Atrial fibrillation (AF) is the most common arrhythmia in Western countries and is associated with high morbidity and mortality rates. It is the leading cause of embolisms and its appearance is also associated with episodes of heart failure, cognitive impairment and a deterioration of quality of life.[1]
It is the most frequent arrhythmia, especially in the elderly, and to which a large amount of health resources must be devoted. Although it occurs in people with all types of heart disease or with some systemic diseases, it can also occur in otherwise healthy individuals.[2]
It has become a serious public health problem due to its increasing prevalence, its impact on the survival rate and quality of life of patients and the high health costs involved.[3]
The prevalence of AF is estimated to be at 0.4% in the general population, with this prevalence increasing with age. Some studies have shown that the prevalence in individuals under 60 years of age is 1%, increasing to 6% in people over 80 years of age. It is more prevalent in males. It is 12% in patients with cardiopulmonary disease, in some series reaching 30%. The prevalence of AF doubles with each passing decade, with age being the most important risk factor for its presence.
It is defined as a supraventricular tachycardia, characterized by disordered activation of the atria with subsequent deterioration of mechanical function. This chaotic electrical activity causes an asynchrony of contraction of the atrial myocardial fibers, the activity of the atrium to fill the ventricle stops, the ejection fraction of the ventricle decreases, the heart rate is usually high (which can cause heart failure), and there is blood stasis in the atria, with turbulent flows that favor thromboembolism, increasing the probability of suffering a stroke (the main risk of AF).
In the electrocardiogram (ECG), it is characterized by the absence of clearly defined P waves which are replaced by rapid oscillations (fibrillatory waves, or f waves) that can vary in size, shape and frequency and are associated with an irregular ventricular response when Atrioventricular (AV) conduction is normal.[4]
The appearance and maintenance of AF is conditioned by the characteristics of the atrium itself, such as the atrial mass and its electrophysiological properties (refractory periods and driving speed). Thus, any cardiopathy or intercurrent factor that alters these characteristics can be the cause of AF; therefore, almost any cardiopathy can be the cause of this.1 In approximately 70-80% of patients, AF is associated with organic heart disease.
AF may be related to acute causes and may not recur if the cause disappears. Such is the case with alcohol intake (holiday heart syndrome), electrocution, acute pericarditis and myocarditis, pulmonary embolism, hyperthyroidism[5], etc.
How do I know if I have AF?
The symptomatology of AF can vary, depending on the previous state of the heart, the faster or slower ventricular rate, and the cessation of contractile activity of the atrium.[6]
The most frequent manifestations are fast and irregular palpitations, which may be asymptomatic in cases of paroxysmal AF in healthy subjects.
Why is AF associated with strokes?
AF is the most common cardiac cause of systemic thromboembolism (usually cerebrovascular). Patients with AF have a 15% yearly[7] risk of a cerebrovascular accident (CVA). Several studies establish that, in the presence of AF, the risk of a stroke is approximately 5 times greater, regardless of age. The proportion of stroke-related AF significantly increases with age, from 6.7% for ages 50 to 59 years to 36.2% for ages 80 to 89 years. In addition to symptomatic strokes, AF has been associated with an increase in silent strokes.[4]
AF also increases the risk of an ischemic stroke from 2% to 5% per year.[8] The relative risk of death associated with AF is 1.5 to 1.9 times greater for any cause of death7.
How do I know which type of AF I have?
As AF is a complex condition, there are different classification systems based on different criteria. Three FA types are usually distinguished depending on the duration:
. Paroxysmal covers a duration of less than 48 hours, although it is possible for paroxysms to last up to the following seven days. It may spontaneously remedy itself or need to be remedied with pharmacological or electrical cardioversion. The first 48 hours are highly important because from then on, the probability of spontaneous cardioversion is significantly reduced.[9]
. Persistent lasts more than 7 days and does not remedy itself spontaneously. It is remedied with pharmacological or electrical cardioversion. Within this group, a persistent AF of long duration, fibrillation that has lasted 1 year or more at the time when it is decided to adopt a rhythm control strategy, can be differentiated.
. Permanent, is when it is not remedied (stable rhythm in AF) and the duration exceeds one year. It is accepted by the patient, and restoring the sinus rhythm is impossible or not indicated. [10]
Some patients with paroxysmal AF may sometimes have persistent episodes and vice versa. The predominant form of AF determines its classification category.
What tests should I do for an AF diagnosis?
Various tests or studies exist that should be performed in the presence of AF9:
· Clinical History Data:
Symptoms associated with AF
Type of AF (paroxysmal, persistent, or permanent)
History and evolution of episodes: first episode, frequency and duration of episodes, form of termination, precipitating factors.
Defining the presence of underlying heart disease: HTA, valvular or ischemic heart disease, heart failure, myocardiopathies, previous stroke, etc.
