Increasing evidence shows that the global prevalence of AFib is increasing. A recent study (2023) found that ~60 million individuals are affected and that AFib contributes to >8 million disability-adjusted life years.³  

Although data about the prevalence of AFib in sub-Saharan African countries are scarce, a 2010 study showed the estimated prevalence as 659.8 and 438.1 per 100 000 population for men and women respectively - representing a growth of 3.4% between 1990 and 2010.⁴ 

According to Elliot et al, the increase in AFib can be attributed to lifestyle factors such as hypertension, type 2 diabetes, and physical inactivity. In sub-Saharan Africa, the increase in AFib has been associated with the adoption of a Western lifestyle, which has resulted in an increase in cardiovascular (CV) disease due to hypertension, dyslipidaemia, diabetes, and obesity.^3,4 

Signs and symptoms 

Some patients may be asymptomatic, while others may present with signs and symptoms such as palpitation, shortness of breath, irregularly irregular pulse, or even hypotension.¹ 

AFib is subdivided into five types, based on duration:  

1. New-onset. 
2. Paroxysmal: Self-terminating or intermittent. 
3. Persistent: Fails to self-terminate within seven days and requires treatments (medical or electrical cardioversion).  
4. Long-standing Persistent: Lasts for ≥1-year. 
5. Permanent: Persistent for ≥1-year despite treatment.

How do you decide whether to use a rate or rhythm strategy? 

The decision to use a rate or a rhythm strategy depends on the patient’s haemodynamic stability, candidacy for ablation, and the presence of comorbidities.¹  

The most common comorbidities are hypertension (67%–76%), heart failure (22%–42%), diabetes (20%–24%), obesity (20%–35%), chronic pulmonary disease (10%–18%), thyroid dysfunction (8%–11%), renal failure (11%–22%) stroke/transient ischaemic attack (9%–16%), and neuropsychiatric disturbances (19%).² 

Acute AFib 

The American Heart Association (AHA) recently published a scientific statement on the management of patients with acute AFib, defined as AFib detected in an acute care setting or during an acute illness.⁵  

According to Chyou et al, acute AFib is associated with longer hospital stays, increased risk of morbidity and mortality, and high rates of recurrent AFib.⁵ 

Acute AFib is often incidentally detected in the medical care or surgical setting. In medical patients, incidence rates vary depending on the underlying condition and severity. For example, the incidence of acute AFib varies from 8%-10% in patients with sepsis, to 6%-22% in severe sepsis, and 23%-44% in septic shock.⁵  

In the non-cardiac surgery setting, between 3%-16% of patients develop acute AFib. In the post-cardiac surgery setting, 32% of patients develop acute AFib after coronary artery bypass grafting, 49% after concomitant coronary artery bypass grafting and aortic valve replacement, and 64% after coronary artery bypass grafting and mitral valve replacement.⁵  

 What triggers acute AFib? 

Triggers of acute AFib include:⁵  

• Inflammation 
• Local mechanical stress 
• Oxidative stress 
• Electrolyte imbalance and  
• Shifts in autonomic tone.  

 Potential sources of triggers include:⁵  

• Infection 
• Pericardial effusion and inflammation 
• Long procedural time 
• Haemodynamic shifts 
• Volume loss or overload 
• Intraprocedural and postprocedural pulmonary complications 
• Medications, including inotropic agents. 

 How to manage acute AFib 

The goals of managing acute AFib during hospitalisation are to optimise haemodynamics, alleviate symptoms and reduce the short- and long-term risks of thromboembolism.⁵ 

The AHA recommends tailoring treatment to address the patient’s underlying structural substrates and to identify and treat potential triggers. Structural substrates include for example prior cardiac and thoracic surgeries, pulmonary diseases, pulmonary vein automaticity, pericardial fat pads, atrial scars caused by cardiomyopathy, long-standing hypertension, chronic kidney or underlying valvular diseases.⁵  

A multi-pronged approach is needed that includes, as mentioned, the identification and treatment of triggers (see above), selection and implementation of rate/rhythm control, and management of anticoagulation.⁵ 

