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ATRAIL FIBRILLATION

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By Masooma Hyderbaig

Introduction

Atrial Fibrillation (AF) is a common type of supraventricular tachyarrhythmia characterised by uncoordinated electrical cardiac activity resulting in an irregular and rapid heartbeat. This article delves into the classification, pathology and categories of arrhythmias in addition to the treatment and management of AF. 

Arrhythmias are classified into three main groups:

  1. Supraventricular Arrhythmias: arrhythmias which originate from above the ventricles
  2. Ventricular Arrhythmias: arrhythmias which originate from the ventricles 
  3. Bradyarrhythmias: arrhythmias consisting of a slow heart rate due to sinoatrial node dysfunction or conduction block (1).

Pathology of AF and symptoms

The uncoordinated electrical activity observed in AF results in disorganised contraction of the atria, leading to impaired blood flow to the ventricles and thus ineffective cardiac output. Normal cardiac electrophysiology is dependent on the movement of ions across cell membranes. In arrhythmic states, it is common for abnormalities to occur with these ion channels, causing a reduced refractory period and increased re-entry of cardiac myocytes (2). 

  • Electrical remodeling 

Specific Ion channel changes may include:

  1. Reduced Sodium (Na+) Channel expression: leading to shortened refractory periods and delayed electrical conductivity (3).
  2. Reduced L-type Calcium (Ca2+) channel expression: resulting in shortened effective refractory period and increased sensitivity to AF triggers (2).
  3. Increased potassium (K+) channel expression: the excessive presence of K+ channel subtypes like K2P3.1 can result in shortened action potential duration, further maintaining AF (4). 
  4. Decreased expression of K+ channels: Overtime, however, with atrial fibrosis, a decreased expression of K2P3.1 channels has been observed in AF patients (5), demonstrating a complex relationship between AF pathology and potassium levels.
  • Structural remodelling: Often occurs alongside electrical remodelling. Fibrosis of cardiac tissue can lead to slowed conduction and blocking of electrical signals, enhancing re-entry mechanisms and sustaining AF. Atrial dilation can also occur where enlargement stretches the tissue further maintaining and promoting disorganised electrical conductivity (6). 
  • Embolic stroke risk: The chaotic atrial rhythm can cause blood to pool and stagnate in the atria (abnormal stasis). This increases the risk of clot formation within the heart (hypercoagulability) (7), where these clots can be ejected into the bloodstream (becoming an embolus) and can travel to the brain, causing an embolic stroke. 

Categories

This table summarises the different categories of AF based on the duration and type of symptoms:

Paroxysmal AFAF lasting and resolving within 7 days
Persistent AFAF lasting longer than 7 days and might require intervention (8)
Long-standing persistent AFAF lasting for over a year
Permanent AFWhere rhythm control intervention may be stopped, and treatment is focused on rate control

Diagnosis 

A patient’s medical history, clinical evaluation and diagnostic testing are all used to solidify an AF diagnosis. An electrocardiogram (ECG), where the heart’s electrical activity is observed, makes it easy to identify rapid and irregular heart rhythms. A Holter monitor is a portable ECG  device which enables continuous electrical monitoring for patients with suspected paroxysmal AF. An echocardiogram can help observe blood flow in the heart to assess structural abnormalities and determine atrial size. Finally, blood tests may be done to rule out other causes of proposed AF, like anaemia or thyroid dysfunction (9). 

