Atrial Fibrillation
Definition
Atrial fibrillation (AFib) is a tachyarrhythmia characterized by rapid and irregular atrial contractions (400-600 bpm), often caused by re-entry mechanisms within the atrium. It is one of the most prevalent arrhythmias encountered in clinical practice.
Risk Factors
Non-modifiable Risk Factors:
Advanced Age
Male Sex
European Ancestry
Modifiable Risk Factors:
Sedentary Lifestyle
Smoking
Obesity
Diabetes Mellitus
Obstructive Sleep Apnoea
Elevated Blood Pressure
Structural risk factors and cardiac conditions:
Myocardial Infarction (Heart Attack)
Fibrosis
Scarring
Myocarditis
Pericarditis
Cardiac surgery
Approximately one-third of AFib cases, are considered idiopathic.
Pathophysiology
The pathophysiology of AFib involves the generation of multiple electrical impulses within the atrial conductive system, causing disorganized contractions of the atrium. This disrupts the normal atrial-ventricular coordination, resulting in an arrhytmia, which can be detected in an ECG. Apart from these re-entry mechanisms within the atrium, also triggers from the pulmonary veins are often responsible for causing AFib.
Due to atrial fibrillation haemodynamics can suffer significantly. The persistent tachycardia stemming from atrial fibrillation has the potential to induce sustained stress on the myocardium, potentially even resulting in heart failure. Furthermore, the missing contribution of the atrium during ventricular filling, due to the irregular and uncoordinated contractions, result in a diminished final stroke volume. This decline in stroke volume can trigger a compensatory mechanism, prompting an elevation in heart rate to counterbalance the reduced volume.
Lastly, the ineffective atrial contraction results in blood stasis, increasing the risk of thrombus formation and subsequent embolism significantly. The one-year risk of having a thromboembolic event can be assessed using the CHA2DS2-VASc score.
Signs and symptoms
The most common signs and symptoms in AFib, include palpitations, shortness of breath, fatigue, and dizziness. Sometimes patients may also experience chest discomfort or pain, in these cases a myocardial infarction must always be ruled out. Additionally, the irregular heart rhythm in AFib can compromise the heart's ability to pump blood effectively, leading to reduced exercise tolerance. Intriguingly, approximately one third of patients remain asymptomatic.
Diagnosis
Accurate diagnosis relies on a combination of clinical evaluation and diagnostic tests. The ECG still remains a cornerstone for confirming AFib, capturing the atrial fibrillations and the irregular RR-intervals as an expression of an irregular transmissions coming from the atrium. In cases of paroxysmal atrial fibrillation, a long-term ECG might be necessary to capture the arrhythmia. Besides the ECG, the irregular transmissions from the atrium to the ventricles, are usually auscultable with the stethoscope and palpable while taking the patient’s pulse.
Therapy
The therapy of AFib aims at symptom control, prevention of complications like thromboembolic stroke, and restoration of normal rhythm. Therapeutic strategies include heartrate control and rhythm control through antiarrhythmic drugs or cardioversion and anticoagulation to mitigate the risk of thromboembolic events.
Anticoagulation
Anticoagulation initiation is essential upon diagnosing AFib. The anticoagulant options include Direct Oral Anticoagulants (DOACs) or Vitamin K antagonists. Due to their ease of administration without the need for constant INR monitoring, DOACs are often preferred to Vitamin K antagonists. Prior to commencing anticoagulation, calculating the individual CHA2DS2-VASc score is crucial to assess the risk of thromboembolism within a year. Additionally, evaluating the HAS-BLED score is essential to gauge the risk of bleeding under anticoagulation. These risk assessments aid in tailoring the anticoagulation strategy to the individual patient, balancing the benefits of stroke prevention with the potential risks associated with bleeding.
Heartrate control
To regulate heart rate, various drugs, including beta-blockers, calcium channel blockers (CCBs), and digoxin, can be employed. Among these, beta-blockers like metoprolol are probably the most frequently utilized ones. They regulate the heart frequency by exerting a negative chronotropic effect through the blockage of beta-1 receptors in the heart. Calcium channel blockers such as diltiazem or verapamil target L-type calcium channels in the AV node, slowing down depolarization in this region, again acting negatively chronotropic. Additionally, they induce vasodilation by impeding calcium influx in smooth muscle cells of peripheral blood vessels, thereby inhibiting their contraction. Digoxin, primarily a blocker of Na+/K+ pumps, helps controlling the heart rhythm by indirectly stimulating the vagal nerve's effect on the heart, therefore acting negatively dromotropic.
Heart rhythm control
To regulate heart rhythm, two primary approaches are available: electric cardioversion and the administration of antiarrhythmic drugs.
Cardioversion is employed in situations where the patient is hemodynamically unstable. In these cases, cardioversion can be considered after anticoagulation for three to four weeks before the intervention or, alternatively, if a thrombus has been excluded through transoesophageal echocardiography, but only under heparinization. In both scenarios, post-procedural anticoagulation for 4 weeks is recommended. The risks associated with cardioversion include typical anaesthesia risks and the potential for thromboembolism.
Antiarrhythmic drug therapy commonly involves the use of amiodarone, which predominantly blocks potassium channels but also affects sodium channels and beta receptors. In doing so, it prolongs the action potential and refractory period. Another category of antiarrhythmic drugs are Type Ic antiarrhythmics, which specifically block sodium channels, again leading to a prolongation of the action potential.
It is crucial to highlight that the relapse rate within the first year after restoring sinus rhythm is 70%, and that it can be reduced to 50% with the administration of amiodarone. Due to the numerous side effects associated with amiodarone, especially in long-term use, beta blockers are the preferred alternative. Restoring normal rhythm is essential to alleviate patients' symptoms, and the approach should be tailored based on the severity of the patient's distress.
Interventional Procedures
When the methods mentioned earlier prove insufficient in controlling the patient's symptoms or are contraindicated, an interventional approach becomes can be considered. One option involves electroanatomic mapping using specialized catheters to precisely identify the origin of aberrant signals and subsequent radiofrequency ablation, to impede the origination and propagation of the fibrillations. This procedure, also known as catheter ablation, can target either heart tissue or the pulmonary veins (Pulmonary Vein Isolation), from where the signal often originates. Alternatively, an approach involves ablating the AV-node, followed by the implantation of a pacemaker to allow a ventricular propagation of the physiological electric stimulus after the ablation of the AV-node.
References
Staerk L, Sherer JA, Ko D, Benjamin EJ, Helm RH. Atrial Fibrillation: Epidemiology, Pathophysiology, and Clinical Outcomes. Circ Res. 2017 Apr 28;120(9):1501-1517. doi: 10.1161/CIRCRESAHA.117.309732. PMID: 28450367; PMCID: PMC5500874.
Joglar JA, Chung MK, Armbruster AL, Benjamin EJ, Chyou JY, Cronin EM, Deswal A, Eckhardt LL, Goldberger ZD, Gopinathannair R, Gorenek B, Hess PL, Hlatky M, Hogan G, Ibeh C, Indik JH, Kido K, Kusumoto F, Link MS, Linta KT, Marcus GM, McCarthy PM, Patel N, Patton KK, Perez MV, Piccini JP, Russo AM, Sanders P, Streur MM, Thomas KL, Times S, Tisdale JE, Valente AM, Van Wagoner DR. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024 Jan 2;149(1):e1-e156. doi: 10.1161/CIR.0000000000001193. Epub 2023 Nov 30. Erratum in: Circulation. 2024 Jan 2;149(1):e167. PMID: 3803308