9 Atrial fibrillation
Salient features
History
• Asymptomatic and atrial fibrillation (AF) is discovered incidentally
• History of ischaemic heart disease, hypertension, valvular heart disease, rheumatic heart disease, chronic obstructive airway disease (COPD), congenital heart disease (atrial septal defect, ventricular septal defect), thyrotoxicosis (p. 506)
• History of consumption of caffeine, digitalis, theophylline.
Examination
• Irregularly irregular pulse (patients are often digitalized and in slow AF)
• Elevated JVP without ‘a’ waves
• Varying intensity of first heart sound (the intensity is inversely related to the previous RR cycle length; a longer cycle length produces a softer first heart sound)
• Pulse deficit, which is the difference between the rate of the apex and the pulse rate (because of varying stroke volumes resulting from varying periods of diastolic filling, not all ventricular beats produce a palpable peripheral pulse). The pulse deficit is greater when the ventricular rate is high
• If you are not sure tell the examiner that you would like to differentiate from ventricular ectopics by asking the patient to exercise: after exercise, ventricular ectopics diminish in frequency whereas there is no change in the rhythm of AF
• Look for the underlying cause:
• Calculate the CHAD2 score (see below) to determine the eligibility for anticoagulation.
Questions
What are the components of the bleeding risk index?
The annual risk of stroke (based on points accrued) is then:
Mention common sites of systemic embolization
Brain, leg, kidney, superior mesenteric artery, coronary artery and spleen.
How would you investigate this patient?
• ECG shows absent P waves. Fibrillatory or ‘f’ waves are present at a rate that may vary between 350 and 600 beats/min and the ‘f’ waves vary in shape, amplitude and intervals. The RR interval is irregularly irregular. Narrow QRS complex with varying RR interval (irregular unless there is an underlying ventricular conduction defect). It should be differentiated from sinus arrhythmia (Figs 9.1 and 9.2).
• Echocardiogram (transthoracic and transoesophageal) is useful to determine left atrial size and left ventricular systolic function, and to exclude underlying valvular heart disease and intracardiac thromboemboli. Transoesophageal echocardiography prior to cardioversion.
• Test of thyroid function to exclude thyrotoxicosis.
• Exercise treadmill will identify AF precipitated by exercise.
• Holter monitor is useful in paroxysmal AF to determine whether it was triggered by another arrhythmia, such as when a premature atrial complex during a rapid paroxysmal atrial tachycardia may cause the immediate onset of AF.
Advanced-level questions
What is the clinical classification of atrial fibrillation?
1 Recent onset or first detected: first diagnosed episode (sometimes an incidental diagnosis and precise duration is not known); may or may not recur.
2 Recurrent: when a patient has had two or more episodes:
3 Permanent: cardioversion has failed or restoration of sinus rhythm is no longer considered possible; or established. (The definition of permanent AF is often arbitrary.) The duration of AF refers both to individual episodes and to how long the patient has been affected by the arrhythmia. Thus, a patient with paroxysmal AF may have episodes that last seconds to hours occurring repeatedly for years.
4 Secondary AF that occurs following acute myocardial infarction, hyperthyroidism, cardiac surgery, pericarditis, myocarditis, pulmonary embolism, pneumonia, or other acute pulmonary disease.
5 Lone AF occurs in the absence of cardiopulmonary disease or a history of hypertension and before the age of 60 years. Such patients have a low risk of stroke (0.5% per year).
Notes
• Termination with pharmacological therapy or direct-current cardioversion does not change the designation.
• First-detected AF may be either paroxysmal or persistent.
• The category of persistent AF also includes long-standing AF (e.g. greater than 1 year), usually leading to permanent AF, in which cardioversion has failed or has not been attempted.
• These categories are not mutually exclusive in a particular patient, who may have several episodes of paroxysmal AF and occasional persistent AF, or the reverse. Regarding paroxysmal and persistent AF, it is practical to categorize a given patient by the most frequent presentation.
How would you treat a patient with atrial fibrillation?
• Attempt to restore slow ventricular rate:
• Attempt to restore sinus rhythm by cardioversion if the following conditions apply:
• Anticoagulation with warfarin is advised for certain patients:
What is the role of oral anticoagulants in chronic atrial fibrillation?
