Atrial Fibrillation Management

What is atrial fibrillation?

Atrial Fibrillation (AF) is the most common type of abnormal heart rhythm and is found in more than six million people worldwide. AF is avery fast and disorganised heartbeat that occurs in the upper chamber of the heart (the atrial). During AF, the atria beats between 350 and 600 times per minute. If you AF, you may experience symptoms such as dizziness, fatigue and shortness of breath.
During AF, blood does not empty properly from the upper chambers of your heart. The blood can pool and sometimes clot. This can ultimately lead to a stroke.

Symptoms of AFib

Many people with AFib feel no symptoms at all. Others can tell as soon as it happens. The symptoms of AFib are different for each person. This depends on age, the cause of the AFib (such as heart problems or other diseases), and on how much AFib affects the pumping of the heart. Symptoms include:
A faster-than-normal or irregular pulse (switching between fast and slow)
Shortness of breath
Heart palpitations (your heart may feel like it is racing, pounding, or fluttering)
Trouble with everyday exercises or activities
Pain, pressure, tightness, or discomfort in your chest
Dizziness, lightheadedness, or fainting
Increased urination (using the bathroom more often)

Treatment goals

Recent advances in the atrial fibrillation management therapies provide new solutions for those suffering from this condition.
Restore a normal heart rhythm
Control your heart rate
Reduce the potential for blood clot formation
Reduce your stroke risk
Your doctor will work with you to develop a treatment plan. The treatment prescribed will depend on your type of AF, your symptoms, and your lifestyle.

Treatment options

Your AF treatment plan may include:
Medication: A number of different medications may be prescribed to manage your heart’s rate or rhythm and reduce the risk of stroke.
Electrical cardioversion: AF can be treated electrically with a procedure called cardioversion. During the procedure, an electrical shock is delivered to your heart in order to restore a normal heart rhythm. The procedure is performed using short- acting anesthesia.
Catheter ablation: Catheter ablation is a procedure to burn the tissue with radio frequency heat responsible for AF. During the procedure, small catheters are placed into the heart to study its electrical activity and help locate the problem areas. These problem areas are then destroyed (ablated).
Implantable devices: In select cases, a pacemaker may be implanted after a AF ablation procedure to keep the heart rate stable.
Surgical therapy for AF: Surgical therapy may be an option for people with persistent or permanent AF that cannot be managed with drugs or other therapies. These procedures require open heart surgery and general anesthesia. For patients who have AF in addition to heart problems requiring surgery, it may be possible to perform both surgeries at the same time.

Risk Factors for AFib

Even people committed to healthy lifestyles and who have no other medical problems can develop AFib. The most common risk factors include:
  • Age over 60
  • High blood pressure
  • Coronary artery disease
  • Heart failure
  • Heart valve disease
  • Untreated atrial flutter (another type of abnormal heart rhythm)
  • Prior open-heart surgery
  • Sleep apnea
  • Thyroid disease
  • Diabetes
  • Chronic lung disease
  • Excessive alcohol or stimulant use
  • Serious illness or infection

Taking care of yourself
  • Obesity
  • Diabetes
  • High blood pressure
  • Heart disease

