Atrial Fibrillation and Atrial Flutter



Atrial Fibrillation and Atrial Flutter


Aron Bender

Joseph Hadaya

Peyman Benharash

Eric Buch

Richard J. Shemin



INTRODUCTION


Epidemiology

Atrial fibrillation is the most common arrhythmia encountered clinically, and is a major driver of health care utilization. Data from the 2010 Global Burden of Disease Study estimate the prevalence of atrial fibrillation at approximately 33 million affected individuals worldwide, with higher prevalence in males.1 The incidence of atrial fibrillation continues to increase, with approximately 70 new cases per 100,000 person-years as of 2010.1 A recent database analysis reported a 10% to 20% cumulative risk of developing atrial fibrillation by the age of 80 years.2 Although assessing the cost burden associated with atrial fibrillation presents a challenge given the presence of comorbid conditions, there are at least 450,000 admissions for atrial fibrillation per year, and the annual incremental cost in the United States from atrial fibrillation alone is at least $6 billion.3

Atrial flutter often coexists with atrial fibrillation. As a result, atrial flutter is seen in more than one-third of patients with atrial fibrillation, and the majority of patients presenting with atrial flutter will also have atrial fibrillation.


Risk Factors

The risk factors for both atrial fibrillation and atrial flutter include age, male sex, genetic predisposition, hypertension, heart failure, valvular or ischemic heart disease, obesity, thyroid dysfunction, obstructive sleep apnea, lung disease, and excessive alcohol consumption. For atypical atrial flutter, prior atrial surgery or ablation is nearly a prerequisite.


PATHOGENESIS

Atrial fibrillation is a consequence of a variety of pathologic conditions that result in structural and electrophysiologic remodeling in the atria. The proposed mechanisms for the initiation and maintenance of atrial fibrillation are based on the concepts of triggers and substrate. Focal atrial tachycardia (most commonly originating in the pulmonary veins, less commonly in the right atrium, superior vena cava, left atrial appendage, or coronary sinus) can initiate fibrillation in the susceptible atria.4 As the duration and burden of atrial fibrillation increases, changes occur in the electrophysiologic characteristics of atrial myocytes, including shortening of the atrial effective refractory period and slowing of conduction velocity, which promote reentry and lead to longer episodes of atrial fibrillation.5 As the burden and duration of atrial fibrillation increases, there is also an increase in triggers beyond the pulmonary veins.6 The autonomic nervous system and a dense network of atrial innervation are also implicated in the initiation and maintenance of atrial fibrillation; procedural modification of ganglionic plexuses is one mechanistic explanation for the efficacy of ablation.7

As opposed to the disorganized electrical activity seen in atrial fibrillation, atrial flutter is an organized macroreentrant rhythm. The most common form of atrial flutter, cavotricuspid isthmus (CTI)-dependent atrial flutter, involves a circuit around the right atrium including a narrow corridor between the tricuspid valve and the inferior vena cava that is usually targeted in catheter ablation. Atypical atrial flutters can occur in either atrium, often as a result of prior surgery or ablation, where electrically inert atrial scar tissue forms an obstacle around which the flutter circuit can propagate (Figure 56.1 A-C).


CLINICAL PRESENTATION


Common Signs and Symptoms

Symptoms of atrial fibrillation and atrial flutter are variable across patients and even between episodes in the same patient. Common symptoms include palpitations, fatigue, dizziness, dyspnea, chest pressure, and exercise intolerance. Some patients are asymptomatic and diagnosed incidentally. The ventricular rate, duration, and stage of atrial fibrillation, as well as the presence of concurrent conditions, all play a role in the development of symptoms. The hemodynamic consequences of an irregular heart rhythm and loss of atrial contraction can be amplified in patients with underlying structural heart disease.8,9 As a result, the development of atrial fibrillation or flutter can lead to decompensated heart failure or angina. Chronically uncontrolled (ie, rapid) ventricular rates and irregularity can lead to cardiomyopathy and heart failure, even in patients without prior evidence of ventricular dysfunction. Syncope occurring in patients with atrial fibrillation or atrial flutter is uncommon, and is most often a result of sinus node dysfunction and resulting post-conversion pauses following termination of episodes.

Thromboembolism is a serious complication of atrial fibrillation and flutter, and may account for up to 15% of ischemic strokes in the United States. Stroke may be the first presentation of atrial fibrillation or flutter in a previously asymptomatic patient.10








Physical Examination Findings

The physical examination in atrial fibrillation is characterized by irregularity or variability in the pulse rate and intensity, loss of the atrial wave in the jugular venous waveform, and variability in the intensity of S1. In very rapidly conducted atrial fibrillation, the auscultated heart rate will be greater than is the heart rate measured by radial artery palpation, resulting in a “pulse deficit.”