Acute rate and rhythm management 

Acute AFib may spontaneously convert to sinus rhythm, therefore an initial rate control and delayed cardioversion ‘wait-and-see’ approach may be reasonable for haemodynamically stable, asymptomatic patients. However, acute triggers should be aggressively treated.⁵  

The authors of the AHA guidance caution that AFib can decrease systemic blood pressure levels and cardiac output, and increase pulmonary vascular pressures, as well as atrioventricular valve regurgitation.  Effects may vary among patients and may be caused by rapid ventricular rates associated with AFib or atrioventricular dyssynchrony, which impact haemodynamics and patient tolerance.⁵  

The authors of the AHA statement stress that the use of a rhythm or rate control strategy depends on the patient and his/her structural substrate, the haemodynamic consequences of AFib, and the adequacy of the rate control strategy.⁵  

Given the risk of acute thromboembolism with acute rhythm control, any decision to proceed needs to be based on the risk of stroke, and the need for adjunctive short- and long-term anticoagulation, they add.⁵ 

Rate control 

Rate control is the treatment of choice in haemodynamically stable patients. Pharmacotherapy approved for rate control reduces the ventricular rate in AFib. These agents work by increasing the refractoriness of the atrioventricular node. Agents approved for rate control include for example: diltiazem, esmolol, and digoxin. The choice of rate control agent should be based on patient characteristics and comorbidities.⁵  

A target heart rate for optimal rate control in the setting of acute AFib has not yet been established. Recent guidelines do, however, recommend <110bpm as a general target for AFib rate control, but a stricter target of a resting heart rate <80bpm for patients with deterioration of left ventricular function, symptoms, concomitant cardiac resynchronisation therapy, or diagnosis of tachycardia-mediated cardiomyopathy.⁵ 

Rhythm control 

Immediate electrical cardioversion with direct current cardioversion (DCCV) is the treatment of choice in haemodynamically unstable patients. In haemodynamically stable patients intolerant of atrioventricular dyssynchrony, acute rhythm control can be achieved either with electrical or pharmacological cardioversion. In the latter, antiarrhythmic drugs (AADs) are recommended (see below).⁵  

Rhythm control should also be considered in patients who are unable to attain clinically adequate rate control despite optimal use of atrioventricular node–blocking agents. The identification and management of acute triggers also play an important role in the management of this patient population.⁵  

Real-world data have demonstrated that both electrical and pharmacological cardioversion are safe and effective. In patients with recently onset AFib, studies have shown high restoration rates of sinus rhythm with either an upfront electrical cardioversion strategy or a stepwise strategy with initial pharmacological cardioversion, followed by DCCV if sinus rhythm control could not be restored using the former.⁵ 

AADs may be used for acute chemical cardioversion or maintenance of sinus rhythm. The choice of antiarrhythmic medication should be individualised based on the safety profiles of each agent.⁵  

AADs for pharmacological cardioversion include for example flecainide and amiodarone. This is what the AHA statement recommends:⁵ 

• Oral flecainide: An option for patients who can swallow a tablet and who do not have underlying structural heart disease. The advantage of oral flecainide is that it can be transitioned to ongoing dosing  
• Amiodarone intravenous (IV): Also has the advantage of transitioning to oral form, but cardioversion with amiodarone takes longer than with the aforementioned agents.  

The authors caution that in critically ill patient, electrical and pharmalogical cardioversions are effective, but relapse is common until the underlying acute illness subsides, or adequate drug levels of rhythm control agents have been reached.⁵  

When should anticoagulation be initiated? 