Complex Arrythmia a.k.a. Ventricular Tachycardia

Sustained ventricular tachycardia (VT) may lead to hemodynamic collapse. Consequently, these patients require urgent conversion to sinus rhythm. The strategy for conversion depends on hemodynamic stability.
Unstable patients have signs or symptoms of insufficient oxygen delivery to vital organs as a result of the tachycardia. Such manifestations may include the following:
  • Chest pain
  • Dyspnea
  • Hypotension
  • Altered level of consciousness
Unstable patients with monomorphic VT should be immediately treated with synchronized direct current (DC) cardioversion. Unstable polymorphic VT is treated with immediate defibrillation. Stable patients have adequate vital end-organ perfusion and thus do not experience signs or symptoms of hemodynamic compromise. Treatment depends on whether the VT is monomorphic or polymorphic and whether left ventricular function is normal or impaired (e.g. reduced left ventricular ejection fraction [LVEF] or heart failure).
In stable patients with monomorphic VT and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide or sotalol. Lidocaine may also be used.
A 12-lead electrocardiogram (ECG) should be obtained for all patients of VT before conversion. It helps to further plan the long term management of these patients.
If left ventricular function is impaired, amiodarone (or lidocaine) is preferred to procainamide for pharmacologic conversion because procainamide exacerbarates heart failure. However, evidence indicates that amiodarone should not be the first-line antiarrhythmic for stable VT, because its effects on myocardial conduction and refractoriness. If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.
Polymorphic VT in stable patients typically terminates on its own. However, it tends to recur. After sinus rhythm returns, the ECG should be analyzed to determine whether the QT interval is normal or prolonged. Polymorphic VT in patients with a normal QT interval is treated in the same manner as monomorphic VT.
If the patient has runs of polymorphic VT punctuated by sinus rhythm with QT prolongation, treatment is with magnesium sulfate, isoproterenol, pacing, or a combination thereof. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide and amiodarone are contraindicated because of their QT-prolonging effects. Magnesium is unlikely to be effective in patients with a normal QT interval.
In patients with electrolyte imbalances (eg, hypokalemia or hypomagnesemia from diuretic use), correction of the abnormality may be necessary for successful cardioversion. In patients with severe digitalis toxicity (eg, with sustained ventricular arrhythmias, advanced atrioventricular AV block, or asystole), treatment with antidigitalis antibody may be indicated.
After conversion of VT, the clinical emphasis shifts to determining the severity of heart disease, assessing the prognosis, and formulating the best long-term management plan. Options, depending on the severity of symptoms and degree of structural heart disease, include the following:
  • Antiarrhythmic medications
  • Implantable cardioverter-defibrillator (ICD)
  • Catheter ablation
Combinations of these therapies are often used when structural heart disease is present.
Antiarrhythmic drugs have traditionally been the mainstays of treatment for clinically stable patients with VT. However, some patients experience unacceptable side effects or frequent recurrence of VT with drug therapy. As a result, cardiologists are increasingly making use of devices and procedures designed to abort VT or to remove the arrhythmogenic foci in the heart. In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.
Congenital long QT syndrome and catecholamine polymorphic VT has been linked to sudden cardiac death. Patients with these disorders are managed with a combination of genetic typing, beta blockers, lifestyle modification, and, in selected cases, ICD placement.
In the 1980s, several centers explored ventricular arrhythmia surgery, using excision and cryoablation of infarct zones to prevent recurrent VT. This strategy has been essentially abandoned as a consequence of the high mortality and the advent of ICDs and ablative therapies.

Cardioversion in Acute Ventricular Tachycardia

The acute emphasis in patients with VT is on achieving an accurate diagnosis and conversion to sinus rhythm. VT associated with loss of consciousness or hypotension is a medical emergency necessitating immediate cardioversion. In a normal-sized adult, this is typically accomplished with a 100- to 200-J biphasic cardioversion shock administered according to standard Advanced Cardiovascular Life Support (ACLS) protocols.
Reversible risk factors for VT should be addressed. Efforts should be made to correct hypokalemia and to withdraw any long-term medications associated with QT-interval prolongation.
When VT occurs in patients with ongoing myocardial ischemia, lidocaine is suggested as the primary antiarrhythmic medication, because the mechanism in these cases is thought to be abnormal automaticity rather than reentry.[45] Although IV lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. In situations involving torsades de pointes, magnesium sulfate may be effective if a long QT interval is present at baseline.
Synchronized cardioversion should be considered at an early stage if medical therapy fails to stabilize the rhythm. The initial shock energy should be 100 J (monophasic), followed by higher shock energies if the response is inadequate.
Occasionally, patients present with wide QRS complex tachycardia of unknown mechanism. In the absence of pacing, the differential diagnosis includes VT and aberrantly conducted supraventricular tachycardia (SVT; see the images below). If hemodynamic compromise is present or if any doubt exists about the rhythm diagnosis, the safest strategy is to treat the rhythm as VT.
Supraventricular tachycardia with aberrancy. Tracing is from patient with structurally normal heart who has normal resting ECG. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note relatively narrow RS intervals in precordial leads.
ECG from 48-year-old man with wide-complex tachycardia during treadmill stress test. Any wide-complex tachycardia tracing should raise possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of supraventricular rhythm. By Brugada criteria, RS complexes are apparent in precordium (V2-V4), and interval from R wave onset to deepest part of S wave is < 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon aVR, which shows no R wave, initial q wave width < 40 ms, and no initial notching in q wave. Last Vereckei criterion examines slope of initial 40 ms of QRS versus terminal 40 ms of QRS complex in aVR. In this case, initial downward deflection in aVR is steeper than terminal upward deflection, yielding Vi/Vt ratio >1. All of these criteria are consistent with aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with sinus tachycardia mechanism.
If the clinical situation permits, a 12-lead ECG should be obtained before conversion of the rhythm. The ECG criteria of Brugada et al[6] may be useful in differentiating the arrhythmia mechanism (see Workup).
Rarely, patients present with repetitive runs of nonsustained VT (see the image below). Prolonged exposure to this (or any other) tachycardia may cause a tachycardia-induced cardiomyopathy, which typically improves with medical or ablative treatment of the VT
Repetitive monomorphic ventricular tachycardia (VT) from asymptomatic 45-year-old female wind-surfer with structurally normal heart. This ECG pattern is typical for idiopathic VT arising from right ventricular (RV) outflow tract. This rhythm is often exertional and, unlike ischemic VT, suppressed by beta blockade or verapamil. Prognosis is good, with 2 exceptions: (1) Sudden death may be seen if RV dysplasia or exceptionally rapid VT is encountered; and (2) occasionally, patients with incessant VT develop congestive heart failure due to tachycardia-induced cardiomyopathy or frequent ectopy. Cardiomyopathy generally resolves when tachycardia is treated.