DIAGNOSIS

The diagnosis of atrial fibrillation or flutter is confirmed electrocardiographically. Although the 12-lead electrocardiogram (ECG) is the gold standard for diagnosis of both atrial fibrillation and atrial flutter, these rhythms are often diagnosed on outpatient rhythm monitors ordered to evaluate for suggestive signs and symptoms or as part of the workup after a thromboembolic event. Atrial arrhythmias are also diagnosed via interrogation of pacemakers and defibrillators.

Atrial fibrillation is characterized on 12-lead ECG by rapid, irregular atrial activity without clear P waves and irregularity in the timing of QRS complexes (Figure 56.2).

The classification of atrial fibrillation is based on duration of episodes and is an important consideration in the planned treatment approach:



  • Paroxysmal atrial fibrillation: Episodes last less than 7 days, either terminating spontaneously or with intervention.


  • Persistent atrial fibrillation: Episodes last 7 days or longer.


  • Longstanding persistent atrial fibrillation: Continuous atrial fibrillation lasting at least 1 year in duration.


  • Permanent atrial fibrillation: This designation marks persistent atrial fibrillation with acknowledgment by both physician and patient that rhythm control will not be pursued.

The identification of CTI-dependent atrial flutter has important implications for developing a treatment plan. “Typical” counterclockwise atrial flutter is characterized by constant, repetitive, undulating atrial activity at 240 to 340 beats per minute (Figure 56.3). These flutter waves are negative in the inferior leads (II, III, aVF) with a gradual downsloping segment, followed by a sharper negative deflection, and then a sharp positive deflection returning above the baseline before the next cycle. Flutter waves tend to be positive in V1, with transition to negative across the precordium by V6. The ventricular rate is most commonly half the atrial rate because of the 2:1 conduction through the atrioventricular (AV) node, although depending on medications and balance in adrenergic input to the AV node, conduction can be a lower integer (3:1 or 4:1 conduction) or at times variable. Clockwise CTI-dependent atrial flutter has a variable ECG appearance, although it can be thought of as the opposite of the counterclockwise version with positive, notched flutter waves in the inferior leads and negative, notched deflections in V1 transitioning to positive deflections by V6.

Atypical atrial flutter is identified by rapid, organized atrial activity that does not fit the patterns consistent with CTI-dependent mechanisms and should be suspected in patients with prior atrial surgery or ablation (Figure 56.4).


MANAGEMENT OF ATRIAL FIBRILLATION


Medical Approach

The goals of treatment in atrial fibrillation and atrial flutter are to reduce the risk of thromboembolism, alleviate symptoms, and prevent the deleterious effects of rapid ventricular rates. The mainstays of therapy are therefore anticoagulation as directed by risk of thromboembolic events, risk factor modification, rate control strategies, and rhythm control strategies, both medical and procedural. The results of the 2002 AFFIRM trial, where a rhythm control approach did not demonstrate
a mortality benefit over a rate control approach, have guided treatment of atrial fibrillation.11 In most patients, a rhythm control approach is indicated for symptom relief, not to prevent stroke or increase life expectancy (Algorithm 56.1). An exception is patients with tachycardia-induced cardiomyopathy despite optimal achievable rate control, in whom rhythm control is the preferred strategy. There is also emerging evidence that patients with left ventricular systolic dysfunction of any etiology might especially benefit from maintenance of sinus rhythm.

















Prevention of Thromboembolic Events

Thromboembolic events, particularly stroke, present the greatest risk of morbidity and mortality in atrial fibrillation and flutter. The decision to pursue anticoagulation therapy should be based on an assessment of the individualized risk for both stroke and bleeding events, regardless of whether a rate control or a rhythm control approach is planned (Table 56.1). The most prominent risk stratification scheme is the CHA2DS2-VASc scoring system, where one point each is assigned for a history of congestive heart failure, female sex, hypertension, age
between 65 and 75 years, diabetes mellitus, or vascular disease, and two points are assigned for either age 75 years or older, or prior transient ischemic attack/stroke. Patients with a CHA2DS2-VASc score of zero are considered at greater risk of bleeding from anticoagulation relative to the benefit derived from anticoagulation; therefore, chronic anticoagulation is not recommended. Therapeutic anticoagulation is recommended for patients with a CHA2DS2-VASc score of 2 or greater unless bleeding risk is felt to be prohibitive. In intermediate-risk patients (CHA2DS2-VASc = 1), either aspirin or anticoagulation is a reasonable approach. Female sex alone without an additional risk factor does not increase stroke risk and should, therefore, be treated as low risk.