmia seen in tissue. This includes shortening of the refractory period of general practice and hospital medicine. It is especially atrial myocytes, which encourages macro re-entry because common in the elderly, with a prevalence of 0.5% in the myocytes are excitable for a greater proportion of each cardiac adult population, rising to 10% among individuals aged over cycle. This process is known as electrical remodelling. 75 years. It is associated with a 5–6-fold increase in the incidence of stroke. A 70-year-old with atrial ﬁbrillation thus has an annual risk of stroke or transient cerebral ischaemic attack of 5%. Risk factors for atrial ﬁbrillation consist mainly Atrial ﬂutter of conditions that lead to increased atrial wall stress. These Atrial ﬂutter is a related arrhythmia that shares the same risk are summarised in Table 2. factors as atrial ﬁbrillation (with the exception of thyrotoxicosis). The mechanisms that underlie these Clinical manifestations arrhythmias are different, resulting in distinct clinical Atrial ﬁbrillation can be paroxysmal, persistent or permanent. manifestations, electrocardiographic characteristics and Paroxysmal atrial ﬁbrillation is characterised by intermittent, treatment options. self-terminating episodes of tachycardia. Sometimes this progresses to persistent atrial ﬁbrillation, in which an Clinical manifestations intervention (such as direct current [DC] cardioversion, pp. Atrial ﬂutter can also present in paroxysms or as a persistent 106–107) may restore sinus rhythm, or permanent atrial arrhythmia. If 2:1 AV block occurs, the presentation may be ﬁbrillation, which is resistant to such treatments. with regular, rapid palpitation. (Rarely, 1:1 AV conduction can Atrial ﬁbrillation may not produce symptoms, especially if occur in young patients, and this may cause an extreme the associated heart rate response is not rapid. If symptoms tachycardia, presyncope or syncope.) Otherwise the clinical occur, their severity is determined by the underlying condition features are similar to those of atrial ﬁbrillation. Atrial stasis can of the heart, and patients’ heart rate at rest and during exercise. occur with atrial ﬂutter (because of loss of atrial contraction) Patients may describe fatigue or reduced effort tolerance, or more deﬁnite symptoms of palpitation, dyspnoea and dizziness. If the heart rate is rapid, cardiac failure or angina may develop in susceptible patients. It is rare for atrial ﬁbrillation to cause syncope, unless the patient has severe left ventricular impairment or valvular stenosis. In some cases, the ﬁrst clinical manifestation of atrial ﬁbrillation is stroke or systemic embolism. This is caused by the development of thrombus in the left atrial appendage (Fig. 2), due to loss of atrial mechanical function and stasis, followed by embolisation. Mechanisms Atrial ﬁbrillation is the result of substrate and trigger. The substrate usually consists of a disease that affects the atria, such as ischaemic heart disease (associated with atrial ischaemia and infarction). The trigger often consists of a rapidly discharging ectopic atrial focus. Although this focus can arise anywhere in the atria, left atrial foci, occurring at or Fig. 2 Transoesophageal echocardiogram showing thrombus in the left atrial appendage caused by stasis. In atrial fibrillation, V1 atrial mechanical function is lost, predisposing to left atrial thrombus and Fig. 1 Rhythm strip of atrial ﬁbrillation. embolic events. 940ftxt06 14/7/04 11:22 am Page 105 Atrial ﬁbrillation and ﬂutter — epidemiology and mechanisms 105 Sino-atrial Pulmonary SVC 5 node veins 4 F F TV F F F F CS 3 6 Eustachian ridge 2 LV IVC 1 RV Fig. 6 ECG leads showing atrial ﬂutter Fig. 4 Schematic of atrial ﬂutter circuit. The Bundle with 4:1 AV block. The ﬂutter waves (F) occur main structures in the right atrium are the of His at a rate of 300 per minute. tricuspid valve (TV), coronary sinus (CS), superior vena cava (SVC) and inferior vena cava (IVC). The Table 3 Key ECG features of atrial ﬂutter circuit itself runs around the tricuspid annulus. Fig. 3 Ectopic beats can arise from sleeves ■ Consistent organised atrial activity of conducting tissue within the (pp. 116–117). The AV node limits the ■ Flutter waves prominent in inferior leads (II, III, aVF) pulmonary veins. These