Atrial Fibrillation

Definition

Most common cardiac arrhytmia involving atria of the hearts.

Classification

(ACC/AHA/ESC guidelines)

AF Category	Defining Characteristics
First detected	only one diagnosed episode
Paroxysmal	recurrent episodes that self-terminate in less than 7 days.
Persistent	recurrent episodes that last more than 7 days
Permanent	an ongoing long-term episode

Additional classification

Lone atrial fibrillation (LAF)	absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years
Nonvalvular AF	absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair
Secondary AF	occurs in the setting of a primary condition which may be the cause of the AF, such asacute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease

Epidemiology
Incidence/prevalence increases with age.
Male > Female
Age <40, <0.1%/year; >80, >1.5%/year
Lifetime risk: 25% for those ≥40 years
Estimated 0.4–1% of general population <60

Pathophysiology
In patients with PAF and no/minimal structural heart disease, triggering premature atrial beats and/or bursts of tachycardia emanate from the pulmonary venous ostia or other sites/
In patients with persistent/permanent AF and significant structural heart disease, multiple reentrant wavelets within atria may be cause.

Aetiology

Cardiovascular	Long-standing hypertension, Ischemic heart disease, CHF. Any form of carditis, Cardiomyopathy, Infiltrative heart disease of any type, Sick sinus syndrome
Respiratory	Pulmonary embolism, Pneumonia, Lung cancer, Hypothermia
Idiopathic	Lone atrial fibrillation is idiopathic and defined as the absence of any known etiologic factors plus normal ventricular function by echocardiography. Most patients with lone atrial fibrillation are younger than 65 years, although age is not used to define lone atrial fibrillation.
Drug use	Stimulants, Excessive alcohol (binge drinking), cocaine
Endocrine	Hyperthyroidism, pheochromocytoma, Low level of K, Mg, Ca
Neurological	Subarachnoid hemorrhage, stroke, Friedreich's ataxia
Familial	associated with defined ion channel abnormalities, especially sodium channels

Commonly Associated Conditions

Sick sinus syndrome

Atrial flutter:

Stroke - 4% a year

Presentation

Maybe asymptomatic. Palpitations, dyspnea, lightheadedness, cardioembolic event,
Irregularly irregular pulse; frequently tachycardic
The apical pulse rate is greater than radial rate, HS 1 is of variable intensity
Sign of underlying causes

Differential Diagnosis

Multifocal atrial tachycardia

Sinus tachycardia with frequent atrial premature beats

Atrial flutter


Investigation

FBC	anaemia, infection
UnE	looking for electrolyte disturbances or renal failure
Cardiac enzyme	CK and/or troponin level - MI
TFT	looking for thyrotoxicosis, a rare, but not-to-be-missed, precipitant
ECG	Absent P waves, replaced by irregular, chaotic fibrillatory waves, in the setting of irregular QRS complexes.Atrial rhtyhm= 300 bpm
Six-minute walk test	assess the adequacy of rate control.
Toxicology	Evaluate drugs toxicity
Transthoracic echocardiogram (TTE)	Evaluate for valvular heart disease, atrial and ventricular chamber and wall dimensions, ventricular function and evaluate for ventricular thrombi, pulmonary systolic pressure (pulmonary hypertension),pericardial disease
Transesophageal echo (TOE)	Evaluate for left atrial (LA) thrombus (particularly in the LA appendage) To guide cardioversion (if thrombus is seen, cardioversion should be delayed)
Holter monitoring	Helpful to establish diagnosis and evaluate rate control.
CXR	Look for radiographic evidence of CHF as well as signs of lung or vascular pathology (pulmonary embolism, pneumonia).
CT/MRI	If atrial fibrillation ablation is planned,
Others	D-dimer, ventilation-perfusion scan, or pulmonary angiography) if pulmonary embolus suspected

Management
Edited from New ECS Guideline (2010)