Presence of precipitating factors: alcohol, hyperthyroidism, etc.
· ECG:
Evaluation of ventricular rate
Presence of left and/or right ventricular hypertrophy
Presence of signs of ischemia, necrosis
Ventricular conduction disorder (branch blocks)
Characteristics of the P wave in sinus rhythm
· Analysis:
Hemogram
Basal glycaemia, total cholesterol, HDL, LDL, triglycerides
Creatinine, ions.
Thyroid function tests: TSH, free T4 (on clinical suspicion and in newly discovered AF, ventricular response difficult to control, prior treatment with amiodarone).
· Echocardiogram: indicated among other tests for assessment and follow-up by the cardiologist and to confirm the presence or absence of heart disease.
The following must be evaluated:
Left atrium size
Diameters and function of the left ventricle
Presence and type of HVI
Global and segmental contractility of the left ventricle.
Anatomy and valve function.
Valuation of the pericardium
Presence of intracavitary thrombi
· Chest x-ray: appropriate if anamnesis or physical examination findings indicate lung disease.
· Other complementary tests:
Holter monitor
Stress or ergometry test
Electrophysiological study
Transesophageal echocardiogram
How can AF be treated?
The treatment of AF has traditionally focused on three, non-mutually exclusive objectives:
. Controlling the ventricular response
. Restoring the sinus rhythm and subsequent maintenance.
. Prevention of thromboembolic events.
There is currently a strong commitment among the scientific associations responsible for setting the standard in atrial fibrillation to promote the idea that therapeutic goals in AF treatment are comprehensive and focus more on the patient than on the electrocardiogram.
According to the American guidelines for the management of AF, when a patient with this condition is initially treated, the general strategy should be discussed with the patient, taking into account, among other factors, type and duration, severity and symptoms, associated cardiovascular disease, the patient’s age, associated medical conditions, short-term and long-term treatment goals, and, lastly, pharmacological and non-pharmacological options.[11]
A. Acute treatment of atrial fibrillation.[12]
Patients who go to the emergency room for AF usually have a rapid ventricular rate; control of the ventricular rate is achieved more quickly with amiodarone, flecainide, propafenone, or beta blockers. If the patient is hemodynamically stable, immediate transthoracic cardioversion may be appropriate. If AF has lasted more than 48 hours or if its duration is uncertain and the patient is not undergoing anticoagulant treatment, cardioversion should be preceded by transesophageal echocardiography to rule out a left atrial thrombus.
If the patient is hemodynamically stable, the decision to restore the sinus rhythm by cardioversion is based on several factors, including symptoms, previous episodes of AF, age, left atrial size, and current antiarrhythmic pharmacotherapy.
When the patient shows signs of AF, it is necessary to try to restore the sinus rhythm in the shortest possible time. Cardioversion can be pharmacological or electrical.
. Pharmacological cardioversion: it has the advantage of not requiring deep sedation. The probability of an immediate recurrence of AF may be lower with pharmacological cardioversion than with electrical cardioversion. However, pharmacological cardioversion is associated with the risk of pharmacological side effects and is not as effective as electrical cardioversion. Drugs that can be given intravenously to produce AF cardioversion include amiodarone, flecainide, and propafenone.
Acute pharmacological cardioversion may be achieved with oral drug administration. The most commonly used oral drugs are amiodarone (600-800mg), propafenone (300-600 mg) and flecainide (100-200 mg).
. Transthoracic Cardioversion: it has approximately 95% efficacy. Biphasic wave pulses modify AF more effectively than monophasic wave pulses and allow the use of lower energy pulses, resulting in a lower risk of skin irritation. The appropriate energy level of the initial biphasic wave pulse is 150 to 200J, followed by higher energy emissions if necessary.
B. Long-term AF treatment
· Pharmacological rate control versus pharmacological control of rhythm.
Several randomized studies have compared the strategy of rate control with that of rhythm control in patients with AF. A very large-scale study is AFFIRM, consisting of 4,060 patients averaging 70 years of age, with AF for 6 hours for 6 months[13]. After 5 years of monitoring, the prevalence of sinus rhythm was 35% in the rate control group and 63% in the rhythm control group. No significant difference was observed between the two study groups in terms of total mortality, stroke rate or quality of life. The AFFIRM study organizers concluded that there is no survival advantage in the rhythm control strategy over that of rate control, and that rhythm control had advantages, such as a lower probability of hospitalizations and pharmacological side effects.
The AFFIRM study has convincingly demonstrated that a rate control strategy is preferable to that of rhythm control in asymptomatic or minimally symptomatic patients over 65 years of age.