Pulseless VT

Pulseless VT, in contrast to other unstable VT rhythms, is treated with immediate defibrillation. High-dose unsynchronized energy should be used. The initial shock dose on a biphasic defibrillator is 150-200 J, followed by an equal or higher shock dose for subsequent shocks. If a monophasic defibrillator is used, the initial and subsequent shock dose should be 360 J.
Shock administration should be followed by immediate chest compressions, airway management with supplemental oxygen, and vascular access with administration of vasopressors. In cases of shock-resistant pulseless VT, the use of antiarrhythmic medications may be considered. IV amiodarone is the drug of choice.
Vasopressors can include epinephrine 1 mg IV given every 3-5 minutes or, in lieu of epinephrine, vasopressin 40 units IV as a 1-time dose.[46] ACLS drug-therapy guidelines recommend the use of IV amiodarone or lidocaine as the first-line adjunctive antiarrhythmic treatment of shock-resistant pulseless VT.

Poststabilization Management

After initial treatment and stabilization, patients with VT generally should undergo the following:
  • Referral to a cardiologist
  • Admission to a monitored bed
  • Further studies, such as electrophysiologic study (EPS)
  • Consideration for radiofrequency ablation (RFA)
  • Consideration for ICD placement
Initiation of antiarrhythmic medications may require telemetry monitoring for drug-induced proarrhythmia. Patients starting class IA and class III drugs should be monitored for corrected QT (QTc) prolongation and torsades de pointes until steady-state drug levels (≥5 clearance half-lives) have been reached. A notable exception is amiodarone, which may require months to achieve steady state; drug loading of amiodarone necessarily is completed on an outpatient basis.
Class IC antiarrhythmics are associated with drug-induced VT and rate-related conduction slowing. Many centers commit their patients to telemetry monitoring and predischarge exercise testing during initiation of agents from this class. Sinus bradycardia and sinus node dysfunction are often exacerbated by antiarrhythmic drugs.
In adult patients with ventricular arrhythmias whose age, gender, and symptoms indicate a moderate or greater likelihood of coronary heart disease, the ACC/AHA/ESC guidelines recommend exercise testing to provoke ischemic changes or ventricular arrhythmias.
Regardless of age, exercise testing is useful in patients with established or suspected exercise-induced ventricular arrhythmias, including catecholaminergic VT, to provoke the arrhythmia, to confirm a diagnosis, and to ascertain the patient’s response to tachycardia.