Initial assessment	ABC ECG- diagnosis Cardiac & arrythymia-related history+exam For severity of symptoms, determine EHRA score Echo for severe symptoms Estimate stroke risk using modified CHADS2 score known as CHA2DS2-VASc score From this, determine Oral Anticoagulant Assess risk of bleeding using HAS-BLED score A score of 3 or more indicates an increased one year bleed risk on anticoagulation which would be sufficient to justify caution or more frequent evaluation. Determine the time of onset: <48h or >48h Find causes :Echo, Thyroid Function test, FBC, Creatinine, Stress test
Management of acute /new onset A-Fib	Management depend on time after onset: i)  AF <48h Haemodically stable Start UFH  i.v. followed by LMWH iv / sc DC Cardioversion UFH or LMWH should be continued until the INR = 2.0 to 3.0 Start OAC after cardioversion only in patients with thrombo- embolic risk factors Haemodically unstable Pharmacological cardioversion: Use iv fleicanide (2mg/kg over 10min), propafenone(2mg/kg over 10min) or ibutilide (1mg/kg over 10min) Use iv amiodarone (5mg/kg over 1h) in structural heart disease i)  AF >48h or doubtful Haemodically stable Can apply 2 strategies: 1. Conventional 3 weeks Oral Antocoagulant (OAC) Give OAC eg: Vitamin K Agonist (VKA) for >3weeks before a cardioversion until INR 2-3 Continue OAC for >4week after cardioversion due to “atrial stunning”- a risk of stroke Continue OAC  lifelong in pt with stroke risk. 2. Transoesophageal Echocardiogram (TOE) strategy. If no LAA thrombus on TOE, start UFH & LMWH, then cardioversion, start 4 weeks OAC, continue longterm OAC if stroke risk If LAA thrombus on TOE, start 3 weeks OAC, if thrombus still present, opt for rate control, start long term OAC Haemodically unstable (angina, myocardial infarction, shock, or pulmonary oedema), Do immediate cardioversion GIve UFH or LMWH before cardioversion. Continue heparin until INR 2-3 After cardioversion, start 4 weeks OAC therapy or life-long if high risk factors for stroke
Left Atrial Appendage Occlusion	Definition Alternative for patients who cannot use oral anticoagulants, eg previous bleeding, non-compliance or pregnancy Techniques During cardiac catheterization, a device (such as the WATCHMAN device or PLAATO) consisting of an expandable nitinol frame is introduced into the left atrial appendage, the source of blood clots in more than 90% of cases. Post TOE to judge completeness of closure and the presence of blood clots. Low dose aspirin and clopidogrel OAC post- WATCHMAN device to allow blood vessel lining to form around the device Result In 210 patients receiving the PLAATO device, there was an estimated 61% reduction in the calculated stroke risk. Complications Pericardial effusion, incomplete LAA closure, dislodgement of the device, blood clot formation on the device requiring prolonged oral anticoagulation, and the general risks of catheter-based techniques (such as air embolism). The left atrium anatomy can also preclude use of the device in some patients.
Acute rate control	b-blockers or nondihydropyridine CCB. In severely compromised patients, i.v. verapamil or metoprolol can be very useful to slow atrioventricular node conduction rapidly. Amiodarone may be used, especiallyin those with severely depressed LV function. AF with slow ventricular rates may respond to atropine (0.5– 2 mg i.v.), Patients with symptomatic bradyarrhythmia may require either urgent cardioversion or placement of a temporary pacemakerlead in the right ventricle
Long-term Rate control	Lenient rate control- used a resting heart rate ,110 bpm in AF as the therapeutic target, Strict rate control aimed at a resting heart rate of ,80 bpm and an adequate increase in heart rate upon moderate exertion. (involve exercise test and 24H ECG) Drugs Choice of drugs depends on the underlying diseases B-blockers Metoprolol 2.5-5 mg iv Bisoprolol Atenolol in symptomatic Myocardial ischaemia Non-dihydropyridine CCB Verapamil 5mg iv Diltiazem for acute/chronic rate control. Avoid inheart failure because of -ve inotropic effect Digitalis glycosides Digoxin 0.5-1mg iv in pt with heart failure and LV dysfunction. Effective at rest. Others Amiodarone 5mg/kg in 1h iv If other measures unsuccessful It may cause severe extracardiac adverse events including thyroid dysfunction and bradycardia. Others Dronedarone for rest & during exercise not approved for permanent AF
