Friday, April 2, 2021

Atrial Fibrillation Case File

Posted By: Medical Group - 4/02/2021 Post Author : Medical Group Post Date : Friday, April 2, 2021 Post Time : 4/02/2021
Atrial Fibrillation Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 11
A 54-year-old man comes to the emergency room with a 3-day history of palpitations. fatigue. and shortness of breath. He has had similar symptoms in the past, but these were always short-lived and he did not previously seek medical attention. He denies chest pain or syncope. His medical history is notable for obesity, treated hypertension, and obstructive sleep apnea. His social history reveals episodic heavy alcohol consumption but no illicit drug use. Family history is unremarkable. On physical examination, the patient is comfortable. His pulse is irregularly irregular with a heart rate of 110 bpm and his blood pressure is 126/87 mmHg. There is no jugular venous distension. Cardiac examination is normal apart from the irregular rhythm. The lung fields are clear, and there is no peripheral edema.

c What is the most likely diagnosis?
c What is the best next diagnostic step?
c What is the best next step in therapy?

Answer to Case 11:
Atrial Fibrillation

Summary: A 54-year-old man with obesity, hypertension, obstructive sleep apnea, and excessive alcohol consumption comes to the emergency room with a 3-day history of palpitations, fatigue, and shortness of breath. He has had similar symptoms in the past, but these were always short-lived and he did not previously seek medical attention. On physical examination, his heart rate is 110 bpm irregularly irregular, and blood pressure is 126/87 mmHg. Cardiopulmonary examination is normal apart from the irregular rhythm.
  • Most likely diagnosis: Paroxysmal atrial fibrillation.
  • Next diagnostic step: Electrocardiogram as shown in Figure 11-1.
  • Next step in therapy: Anticoagulation and rate control.
ANALYSIS

Objectives
  1. Know the diagnostic approach to supraventricular tachycardia. 
  2. Describe the difference between the mechanisms of atrial fibrillation and atrial flutter.
  3. Understand the importance of anticoagulation in atrial fibrillation and atrial flutter.
  4. Be familiar with the role of rate and rhythm control strategies in the management of atrial fibrillation.
Considerations

This 54-year-old patient has several risk factors for the development of atrial fibrillation. Hypertension, obesity, sleep apnea, and heavy alcohol consumption–especially binge drinking–are all associated with a greater risk for atrial fibrillation. Thus, while other supraventricular tachycardias are possible, atrial fibrillation or atrial flutter is the most likely diagnosis. The irregularly irregular pulse is also very suggestive. An ECG should confirm the diagnosis and differentiate between atrial fibrillation and atrial flutter (Figures 11-1 and 11-2). The first priority should be prevention of thromboembolic stroke, which is perhaps the direct consequence of atrial fibrillation or flutter. For most patients and for patients in whom an early rhythm control strategy is planned, stroke prevention requires systemic anticoagulation with warfarin or a novel oral anticoagulant (NOAC). Control of the ventricular rate is also important to limit symptoms and to avoid the deleterious effects of persistent tachycardia on left ventricular function. Rate control is generally achieved with negatively chronotropic drugs such as beta-blockers and nondihydropyridine calcium channel blockers such as diltiazem. Acute cardioversion of atrial fibrillation

Atrial fibrillation

Figure 11-1. Atrial fibrillation. Note the absence of P waves and the fine "f waves" which represent fibrillatory activation of the atria, along with the irregularly irregular ventricular rate.

Atrial flutter

Figure 11-2. Atrial flutter. Note the regular, organized atrial activity, in contrast to atrial fibrillation, The flutter waves are best seen in the inferior leads (II, III, and a VF) and are consistent throughout the rhythm stip. In this case, the ventricular response is variable with a regularly irregular pattern where the interval between each Qr s  complex is a multiple of the atrial flutter cycle length.

or atrial flutter episodes with a definite onset within the last 48 hours can be considered, although in this case the onset of symptoms is outside this timeframe. If spontaneous conversion to sinus rhythm does not occur, cardioversion can be undertaken after either at least 3 weeks of therapeutic anticoagulation or a transesophageal echocardiogram demonstrating the absence of left atrial appendage thrombus. Underlying potentially reversible causes of atrial fibrillation such as hyperthyroidism should be excluded, and an echocardiogram to assess for structural heart disease– especially mitral valve disease and left ventricular dysfunction–should be ordered. Patients with symptoms or signs suggestive of coronary artery disease may require noninvasive testing to exclude active ischemia.

