Treatment of atrial fibrillation
Individualising atrial fibrillation (AF) treatment helps you optimise symptomatic outcomes and reduce stroke risk.
This part of the Learning Zone introduces the various AF treatments. Up to 50% of patients with recent onset AF spontaneously convert to sinus rhythm.20 The remainder need one or more of the treatments covered in this section. The ESC/EHRA guidelines stress the importance of counselling patients starting AF management to prevent unrealistic expectations and to optimise QoL.5
Broadly, patients and clinicians need to decide between rhythm and rate control. Currently, no trial data compares rhythm and rate control as an initial AF treatment. However, consensus guidelines suggest restoring sinus rhythm, which may control AF arising from potentially reversible causes or in those patients experiencing an isolated episode.6
If AF recurs, patients who seem especially suitable for rhythm control include:6
- those who showed a symptomatic improvement during normal sinus rhythm
- young people
- those with AF without underlying heart disease
- patients with substantial symptoms despite control of ventricular rate
Anticoagulation is an important aspect of management to reduce the risk of ischaemic stroke in all AF patients.5,37
Comorbidities and risk factors
Several comorbidities and risk factors contribute to AF and the risk of stroke.
Several modifiable comorbidities and risk factors seem to promote AF development and maintain the arrhythmia (Figure 13).6
Heart rate control
Heart rate control is only suitable for some AF patients; this section suggests when heart rate control may be appropriate.
Antiarrhythmic drugs (AADs) are not routinely used for asymptomatic AF or by people with permanent AF who did not undergo rhythm control.5,6 AADs also have important contraindications and cause dose-limiting adverse events.
Nevertheless, AADs can re-establish normal heart rate and left ventricular function in AF patients with cardiomyopathy and may increase the likelihood of successful electrical cardioversion if initial attempts were unsuccessful.6
Electrical cardioversion is a cornerstone of AF care, but patients still need effective anticoagulation and pretreatment.
Initially, many AF patients require ventricular rate control to reduce the risk that tachycardia will cause cardiomyopathy and CHF, even if the patient does not show left ventricular systolic dysfunction.6 Nevertheless, 20–30% of AF patients show left ventricular dysfunction.5
Patients with emergent AF and haemodynamic instability because of very rapid ventricular rates or structural heart disease may need urgent cardioversion with one or more shocks with direct electrical current producing 200 to 300 joules to restore sinus rhythm.20,32 The electric shock synchronises with the QRS complex, which avoid triggering ventricular fibrillation.32
Find out which patients may be more suitable for pharmacological than electrical cardioversion.
In recent onset AF (Figure 15), the ESC/EHRA guidelines suggest rhythm control to improve symptoms. The guidelines also prefer rhythm to rate control in pre-excited AF (ventricles depolarise prematurely) and AF during pregnancy. Clinicians should also manage cardiovascular risk factors and help patients avoid AF triggers to facilitate sinus rhythm control.5
Invasive treatments offer an option when drugs are contraindicated, poorly tolerated or not fully effective.
Invasive treatments offer an option when drugs are contraindicated, poorly tolerated or not fully effective. The ESC/EHRA guidelines, for instance, suggest considering atrioventricular node ablation to control heart rate in patients unresponsive or intolerant to intensive rate and rhythm control therapy. These patients will, however, become pacemaker dependent.5 This Learning Zone summaries the main invasive approaches used to manage AF.
Introduction to anticoagulation
Learn why most AF patients, other than those at very low stroke risk, should receive anticoagulants.
The coagulation cascade (Figure 19) refers to a series of enzymatic reactions that begins when damage to the endothelium of a blood vessel exposes circulating platelets to collagen in the wall and plasma factor VII/VIIa to extravascular tissue factor. Other proteins (including von Willebrand factor) help platelets bind to the damaged vessel wall. The complex between tissue factor VIIa – the ‘extrinsic pathway’ – activates the coagulation cascade.39
References for Anticoagulation Therapy for Stroke Prevention
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