can trigger episodes ■ Regular or irregular ventricular rhythm may be seen ventricular response to atrial ﬂutter. of atrial ﬁbrillation. ■ A regular, narrow complex tachycardia of 150 bpm Often 2:1 or 4:1 AV block occurs, resulting in a regular ventricular is likely to be atrial ﬂutter with 2:1 AV block. Flutter and thromboembolic complications do waves may be masked by the QRS complexes and occur, although the risk is not as high as rhythm of 150 or 75 beats per minute T waves, but may be unmasked by i.v. adenosine with atrial ﬁbrillation. (Fig. 6). Variable AV block can also (pp. 110–111) occur, resulting in an irregular Mechanisms ventricular rhythm as with atrial Atrial ﬂutter is usually the result of a ﬁbrillation (Table 3). Atrial ﬁbrillation and single, large re-entry circuit within the ﬂutter — epidemiology right atrium (Figs 4 and 5). This circuit is Table 1 Key ECG features of atrial and mechanisms centred round the tricuspid valve ring ﬁbrillation ■ Atrial ﬁbrillation is caused by multiple, (annulus), and the left atrium is ■ No consistent organised atrial activity interlacing re-entry circuits involving ■ Unsteady baseline (ﬁbrillation waves) activated passively from this circuit. In predominantly the left atrium. ■ Irregular ventricular rhythm (unless third-degree most cases the atria depolarise at a rate ■ Risk factors include age, hypertension, AV block also present) of around 300 beats per minute. mitral valve disease, cardiomyopathy and Importantly, the ﬂutter circuit passes Table 2 Risk factors for atrial ﬁbrillation coronary artery disease. through a narrow strip of tissue (known ■ Atrial ﬁbrillation affects around 10% of ■ Advanced age as the ‘ﬂutter isthmus’) in between the ■ Valvular heart disease (especially mitral valve disease) people aged over 75 years. tricuspid annulus and the inferior vena ■ Hypertension ■ Episodes of atrial ﬁbrillation may be cava. This strip of tissue can be targeted ■ Ischaemic heart disease (per se and with heart failure) triggered by ectopic beats originating in for radiofrequency ablation, a potentially ■ Cardiomyopathies the pulmonary veins. curative treatment for this arrhythmia ■ Thyrotoxicosis Fig. 5 Three-dimensional map of right atrial depolarisation obtained during electrophysiological study for atrial ﬂutter. This is a map of the right atrium viewed through the tricuspid annulus (red ring). The depolarisation wave (denoted by concentric colours) passes between the tricuspid annulus (TV6) and the inferior vena cava (IVC). 940ftxt06 14/7/04 11:22 am Page 106 106 ARRHYTHMIAS Atrial ﬁbrillation and ﬂutter — management digoxin are preferable in patients with significant Persistent atrial ﬂutter/ﬁbrillation ventricular impairment. The target is a resting heart rate of Two types of management strategy can be adopted — rate 50–80 bpm. control and rhythm control. With rate control, the atrial In atrial ﬂutter, rate control is difﬁcult because the AV node arrhythmia itself is not terminated and treatment is directed blocking response is not linear, and is usually a whole at controlling the ventricular response and preventing fraction of an atrial rate of around 300 min –1. Thus, a embolic complications. With rhythm control, treatment is therapeutic dose of digoxin may not reduce heart rate from directed at restoring and maintaining sinus rhythm. Both 150 bpm (2:1 AV block), but an additional agent may cause it strategies have advantages and disadvantages. The choice is to fall abruptly to 75 bpm (4:1 block) or lower. governed by risk of thromboembolic complications, severity of symptoms and an assessment of whether the patient is Table 1 Rhythm control strategy Advantages Disadvantages likely to maintain sinus rhythm. Patients with long-standing ■ Restoration of atrial contraction ■ General anaesthetic risk (not a major concern atrial ﬁbrillation (especially if due to mitral valve disease, — ↑ cardiac output with exercise for most patients) hypertension or advanced LV dysfunction) are least likely to — appropriate rate response to ■ Drugs used to maintain sinus rhythm generally maintain sinus rhythm after cardioversion. Recent evidence exercise have more proarrhythmic potential than do the (the AFFIRM trial) suggests that aggressive attempts to AV node blocking drugs used for rate control. restore