Long-Term Treatment

Patients with monomorphic VT who have structurally normal hearts are at a low risk of sudden death. Consequently, ICDs are rarely necessary in this setting; these patients are almost always managed with medications or ablation.
Antiarrhythmic drug trials have been disappointing, particularly in patients with left ventricular dysfunction. Some antiarrhythmic drugs may actually increase sudden-death mortality in this group. This is a particular concern with Vaughan Williams class I antiarrhythmics, which slow propagation and reduce tissue excitability through sodium-channel blockade. For most patients with left ventricular dysfunction, current clinical practice favors class III antiarrhythmics, which prolong myocardial repolarization through potassium-channel blockade.
Amiodarone is a complex antiarrhythmic drug that deserves special mention. It is generally listed as a class III agent but has measurable class I, II, and IV effects. Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction.
As per the ACC/AHA/ESC 2006 guidelines, amiodarone, when used in combination with beta blockers, can be useful for patients with left ventricular dysfunction due to previous myocardial infarction (MI) and symptoms due to VT that do not respond to beta blockers.
In the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) trial, which compared long-term treatment with 7 antiarrhythmic drugs (not including amiodarone) in patients with VT, the risks of adverse drug effects, arrhythmia recurrence, or death from any cause were lowest with sotalol.[50] The other antiarrhythmic drugs studied in the ESVEM trial were imipramine, mexiletine, pirmenol, procainamide, propafenone, and quinidine.
In patients with heart failure, the best-proven—albeit nonspecific—antiarrhythmic drug strategies include the use of the following:
  • The beta receptor–blocking drugs carvedilol, metoprolol, and bisoprolol
  • Angiotensin-converting enzyme (ACE) inhibitors
  • Aldosterone antagonists
According to the ACC/AHA/ESC guidelines, statin therapy is advantageous in patients with coronary heart disease, to reduce the risk of vascular accidents, ventricular arrhythmias (possibly), and sudden cardiac death.
Although idiopathic VTs often respond to verapamil, this agent may cause hemodynamic collapse and death when administered to treat VT in patients with left ventricular dysfunction. Therefore, verapamil (or any other calcium-channel blockers) is contraindicated in any patient with wide-complex tachycardia of uncertain etiology.

Catheter Ablation

RFA via endocardial or epicardial catheter placement can be used to treat VT in patients with left ventricular dysfunction from previous MI, cardiomyopathy, bundle-branch reentry, and various forms of idiopathic VT (see the image below).
Curative ablation of ventricular tachycardia (VT). Patient had VT in setting of ischemic cardiomyopathy. VT was induced in electrophysiology laboratory, and ablation catheter was placed at critical zone of slow conduction within VT circuit. Radiofrequency (RF) energy was applied to tissue through catheter tip, and VT terminated when critical conducting tissue was destroyed.
Current techniques include 3-dimensional scar, late potential, and activation mapping, followed by high-energy RFA with irrigated-tip catheters capable of creating deeper lesions in the thicker left ventricular wall. In some patients, percutaneous epicardial ablation can be used successfully when endocardial lesions fail.
Catheter ablation is used early in patients with idiopathic monomorphic VT (ie, VT in a structurally normal heart arising from a focal source) that is resistant to drug therapy, as well as in those who are drug-intolerant or do not wish to have long-term drug therapy.[27] In these patients, ablation is used to treat symptoms rather than to reduce the risk of sudden death. In patients with structurally normal hearts, Catheter ablation can eliminate symptomatic VT arising from the right or left ventricle.
Catheter ablation may also be used in patients with cardiomyopathy. The goal in these cases is to reduce arrhythmia burden and thereby minimize the number of ICD shocks.
The ACC/AHA/ESC guidelines recommend ablation in patients with bundle-branch reentrant VT. Most ischemic reentrant VT requires a slow conduction zone, which is usually located along the border of a scarred zone of myocardium. The small physical size of the slow conduction zone makes it an ideal target for focal ablation procedures. Cell disruption can be achieved by using RFA or cryoablation via transvenous catheters during closed-chest procedures.
A 2-center study examined the use of a percutaneous left ventricular assist device (pLVAD) in patients undergoing ablation for scar-related VT.[54] Use of a pLVAD allowed maintenance in VT for a significantly longer period by virtue of its ability to maintain end-organ perfusion. Whether this effect will translate into clinical benefits is unclear. At the least, however, this study demonstrates the benefit of pLVADs in patients with scar-related unstable VT.
Because patients with ischemic VT often have multiple reentrant circuits, ablation is typically used as an adjunct to ICD therapy. If VT arises from an automatic focus, the focus can be targeted for ablation.
In patients with structurally normal hearts, the most common form of VT arises from the right ventricular outflow tract (RVOT). The typical outflow tract ectopic beat shows a positive QRS axis in the inferior leads. Abnormal or triggered automaticity is the most likely mechanism, and focal ablation is curative in these patients. Ablation cure rates typically exceed 95% if the arrhythmia can be induced in the electrophysiology laboratory. Difficulty of outflow tract ablation may be predicted by ECG morphology.
Reentrant tachycardia may arise from the RVOT in patients with right ventricular dysplasia or repaired tetralogy of Fallot. These circuits are usually amenable to catheter ablation (see the image below).
Posteroanterior view of right ventricular endocardial activation map during ventricular tachycardia in patient with prior septal myocardial infarction. Earliest activation is recorded in red, late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
Bohnen et al performed a prospective study to assess the incidence and predictors of major complications from contemporary catheter ablation procedures.[57] Major complication rates ranged from 0.8% (SVT) to 6% (VT associated with structural heart disease), depending on the ablation procedure performed. These researchers reported that renal insufficiency was the only independent predictor of a major complication.