Approach To:
Atrial Fibrillation and Atrial Flutter

DEFINITIONS

ATRIAL FIBRILLATION: A chaotic atrial rhythm characterized by very rapid and uncoordinated depolarization (fibrillation) of the atria with resultant loss of atrial mechanical contraction and an irregular, often rapid, ventricular rate.

ATRIAL FLUTTER: A macroreentrant atrial tachycardia around structural or functional barriers in the atria and characterized by rapid atrial contraction at 250–300 bpm with ventricular response that is often fast and regular because of 2:1 conduction over the AV node.

PAROXYSMAL: Episodes of atrial fibrillation lasting <7 days (typically hours) before spontaneously terminating.

PERSISTENT: Episodes of atrial fibrillation lasting >7 days, typically until electrical or pharmacologic cardioversion.

PERMANENT: Continuous atrial fibrillation present for >1 year, or when a decision has been made not to attempt rhythm control.

LONE ATRIAL FIBRILLATION: Atrial fibrillation in patients younger than 60 years and without cardiopulmonary disease.

RATE CONTROL: A strategy to alleviate the symptoms of atrial fibrillation by controlling the ventricular rate with medications and occasionally ablation of the AV node along with pacemaker implant, without attempts to convert the rhythm to sinus rhythm.

RHYTHM CONTROL: A strategy to reestablish and maintain sinus rhythm through the use of antiarrhythmic drugs, cardioversion, and catheter or surgical ablation.


CLINICAL APPROACH

Etiologies
Atrial fibrillation and flutter do not have a single unifying cause. Instead, a number of predisposing conditions are described, especially for atrial fibrillation (Table 11-1). Paroxysmal atrial fibrillation is assumed to arise from rapid repetitive atrial depolarizations originating near the pulmonary vein ostia, while persistent atrial fibrillation requires additional abnormalities, especially in the left atrium, for its maintenance. Atrial flutter is less common but also occurs in conditions that cause atrial dilatation, such as pulmonary embolus, mitral or tricuspid valve disease, and congestive heart failure. Typical atrial flutter results from macroreentry around the tricuspid valve and variable amounts of the right atrium. Atypical atrial flutter occurs usually after cardiac surgery or ablation, and is due to reentry around atrial incisions or scars.

increased risk of atrial fibrillation

Clinical Presentation
The most common symptoms of atrial fibrillation are fatigue, reduced exercise tolerance, and palpitations. For younger patients in whom ventricular rates are generally higher, palpitations predominate. In older patients and in those in whom rates are better, controlled fatigue and exercise intolerance, which can be insidious, are more prominent. Patients with coronary artery disease may present with angina due to rate-related ischemia. Those with heart failure often present with acute decompensation due to loss of atrioventricular synchrony and tachycardia. Most patients have some symptoms that may be manifest as an improvement in exercise capacity after restoration of sinus rhythm, but some are truly asymptomatic. Some patients present with stroke or transient ischemic attack (TIA), or with heart failure due to prolonged tachycardia.

Treatment
The first line of treatment of atrial fibrillation is anticoagulation to reduce the risk of stroke or systemic embolism. The risk for stroke is approximately 5 times higher in patients with atrial fibrillation than in the general population, but that risk can be reduced by nearly two-thirds with appropriate anticoagulation. Heparin or lowmolecular- weight heparin are used in recent-onset atrial fibrillation in hospitalized patients. The decision to prescribe long-term anticoagulation is based on risk stratification using clinical risk assessment tools such as the CHADS2 (where CHADS is Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus, Stroke) or CHA2DS2-VASc (vascular disease history) score (Table 11-2) and should be weighed against the risk for major bleeding due to anticoagulation using similar risk assessment tools such as HAS-BLED [Hypertension, abnormal kidney or liver function, stroke history, bleeding predisposition, Labile INR, Elderly (age 65 or older),

CHADS2 and CHA2DS2-VASc SCORES

Note: Each risk factor is given 1 point except stroke/TIA/ peripheral embolism, which is given 2 in both systems, and age ≥75 in the CHA2DS2-VASc score. A score of ≥ 2 is considered an indication for anticoagulation, whereas either aspirin or anticoagulation is recommended for a score of ≥ 1, and aspirin for a score of 0.

drug or alcohol abuse]. In patients with one or more CHADS2 risk factors, anticoagulation with warfarin (with an INR of 2.0–3.0), dabigatran, rivaroxaban, or apixaban is preferred. Aspirin is used for low-risk patients, although its role is less clear. The risk of stroke and the benefit of anticoagulation is similar in patients who have paroxysmal and persistent atrial fibrillation. The role of anticoagulation is less well studied in patients with atrial flutter, but as this arrhythmia frequently coexists with atrial fibrillation, the same guidelines are used.