sinus rhythm in asymptomatic patients may be ■ Recent evidence suggests embolic risk may be harmful and increase the risk of stroke. increased Rhythm control strategy Table 2 DC cardioversion protocol The rhythm control strategy (Table 1) uses cardioversion to ■ Ensure patient has had at least three weeks of effective (INR>2) anticoagulation restore sinus rhythm. Cardioversion is most often achieved ■ Check serum K+ (success greater if > 4.0 mmol. L1-1) ■ Patient fasting > 6 hours using a synchronised direct current (DC) shock applied to ■ i.v. access the chest with paddles placed over the apex and base of the ■ General anaesthesia with short-acting induction agent heart. This procedure is performed under general ■ Cardiovert using following protocol (start at 200 J for atrial ﬁbrillation): anaesthesia. Cardioversion can also be achieved using — 100 J synchronised shock (or 50 J biphasic) if fails → antiarrhythmic drugs such as ﬂecainide or amiodarone; this — 200 J synchronised shock (or 100 J biphasic) if fails → pharmacological cardioversion is normally used to restore — 360 J synchronised shock (or 150 J biphasic) if fails → sinus rhythm in patients with acute atrial ﬁbrillation (of less — 360 J anteroposterior shock than 48 hours duration). For patients with established atrial — [lower shock energies used (up to 150 J) with biphasic shock deﬁbrillator] ﬁbrillation, four weeks of prior anticoagulation (target INR ■ Continue warfarin for at least 3 months if cardioversion successful 2.0 to 3.5) is mandatory. Here, cardioversion is dangerous ■ If cardioversion unsuccessful, consider repeating at later date after pre-treatment with without prior anticoagulation. Restoration of atrial antiarrhythmic agent (e.g. amiodarone) mechanical function can cause ejection of clot from the left Table 3 Drugs to maintain sinus rhythm atrial appendage in the days following the procedure. Class Ic drugs (sodium channel blockers) Warfarin should be continued for at least 12 weeks after These agents should be avoided in patients with IHD or heart failure. In patients with cardioversion, and only stopped if sinus rhythm is still structurally normal hearts, the incidence of proarrhythmia is around 1% maintained and likelihood of recurrence considered low. ■ ﬂecainide 50–100 mg BD ■ propafenone 150 mg BD to 300 mg TID DC cardioversion Class II drugs (β-blockers) Long-term success rates are disappointing with cardioversion These have little proarrhythmic effect, and are a sensible ﬁrst-line agent, especially when (< 50% of patients maintain sinus rhythm at six months) ischaemia or heart failure is implicated as a cause (Table 2). Concomitant use of antiarrhythmic drugs increases ■ atenolol 25–100 mg D the proportion of patients that maintain sinus rhythm. ■ metoprolol 25–100 mg BD Amiodarone, sotalol, propafenone and ﬂecainide are effective Class III drugs (potassium channel blockers) but can be proarrhythmic and have other signiﬁcant side Sotalol has combined β-blocking and class III activity. It causes proarrhythmia by causing abnormal ventricular repolarisation (seen as QT interval prolongation). This can lead to effects (Table 3). Therefore, unless the patient has a history of polymorphic ventricular tachycardia/sudden death. Proarrhythmia with sotalol is more intermittent atrial ﬁbrillation progressing to chronic atrial common in women and in patients with LVH. Amiodarone is the safest agent in patients with ﬁbrillation or has had a previous cardioversion with signiﬁcant LV compromise. It has many side effects (see pp 104–105, Fig. 4) and should be recurrence, antiarrhythmic drugs are not normally given. avoided in young patients unless no effective alternative is found ■ sotalol 60–120 mg BD Rate control strategy ■ amiodarone 100–400 mg D (usual dose 200 mg D) Recent trials suggest that the rate control strategy (Table 4) is For all of the above agents, except β-blockers, ambulatory monitoring within the ﬁrst ﬁve at least as safe as rhythm control, and is especially days of treatment is sensible to identify proarrhythmia appropriate in asymptomatic patients — it avoids the hazards Table 4 Rate control strategy of cardioversion and antiarrhythmic drugs. Advantages Disadvantages ■ More appropriate for patients with valve ■ Loss of atrial contribution to Drugs for rate