Implantable Cardioverter-Defibrillator Placement

The ICD has changed the face of ventricular arrhythmia management. Like pacemakers, these devices can be implanted transvenously in a brief, low-risk procedure. Once implanted, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or antitachycardia pacing algorithms (see the image below).
Termination of ventricular tachycardia (VT) with overdrive pacing. Patient has reentrant VT, which is terminated automatically by pacing from implantable cardioverter-defibrillator. Newer guidelines recommend ICD therapy to augment medical management for the following
  • Most patients with hemodynamically unstable VT
  • Most patients with prior MI and hemodynamically stable sustained VT
  • Most cardiomyopathy patients with unexplained syncope
  • Most patients with genetic sudden death syndromes when unexplained syncope is noted
In patients with prior VT or ventricular fibrillation (VF), the Antiarrhythmics Versus Implantable Defibrillators (AVID) study, the Canadian Implantable Defibrillator Study (CIDS), and the Cardiac Arrest Study, Hamburg (CASH), demonstrated better survival with ICD therapy than with antiarrhythmic therapy with amiodarone or sotalol. The survival difference was statistically significant in AVID, of borderline significance in CIDS, and insignificant in CASH. A meta-analysis of the 3 trials found a 28% reduction in relative risk of death.
Current guidelines also recommend ICD placement in patients with nonischemic dilated cardiomyopathy and considerable left ventricular dysfunction, or arrhythmogenic right ventricular cardiomyopathy, who have sustained VT or VF. These patients should be receiving optimal long-term medical therapy and may reasonably be expected to survive with good functional status for more than 1 year.
ICDs are not used for the following
  • Patients with VT or VF occurring during an acute ST-segment elevation MI (STEMI)
  • Patients with reversible, drug-induced VT
  • Patients with poor expected survival as a consequence of comorbid conditions
Because ICDs treat, rather than prevent, ventricular arrhythmias, as many as 50% of ICD recipients require therapy with antiarrhythmic drugs to reduce the potential for ICD shocks. The 2006 ACC/AHA/ESC guidelines support the use of catheter ablation in patients with an ICD who are receiving multiple shocks because of sustained VT that is not manageable by changing drug therapy or who do not wish to undergo long-term drug therapy.

Diet and Activity

Patients with ischemic VT may benefit from low-cholesterol diets, low-salt diets, or both. Patients with idiopathic VT may notice a reduction in symptoms when stimulants (eg, caffeine) are avoided.[59] Fish oil supplementation does not reduce the risk of VT or VF in ICD patients with recent sustained ventricular arrhythmia.
VT may be precipitated by increased sympathetic tone during strenuous physical exertion. One goal of successful VT management is to allow the patient to return to an active lifestyle through medications, ICD implantation, ablation therapy, or some combination thereof.
The 2006 ACC/AHA/ESC guidelines recommend that smoking be strongly discouraged in all patients who have, or who are thought to have, ventricular arrhythmias, aborted sudden cardiac death (SCD), or both. Cigarette smoking is an independent risk factor for SCD, typically from arrhythmia and regardless of underlying coronary heart disease, and smoking cessation significantly reduces the risk of SCD.
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    Dr. Vanita Arora is Senior Consultant Cardiac Electrophysiologist & Interventional Cardiologist at Apollo Hospital, Delhi. She has been a successful Cardiologist in India for the last 28 years. She is a DNB Cardiology, MD - Medicine, M.B.B.S . You can visit her at Apollo Hospital, Delhi. To book an appointment online with Dr. Vanita Arora - the best cardiologist in India, please contact us.

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