Two strategies can be used to control the arrhythmia itself: (1) rhythm control, where attempts are made to restore and maintain sinus rhythm through the use of antiarrhythmic drugs, cardioversion, and catheter-based or surgical ablation; and (2) rate control, where atrial fibrillation is accepted as the rhythm but the ventricular rate is controlled with drugs, or occasionally pacemaker implantation with ablation of the AV node in patients with refractory tachycardia. Mortality rates are equivalent between these two approaches, and as most strokes occur when anticoagulation is stopped, this should be continued in patients with risk factors even when sinus rhythm is restored, because of the possibility of asymptomatic recurrences. Studies of drug-treated patients using long-term ambulatory monitoring have demonstrated that asymptomatic paroxysms of atrial fibrillation are common even when office ECGs consistently reveal sinus rhythm during follow-up.

Quality of life and functional status is consistently better in patients who successfully maintain sinus rhythm; however, current antiarrhythmic drug therapy is characterized by limited efficacy and toxicity. Nonetheless, this approach is favored in patients who have significant symptoms as a consequence of their atrial fibrillation.

Rate control is achieved primarily with beta-blockers and nondihydropyridine calcium channel blockers (eg, diltiazem or verapamil). Digoxin has a limited role as its vagotonic effect is quickly overcome by adrenergic states such as exercise and should rarely be used as the sole rate control agent. Atrial flutter is often more symptomatic and is generally more difficult to rate-control than atrial fibrillation, due to the rapid organized atrial depolarizations. In cases of refractory symptoms or hemodynamic compromise due to rapidly conducted atrial fibrillation, ablation of the AV node with implantation of a pacemaker is a useful strategy. The disadvantage of this approach is that it renders the patient permanently pacemaker-dependent. In patients with left ventricular dysfunction, biventricular pacing should be considered.

Class 1C or class 3 antiarrhythmic drugs are used to establish and maintain sinus rhythm in the rhythm control strategy. Class 1C drugs (flecainide or propafenone) are used in patients without structural heart disease. The class 3 drugs sotalol and dofetilide are options in patients with coronary artery disease, but are contraindicated in those with significant renal impairment. Dofetilide and another class 3 drug amiodarone are the only reasonable antiarrhythmic options for patients with left ventricular dysfunction as the 1C agents are associated with an increased risk for dangerous arrhythmia in patients with reduced pump function, and sotalol has significant negative inotropic properties. Amiodarone is perhaps the most effective antiarrhythmic for the treatment of atrial fibrillation but is limited by significant dose-dependent toxicities, especially thyroid and pulmonary. Dronedarone is an amiodarone analog that is contraindicated in patients with heart failure and those with permanent atrial fibrillation.

Cardioversion is used in patients with persistent atrial fibrillation. Therapeutic anticoagulation for at least 3 weeks prior to this is needed to ensure the absence of thrombus in the left atrial appendage, and for 4 weeks after, regardless of the baseline risk of thromboembolism. With the return of left atrial contractile function in sinus rhythm, the postcardioversion period presents a higher risk as any such thrombi may be dislodged. In patients who have not been anticoagulated. a transesophageal echo can be performed to exclude the presence of left atrial appendage thrombi; however, therapeutic anticoagulation after cardioversion is still required. Pharmacologic cardioversion can be achieved with oral flecainide or propafenone, or with intravenous ibutilide or amiodarone. Electrical cardioversion is performed by a cardiologist under anesthesia via an external defibrillator. A biphasic shock is delivered through the chest that alters transmembrane gradients via an incompletely understood mechanism, leading to the cessation of atrial fibrillation and the resumption of sinus rhythm. The use of antiarrhythmic drugs after cardioversion delays recurrence of atrial fibrillation and should be strongly considered.