Treatment and Management

Treatment and management of AF focuses on alleviating and preventing future complications while reducing the risk of adverse events. Direct current cardioversion (DDCV) is considered for new onset AF if symptoms in the patient starts within 48 hours and the patient is hemodynamically unstable. Drug therapy consists of rate control, rhythm control and stroke prevention. For rate control, beta-blockers, rate-limiting calcium channel blockers and digoxin (as monotherapy or combined therapy with beta-blockers or calcium channel blockers) are considered, depending on the patient’s preference, tolerance and comorbidities. If the AF requires rhythm control, antiarrhythmic drugs like flecainide (class 1c)  and amiodarone (class 3) are used. For paroxysmal AF, which is infrequent or triggered by short-term factors like increased alcohol or caffeine consumption, no drug therapy can be considered, or a ‘pill-in-pocket’ approach can be implemented where patients only take a tablet when they experience the onset of their symptoms. For stroke prevention, patients with AF are assessed and then put on anticoagulation therapy, where direct oral anticoagulants (DOACs) are preferred, but vitamin K antagonists (warfarin) may be chosen in patients where DOACs are contraindicated. Regarding non-pharmacological management, weight management, limiting risk factors (alcohol, tobacco, caffeine, infections), and regular exercise can all contribute to enhancing treatment and improving patients’ quality of life (10). 

Edited by Romanea Kimhor

REFERENCES

1.National Heart, Lung, and Blood Institute. Arrhythmias – Types | NHLBI, NIH [Internet]. http://www.nhlbi.nih.gov. 2022 [cited 2025 Mar 9]. Available from: https://www.nhlbi.nih.gov/health/arrhythmias/types

2.Han P, Zhao X, Li X, Geng J, Ni S, Li Q. Pathophysiology, molecular mechanisms, and genetics of atrial fibrillation. Human Cell. 2024 Nov 6;38(1).

3.An R, Liu J, Zhang J, Yao F, Tian D, Liang F, et al. Risk factors and SCN5A-H558R polymorphism for atrial fibrillation in Tibetans living at different altitudes. Medicine [Internet]. 2022 Nov 18 [cited 2025 Mar 9];101(46):e31778–8. Available from: https://journals.lww.com/md-journal/fulltext/2022/11180/risk_factors_and_scn5a_h558r_polymorphism_for.83.aspx

4.Arnela Saljic, Jordi Heijman, Dobromir Dobrev. From Atrial Small-conductance Calcium-activated Potassium Channels to New Antiarrhythmics [Internet]. Radcliffe Cardiology. 2024 [cited 2025 Mar 9]. Available from: https://www.ecrjournal.com/articles/atrial-small-conductance-calcium-activated-potassium-channels-new-antiarrhythmics

5.Vadim Mitrokhin, Nikola Hadzi-Petrushev, Viktor Kazanski, Stanislav Schileyko, Kamkina O, Rodina A, et al. The Role of KACh Channels in Atrial Fibrillation. Cells [Internet]. 2024 Jun 10 [cited 2025 Mar 9];13(12):1014–4. Available from: https://www.mdpi.com/2073-4409/13/12/1014

6.Yue L, Xie J, Nattel S. Molecular determinants of cardiac fibroblast electrical function and therapeutic implications for atrial fibrillation. Cardiovascular Research. 2010 Oct 20;89(4):744–53.

7.Watson T, Shantsila E, Lip GYH. Mechanisms of thrombogenesis in atrial fibrillation: Virchow’s triad revisited. Lancet (London, England) [Internet]. 2009 Jan 10 [cited 2025 Mar 9];373(9658):155–66. Available from: https://pubmed.ncbi.nlm.nih.gov/19135613/?dopt=Abstract

8.National Heart, Lung, and Blood Institute. Atrial Fibrillation [Internet]. 2022 [cited 2025 Mar 20]. Available from: https://www.nhlbi.nih.gov/health/atrial-fibrillation/types

9.Mayo Clinic. Atrial fibrillation [Internet]. Mayo clinic. 2024 [cited 2025 Mar 20]. Available from: https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624

10.NICE. Recommendations | Atrial fibrillation: diagnosis and management | Guidance | NICE [Internet]. http://www.nice.org.uk. 2021 [cited 2025 Mar 20]. Available from: https://www.nice.org.uk/guidance/ng196/chapter/Recommendations#stroke-prevention

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