The decision to initiate anticoagulation has to be based on the risk of thromboembolism against the risk of bleeding. General considerations for anticoagulation for patients with AFib are based on substrates, with a CHA2DS2-VASc score of ≥2 for men or ≥3 for women as an accepted indication for anticoagulation in the absence of contraindications and significant bleeding risks.⁵  

In the setting of acute illness, potential prothrombotic coagulopathic and periprocedural haemostasis may also need to be considered, stress the authors.⁵  

Consistent with newly detected AFib in general, there is uncertainty about the optimal threshold to initiate anticoagulation. However, state the authors,  anticoagulation should be initiated as soon as possible before AFib cardioversion. When intracardiac thrombus is excluded, cardioversion may proceed in patients treated with anticoagulants.⁵  

After cardioversion, uninterrupted anticoagulation is recommended for four weeks. Interrupted post-cardioversion anticoagulation may be considered in patients with CHA2DS2-VASc of 0 in men or 1 in women with very low associated thromboembolic risks.⁵  

The decision to cardiovert a haemodynamically stable patient with acute AFib should include care team discussions, and patient counselling to stress the importance of uninterrupted anticoagulation therapy following acute cardioversion.⁵  

If interruption of anticoagulation is anticipated (due to eg planned surgical procedures) in a haemodynamically stable patient with acute AFib, rate control should be initiated first, and cardioversion should be postponed until no further interruption of anticoagulation is anticipated.⁵ 

Options for anticoagulation during acute hospitalisation include parenteral and oral formulations. Approved agents include:⁵   

• Warfarin: Contraindicated in known bleeding complications 
• Heparin: May be used as the initial parenteral anticoagulation as a bridge to therapeutic oral anticoagulation with warfarin. Contraindications include active bleeding, severe thrombocytopenia, heparin-induced thrombocytopenia (HIT), heparin-induced thrombocytopenia and thrombosis (HITT), and thrombocytopenia with pentosan polysulphate. 
• Enoxaparin and dalteparin: May be used as the initial parenteral anticoagulation as a bridge to therapeutic oral anticoagulation with warfarin. Contraindications for enoxaparin include active bleeding, severe HIT, and HITT. Contraindications for dalteparin include a history of HIT within the past 100 days or in the presence of circulating antibodies and active bleeding. 
• Argatroban and bivalirudin: May be used in lieu of heparin-containing parenteral anticoagulants in HIT patients. Contraindications for both agents include active bleeding. 

Given rapid time to therapeutic efficacy and ease of continuation, direct oral anticoagulants have been recommended for thromboembolic prophylaxis including in the setting of cardioversion for AFib, barring contraindications. Approved DOACs include:⁵ 

• Dabigatran and rivaroxaban: Not recommended if creatinine clearance is <15ml/min. 
• Apixaban: Not recommended in patients with severe hepatic impairment (Child-Pugh C).

Conclusion  

Patients with acute AFib have high rates of recurrence. The five-year AFib recurrence rates are 42%-68%, 39% and 76% in patients with acute medical illness, non-cardiac surgeries, and cardiac surgeries respectively. Therefore, patients with acute AFib warrant long-term outpatient follow-up evaluation and management.⁵ 

Follow-up should include an assessment of family history, associated conditions and risk factors, structural heart disease, thromboembolic risk, and symptoms. Further management of AFib, anticoagulation, and considerations for monitoring and guidance on appropriate risk factor modification are key aspects of the long-term management of patients with acute AFib.⁵  

REFERENCES: 

1. Desai DS, Hajouli S. Arrhythmias. [Updated 2022 Jun 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558923/ 
2. Naser N, Dilic M, Durak A, et al. The Impact of Risk Factors and Comorbidities on The Incidence of Atrial Fibrillation. Mater Sociomed, 2017. 
3. Elliott AD, Middeldorp ME, Van Gelder IC, et al. Epidemiology and modifiable risk factors for atrial fibrillation. Nat Rev Cardiol, 2023  
4. Linz D, Sanders P, Pitman B, Dobrev D, Lau DH. Atrial fibrillation in sub-Saharan Africa: The knowns and unknowns? Int J Cardiol Heart Vasc, 2019. 
5. Chyou JY, Barkoudah E, Dukes JW, et al. Atrial Fibrillation Occurring During Acute Hospitalization: A Scientific Statement From the American Heart Association. Circulation, 2023.