Long term rhythm control	Goal: reduce AF-related symptoms Disopyramide 100-250mg t.i.d CI: systolic heart failure, caution when using concomitant QT prolonging drug Fleicanide 810-200 mg b.i.d CI: if Creatinine clearance <50mg/ml, coronary artery disease, reduced LVEF Fleicanide XL 200mg o.d Caution in the presence of conduction system disease Propaferone 150-300mg t.i.d CI: coronary artery disease, reduced LV ejection fraction Propaferone SR 225-425mg b.i.d Caution in the presence of conduction system disease, renal impairement D,I- Sotalol 80-160 mg b.i.d CI: LVH, systolic heart failure, pre-existing prolong QT Amiodarone 600mg o.d for 4 weeks 400mg o.d. for  4 weeks then 200mg o.d Caution when using concomitant medication with QT-prolonging drugs, hart failure Dronedarone 400mg bid CI: NYHA III-IV, unstable HF, concomitant QT prolonging drugs, CrCl<30mg/ml
Procedure	Atrioventricular node ablation (source; materprivate.ie) + pacemaker implantaion Definition Selective catheter-mediated destruction of the atrioventricular node or His bundle, with radiofrequency current serving as the predominant source of ablation energy to achieve complete heart block. Use Palliative or pt who fails pharmacological therapy Others: Wolff-Parkinson-White syndrome, supraventricular tachycardia, ventricular tachycardia, atrial fibrillation or atrial flutter. Pre Aspirin and Plavix or Warfarin for at least 1 week before the procedure TOE may be performed to confirm the absence of a clot. Steps The procedure can take 2–4 hours to perform Anaesthetise the groin and insert a cathether into a vein Wires are threaded along the cathther, guided by X-ray A different catheter is inserted to deliver radiowave energy to destroy the selected tissue. After that pace maker is fitted Post Bed rest 4-6h, monitor rhythm 2d hosp stay Anticoagulation for 1-3 month after ablation Video Result The likelihood of further AF is about 35%in patients with paroxysmal fibrillation and about 50% in patients with persistent fibrillation. Complication Allergy reaction Bruising, mild soreness/ oozing Rare: blood clot, stroke (<1%), infection, damage to vessels, damage tooesophagus (1/10,000), Death (<1/5000) Pacemaker choice CRT pacemaker Any type of AF, LVEF <45%, NYHA II DDD pacemaker paroxysmal AF, nomal LV function Single-chamber (WIR) pacemaker Persistent or permanent AF and normal LV function
Surgery	Maze Procedure Definiton a complicated set of incisions made in a maze-like pattern on the left and right atria to permanently interrupt the abnormal electrical signals that cause irregular heartbeats Over time it evolved into Cox Maze IV- uses surgical ablation instead of incision Type: Open chest, or Close chest: Mini Maze Uses Patients with paroxysmal AF have been considered the best candidates, Patients who fail rhythm or antiarrhythmic drugs and/or rate control drugs, or intolerant to them Pre-op complete phisical, ECG, echo, stress test, CXR, XT, Holter monitor, TOE, blood work. Fast 12h prior Op 3-4 small incisions on each side of the chest An ablation device, and a thoracoscope are inserted A surgical ablation energy source is used to create a conduction block that isolates the pulmonary veins and stops the chaotic electrical signals from disrupting the heart. While in there, the surgeon treats the Ligament of Marshall and nerve bundles that are called the ganglionic plexi, and removes or clamps off the left atrial appendage to reduce the risk of blood clots and stroke. Video Results 0%–90% range for paroxysmal AF 50%–75% range for persistent and longstanding AF freedom from stroke in excess of 99%. Complications Collapsed lung from deflating the lung in surgery, which is correctable with a chest tube Vein inflammation (phlebitis) Heart tissue inflammation (pericarditis) Blood vessel or heart damage Death
Upstream Therapy	Def Treatment with ACEIs, ARBs, aldosterone antagonists, statins, and omega-3 polyunsaturated fatty acids (PUFAs) are usually referred to as ‘upstream’ therapies for AF Aim Prevent or delay myocardial remodelling associated with hypertension, heart failure, or inflammation (e.g. after cardiac surgery) May deter the development of new AF (primary prevention) May deter progression to permanent AF

Complications

• Embolic stroke
• Peripheral arterial embolization
• Bleeding with anticoagulation
• Tachycardia-induced cardiomyopathy with prolonged periods of inadequate rate control

Prognosis

• Warfarin anticoagulation reduces annual embolic stroke rate from ~5% to 1–2%. Aspirin reduces risk to 3–4% annually.
• Clinical risk factors for stroke include >65, diabetes, HTN, history of stroke or TIA, history of heart failure.
• AF increases risk of morbidity and mortality, but prognosis is a function of underlying heart disease.