control disease or previous failed cardioversions cardiac output AV node blocking drugs are used to control heart rate. A ■ Less proarrhythmic potential from rate ■ Risk of embolic complications hierarchy of drugs is given in Table 5. β-blockers and controlling drugs 940ftxt06 14/7/04 11:23 am Page 107 Atrial ﬁbrillation and ﬂutter — management 107 I III aVF V1 RA 1,2 RA 3,4 RA 5,6 RA 7,8 RA 9,10 RA 11,12 RA 13,14 Fig. 2 Surface (ECG (top four traces) and intracardiac electrograms from right atrium, (RA) during successful ablation of atrial ﬂutter. Rapid, regular atrial depolarisation is seen to proceed around the right atrium until sinus rhythm is restored by blocking the ﬂutter circuit (see pp. 116–117). Fig. 1 Computer-generated map of the left atrium in a patient 104–105 is targeted. Current success rates are 80–90%. with atrial ﬁbrillation due to pulmonary vein ectopy. The red dots Ablation can also be used to treat atrial ﬁbrillation, by around the right upper pulmonary vein (RUPV) denote ablation lesions delivered during the procedure. (RLPV, right lower pulmonary vein.) targeting triggering foci in the pulmonary veins (Figs 1 and 2). This evolving treatment has a success rate of around 65% in patients with otherwise normal hearts. ‘Dynamic overdrive’ pacemakers have recently been developed to suppress rate changes and ectopic activity that may trigger atrial ﬁbrillation (Fig. 3). The pace and ablate strategy is used as a last resort for symptomatic patients in whom drug treatment is ineffective or poorly tolerated. Rate control is achieved by ablation of the AV node and implantation of a permanent pacemaker. Table 5 Oral drugs for rate control in atrial ﬁbrillation Fig. 3 AF suppression pacemaker. This device paces the atria slightly First line faster than the sinus rate, preventing bradycardia and atrial ectopy that Digoxin 250 µg D (after leading with 600–1200 mg for one week) OR otherwise trigger atrial ﬁbrillation. Verapamil 240 to 480 mg D OR Diltiazem 200 to 500 mg D OR Anticoagulation β-blocker (e.g. atenolol 50 to 100 mg D) Most patients with chronic atrial ﬂutter/ﬁbrillation require If digoxin ineffective, ensure blood level therapeutic before adding a second agent long-term anticoagulation with warfarin. Exceptions are Second line patients who, from anticoagulation trials, are considered low Combination of digoxin and either verapamil or β-blocker risk. In these cases, low-dose aspirin 75–300 mg daily is Third line sufﬁcient prophylaxis. The European Society of Cardiology Amiodarone 100 to 400 mg daily (after loading ⊗) has produced anticoagulation guidelines which are Table 6 ESC guidelines for anticoagulation in atrial ﬁbrillation summarised in Table 6. ■ Age > 60 years with diabetes or CAD ■ Age > 75 years (esp. women) ■ Current or prior hypertension Intermittent atrial ﬂutter/ﬁbrillation ■ Heart failure Intermittent atrial ﬂutter/ﬁbrillation may be a prelude to ■ History of TIA, stroke or other embolic event* chronic atrial ﬁbrillation, but can exist as a separate entity. ■ Rheumatic heart disease or prosthetic valve* The need for antiarrhythmic drugs is dictated by the severity Warfarinise, INR range 2.0–3.0 except highest risk cases (*) where target range is 2.5–3.5. of symptoms. Anticoagulation may be needed if prolonged (> 24 hours) episodes occur. Ambulatory ECG monitoring Atrial ﬁbrillation and ﬂutter — management helps guide treatment. Identiﬁcation and treatment of potential precipitants (e.g. hypertension, alcohol, valve ■ The rate control strategy is directed at limiting the ventricular response disease) should be done before committing to long-term to atrial ﬁbrillation by using AV node blocking drugs such as digoxin, antiarrhythmic treatment. ß-adrenoceptor antagonists and verapamil. ■ The rhythm control strategy uses cardioversion and antiarrhythmic Non-pharmacological treatments drugs to restore and maintain sinus rhythm. Radiofrequency ablation ■ Anticoagulation with warfarin should be considered for patients with Radiofrequency ablation can be used to treat intermittent or atrial ﬁbrillation and risk factors for stroke. persistent atrial ﬂutter; the isthmus zone described on pages ■ Pacemaker implantation and AV nodal ablation can be used to control heart rate in patients for whom drugs fail or are not tolerated.