• Non-rheumatic AF is an important risk factor for stroke (AF raises the risk of ischaemic stroke by a factor of four to five, primarily as a result of cardioembolism of a fibrin-rich thrombus), even though it is recognized that only 80% of strokes in such patients are caused by embolism from the heart. All patients with non-rheumatic AF should receive warfarin for anticoagulation unless there are contraindications (Br J Hosp Med 1993;50:452–7).
• Oral anticoagulation is highly efficacious for prevention of all stroke (both ischaemic and haemorrhagic), with a risk reduction of 62% (95% CI, 48–72) versus placebo identified in a meta-analysis of five large randomized trials. This reduction was similar for both primary and secondary prevention and for both disabling and non-disabling strokes. By on-treatment analysis (excluding patients not undergoing oral anticoagulation at the time of stroke), the preventive efficacy of oral anticoagulation exceeded 80%.
• Aspirin offers only modest protection against stroke for patients with AF. Meta-analysis of the five randomized trials showed a stroke reduction of 19% (95% CI, 2–34).
• The Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events (ACTIVE) investigators reported that the combination of clopidogrel and aspirin significantly reduced the rate of major vascular events in certain patients with AF (in those not eligible for vitamin K-antagonist therapy such as warfarin), driven primarily by fewer strokes, when compared with aspirin alone (N Engl J Med 2009;360:2066–78). One disabling or fatal stroke would be prevented for approximately 200 patients treated for 1 year with clopidogrel added to aspirin. One extra major bleeding episode and one extra intracranial haemorrhage would occur for approximately 143 and 500 patients, respectively, treated for 1 year with clopidogrel added to aspirin. The same investigators in a separate study found that vitamin K-antagonist therapy was more efficacious than clopidogrel plus aspirin in patients at high risk for stroke.
• The Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) reported that dabigatran, a direct oral thrombin inhibitor, given at a dose of 110 mg was associated with rates of stroke and systemic embolism that were similar to those associated with warfarin, as well as lower rates of major haemorrhage (N Engl J Med 2009;361:1139). The number needed to treat to prevent one (non-haemorrhagic) stroke with dabigatran (150 mg twice daily) was 357.
• Dabigatran etexilate, after conversion to its active form by a serum esterase that is independent of cytochrome P450, competitively inhibits thrombin. Therefore, dabigatran should be less susceptible to dietary and drug interactions and to genetic polymorphisms that affect warfarin. Furthermore, neither anticoagulation monitoring nor dose adjustments are necessary with dabigatran. P-glycoprotein inhibitors, including verapamil, amiodarone and especially quinidine, raise dabigatran serum concentrations considerably. The long-term hepatic risks of dabigatran are unclear but in the short term it was similar to warfarin (ximelagatran, an earlier direct thrombin inhibitor, appeared to be similar to warfarin with respect to efficacy and safety but was found to be hepatotoxic). Dabigatran is excreted by the kidney and has a half-life of 12 to 17 h. In a separate study, dabigatran was also found to be comparable to warfarin in the management of deep venous thromboembolism (N Engl J Med 2009;361:2342).
• Rivaroxaban is a direct factor Xa inhibitor which has been shown to prevent strokes in the ROCKET AF (Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation) trial (N Engl J Med 2011).
What is the role of surgery in the treatment of atrial fibrillation?
• The Maze procedure involves multiple incisions in the atria to prevent re-entrant loops (Clin Cardiol 1991;14:827–34). This procedure is highly effective in preventing AF, with only 1 patient out of 65 suffering a clinical recurrence of the arrhythmia 3 or more months after the procedure. Although the long-term outcome is not known, it remains a promising procedure when AF is not controlled by medical therapy or in those complicated by recurrent thromboembolism.
• The ‘corridor’ procedure effectively isolates both the left and right atrium, leaving a strip of myocardium connecting the sinus node to the atrioventricular node. This procedure does not prevent AF but isolates the fibrillating atria. Although a 70% ‘cure’ rate is reported, sequential atrioventricular contraction is not restored (with the consequent haemodynamic effects), and there is a risk of thromboembolism.
Rhythm control versus rate control for atrial fibrillation and heart failure
Mention newer antiarrhythmic drugs for AF:
• Vernakalant, a new atrial selective agent, is effective for rapid cardioversion of recent onset AF
• Dronedarone, a derivative of amiodarone, is more effective than placebo in maintaining sinus rhythm and reducing admission to hospital but increased mortality in patients with heart failure (the results from a study comparing dronedarone with amiodarone are expected soon).