Catheter-based ablation uses radiofrequency energy to isolate the pulmonary veins from the left atrium, thereby preventing the rapid discharges that form the electrophysiologic basis of paroxysmal atrial fibrillation from reaching the atrium. Catheter-based ablation is superior to antiarrhythmic drug therapy in the maintenance of sinus rhythm. Success rates are highest in patients with paroxysmal atrial fibrillation, normal or mildly dilated left atria, and without structural heart disease. The procedure is time-consuming and technically challenging, and effects on longterm stroke and mortality rates remain under investigation. Surgical ablation of atrial fibrillation is often combined with concomitant heart surgery (valve surgery or coronary artery bypass), although it can also be performed as a standalone procedure. Results may be comparable to catheter ablation, although recovery time and complication rates are higher, and standalone surgical ablation is generally reserved for those who have failed at or been turned down for catheter ablation.

Ablation of atrial flutter is technically more straightforward and associated with higher success rates (95%) and is superior to antiarrhythmic drugs, even as a firstline approach. Patients with symptomatic atrial flutter should be evaluated for catheter ablation rather than repeated cardioversions and extended antiarrhythmic drug therapy. The risk of developing atrial fibrillation in a patient with atrial flutter is approximately 10% per year, so continuation of anticoagulation in patients with risk factors for thromboembolism, even after successful ablation of atrial flutter, should be carefully considered.


COMPREHENSION QUESTIONS

Choose the correct answer (A–E) to the following statements:

11.1 An 83-year-old man with a history of hypertension and diabetes is referred to you for management after presenting to the emergency department last week with several hours of recent-onset palpitations. He was found to be in atrial fibrillation with a rapid ventricular rate and underwent successful electrical
cardioversion. He was discharged to home from the ED with prescriptions for metoprolol and a limited supply of low-molecular-weight heparin to use while he began warfarin therapy. His point-of-care INR in the office today is 2.2 on warfarin 5 mg daily. The patient is questioning his need for anticoagulation, citing the fact that he is now back in normal rhythm after cardioversion and is not in atrial fibrillation permanently. He reports that his 50-year-old nephew has a diagnosis of atrial flutter and takes aspirin only for stroke prevention. He considers himself healthier than the average 83-year-old man and feels that his risk for stroke must be relatively low. He would like to know more about atrial fibrillation and his risk for stroke. You should tell him which of the following?
A. His stroke risk is similar regardless of whether his atrial fibrillation is paroxysmal, persistent, or permanent.
B. His stroke risk would be considerably lower if he had atrial flutter like his nephew.
C. His stroke risk is similar to that of the age-matched general population.
D. His stroke risk 1 week after cardioversion is lower than it was prior to cardioversion
E. His stroke risk should be reduced to a similar extent by aspirin and warfarin.

11.2 A 75-year-old woman with rheumatic mitral valve disease treated with a mitral bioprosthesis 10 years ago is referred to you for management of her permanent atrial fibrillation. She has been in atrial fibrillation for the past 4 years and was initially asymptomatic, but over the past year she has developed progressive exertional dyspnea, ankle swelling, and fatigue. This correlates with a gradual increase in her resting average heart rate from 89 bpm 1 year ago to 128 bpm as assessed by a recent 48-hour ambulatory monitor. Her primary care physician has attempted to treat her with metoprolol, but her dose has been limited by hypotension. Digoxin was also added, but this did not significantly improve her heart rate. She takes dose-adjusted warfarin for stroke prevention. She has failed numerous electrical cardioversions even in the setting of previous antiarrhythmic therapy with amiodarone and sotalol.

Her examination is noteworthy for distended jugular veins, an irregularly irregular tachycardia, faint bibasilar rales, and bilateral pitting edema of the legs. Her ECG reveals atrial fibrillation with a rate of 115 bpm and ST segment findings consistent with digoxin effect. Her QTc interval is 520 ms. You arrange for an office echocardiogram, and this reveals a mildly dilated left ventricle with an ejection fraction of 35%, a dilated right ventricle with mild systolic dysfunction, an intact mitral prosthesis with an average mean gradient of 7 mmHg and trivial regurgitation, and a markedly enlarged left atrium. Her ejection fraction by echocardiogram last year was 55%. In addition to proper medical management of her newly discovered heart failure, what is the most appropriate next step?
A. Treatment with dofetilide for rhythm control.
B. Treatment with propafenone for rhythm control.
C. Referral for catheter-based ablation of her atrial fibrillation.
D. Referral for catheter-based ablation of the AV node and pacemaker
implantation.
E. Referral for redo mitral valve replacement and surgical MAZE procedure.