In patients with persistent AF, it is reasonable to attempt to restore the sinus rhythm with antiarrhythmic treatment or transthoracic cardioversion, at least once in patients ≤ 65 years of age and in patients ≥ 65 years of age with symptomatic AF, despite adequate heart rate control. If AF has been continuous for more than one year or if the left atrial diameter is very wide (> 5 cm), there is a high probability of early recurrence of AF, which should be taken into account when deciding on the best strategy. After cardioversion, the decision to keep the patient on antiarrhythmic treatment to delay the next AF episode is based on the perceived risk of an early recurrence of AF and the duration of sinus rhythm between previous cardioversions. Cardioversion treatment without daily pharmacotherapy with antiarrhythmics is acceptable if AF episodes are at least 6 months apart. Treatment with a rhythm-controlling drug is usually adequate when there is an AF relapse a few months after cardioversion.
· Pharmacological rate control.
An excessively fast ventricular rate during AF often causes bothersome symptoms and decreased stress tolerance, and can lead to tachycardia-induced cardiomyopathy, if it occurs over a period of several weeks to months.
The optimal heart rate during AF varies with age and should be similar to the heart rate that a patient would have under a particular degree of stress while in sinus rhythm. The heart rate will be assessed both at rest and during exertion. The ideal ventricular rate at rest during AF is between 60 and 75 bpm. During mild to moderate exertion, such as brisk walking, the rate should be 90 to 115 bpm while during intense exercise, the ideal rate is 120 to 160 bpm. An optimal assessment of the degree of heart rate control is provided on an outpatient basis with a 24-hour Holter monitor or with a stress test.
Strict rate control is a suitable goal for improving symptoms, increasing functional ability, and preventing tachycardia-induced cardiomyopathy in long-term progression.[14]
· Pharmacological control of rhythm.
The results of published studies on the efficacy of antiarrhythmic drugs for AF suggest that all available drugs, except amiodarone, have similar efficacy and are associated with a 50% to 60% reduction in the likelihood of AF recurrence one year after treatment. The only drug that stands out is amiodarone, with an efficacy of more than 60 to 70%.[14]
C. Non-pharmacological treatment of AF
· Pacemaker implantation.
Randomized clinical trials comparing double chamber pacemaker stimulation with right ventricular pacemaker stimulation have concluded that atrial pacemaker stimulation avoids AF.
In patients with bradycardia, indicative of pacemaker placement and who are experiencing paroxysmal AF or recurrent episodes of persistent AF, the available data clearly supports the use of atrial pacemaker stimulation and programming to minimize the degree of stimulation with ventricular pacemakers.
· Atrioventricular Node Ablation.
Radiofrequency catheter ablation of the AV node causes complete blockage of the AV node and replaces an irregular, fast original rhythm with a regular, pacemaker-stimulated rhythm. It is an effective strategy in patients with symptomatic AF because the rapid ventricular rate could not be sufficiently controlled pharmacologically, due to pharmacological inefficacy or intolerance, and they are not suitable candidates for AF ablation, or AF ablation has already been attempted with negative results.
In patients with AF and an uncontrolled ventricular rate, AV node ablation improves the ventricular ejection fraction in the presence of tachycardia-induced cardiomyopathy. AV node ablation has also been shown to improve symptoms, quality of life and functional ability, and reduce the use of health care resources. There is no evidence that AV node ablation benefits patients whose ventricular rate is adequately controlled by pharmacotherapy.
The drawbacks of AV node ablation are the lifelong need for ventricular stimulation with pacemakers and the inability to restore AV synchrony.
AV node ablation is a simple technique with an acute and long-term success rate of 98% or higher and a very low risk of complications. In patients with persistent AF, a ventricular pacemaker is implanted; with paroxysmal AF, a double chamber pacemaker is suitable. Most patients have good clinical results with the right ventricular pacemaker, but in those with borderline or reduced left ventricular function, the biventricular pacemaker is suitable as a cardiac resynchronization treatment. In patients with ischemic or non-ischemic cardiomyopathy and with an ejection fraction ≤ 30-35%, an Implantable Automatic Defibrillator (IAD) may be suitable for the primary prevention of sudden death. However, an ICD-free pacemaker is often sufficient in patients with an intermediate ejection fraction (30 to 35%) and a rapid ventricular rate, as the ejection fraction is likely to improve > 35% after controlling the ventricular rate via ablation of the AV14 node. [14]
· Balloon cryoablation of pulmonary veins.
Unlike point-by-point radiofrequency ablation around the pulmonary veins, balloon cryoablation is designed to fit into the antrum of a pulmonary vein and create a circumferential ablative lesion through cryoenergy. An advantage of cryoablation over radiofrequency energy is that it is much less likely to cause pulmonary vein stenosis or esophageal injury. Experienced professionals are able to accurately achieve complete isolation of the pulmonary veins using only a cryoablation catheter in 98% of patients.
Francisca Esteve is Professor of Nursing in the Grado de Enfermería
Bibliografía
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