11.3 Which of the following statements regarding atrial flutter is true?
A. Ablation of atrial flutter is more difficult than that of atrial fibrillation.
B. Atrial flutter presents a risk of thromboembolism similar to that for atrial fibrillation.
C. Rate control in atrial flutter is easier than rate control in atrial fibrillation.
D. Atrial flutter is associated with fewer symptoms than atrial fibrillation.
E. Atrial flutter is caused by chaotic irregular atrial depolarizations.


ANSWERS

11.1 A. The stroke risk associated with atrial fibrillation is similar regardless of whether the atrial fibrillation is considered paroxysmal, persistent, or permanent. This is because a large percentage of patients with paroxysmal atrial fibrillation have clinically silent recurrences and some of these episodes can exceed 24 hours in length. Mechanical atrial contraction can remain impaired for days to weeks after cardioversion before normalizing, and for this reason patients are considered to be at increased risk for stroke in the weeks immediately after cardioversion. Atrial flutter is felt to confer approximately the same stroke risk as atrial fibrillation. Given this patient’s elevated CHA2DS2- VASc score, his stroke risk would be expected to exceed that of the general population and he would be expected to derive a greater benefit from warfarin than aspirin.

11.2 D. This patient has failed reasonable attempts at both rate and rhythm control, and AV nodal ablation with pacing is the most definitive treatment option. This patient’s symptoms are most likely due to heart failure, which is likely the result of a tachycardia-mediated cardiomyopathy. Antiarrhythmic therapy with dofetilide or propafenone is unlikely to succeed, and both of these agents are contraindicated in this patient (for QT prolongation and LV dysfunction, respectively). With her longstanding atrial fibrillation and marked atrial enlargement, atrial fibrillation ablation would also be unlikely to succeed. Warfarin is the most appropriate choice for her anticoagulation as newer agents such as rivaroxaban have not been studied for use in patients with rheumatic mitral valve disease. This patient has a functional mitral prosthesis and does not require redo open-heart surgery.

11.3 B. Atrial flutter is a fast, organized rhythm that follows a rather predictable circuit involving the right atrium and tricuspid valve isthmus in most cases. Atrial flutter is generally more difficult to rate-control and less responsive to antiarrhythmic therapy than atrial fibrillation, but its predictable pathway makes it quite amenable to successful ablation. The stroke risk related to atrial fibrillation and atrial flutter is considered to be similar.

CASE CORRELATION
  • See also Case 11 (atrial fibrillation and flutter).

CLINICAL PEARLS
C Fatigue and exercise intolerance are common symptoms of atrial fibrillation, especially in the elderly.

C The risk of thromboembolism is similar in paroxysmal and persistent atrial fibrillation.

C Anticoagulation should be considered in all patients with risk factors for stroke.

C Anticoagulation should be continued in patients with a diagnosis of atrial fibrillation who are in sinus rhythm, as recurrences can be silent or present late.

C digoxin is a third-line rate control medication and should rarely be used as the sole therapy.

C Atrioventricular node ablation and pacemaker implant is useful for rate control if refractory to medical therapy.

C The choice of antiarrhythmic drug to achieve rhythm control is complex and should be initiated under expert supervision.

C Catheter ablation of atrial fibrillation is superior to antiarrhythmic drugs in the maintenance of sinus rhythm.

References

Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Analysis of pooled data from five randomized controlled trials. Arch Intern Med. 1994;154(13):1449–1457. 

Da Costa A, Thévenin J, Roche F, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114(16):1676–1681. 

Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114(7):e257–e354. 

Haïssaguerre M, Jaïs P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339(10):659–666. 

Lip GY. Implications of the CHA2DS2-VASc and HAS-BLED scores for thromboprophylaxis in atrial fibrillation. Am J Med. 2011;124:111–114. 

Wilber DJ, Pappone C, Neuzil P, et al. Comparison of antiarrhythmic drug therapy and radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation: a randomized controlled trial. JAMA. 2010;303(4):333–340. 

Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: The Framingham Study. Stroke. 1991;22(8):983–988. 

Wyse DG, Waldo AL, DiMarco JP, et al. Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347(23):1825–1833.

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