CHAPTER 13

The estimated prevalence of AF is 1% to 2% of the population.1,2 Data from the Framingham Heart Study has shown that the lifetime risk for men or women aged 40 years or older to develop AF is 1 in 4.³ AF is a disease of advancing age and is associated with an increase in CV and total mortality and morbidity.⁴ AF is associated with a 5-fold increase in the risk of stroke, a 3-fold increase in the risk of heart failure, and an increase in the risk of hospitalization.⁵ Furthermore, AF has a significant deleterious impact on quality-of-life measures.⁶ Last, but not least, is the incremental cost that managing this complex disease places on an already burgeoning healthcare expenditure. The management of AF is estimated to add another $26 billion to annual healthcare expenditures.⁷

DIAGNOSING AF

Given the consequences of AF, it is imperative for healthcare practitioners to recognize the signs and symptoms of AF. The range of symptoms varies from no symptoms to severe debilitation. The most common symptom associated with AF is fatigue.⁸ Other common symptoms are palpitations, chest pain, dyspnea, and lightheadedness. A distinct fraction of patients with AF, particularly in the elderly age group, are asymptomatic.9 However, mortality and the risk of cerebrovascular disease was not lower than their symptomatic counterparts.⁹

Symptoms are due to the rapid ventricular rate associated with AF, the beat-to-beat variability in rate, and loss of functional atrial contraction and atrio-ventricular synchrony. Furthermore, patients with underlying cardiovascular disease such as heart failure, hypertrophic cardiomyopathy, and mitral stenosis, suffer with the inception of AF and sudden exacerbation of their underlying cardiovascular disease. Such an exacerbation in symptoms should alert the clinician to the possibility that the inception of AF may have triggered the acute decline. Without recognizing the precipitating arrhythmia, the downward course would be hard to reverse, and the consequences of AF, such as thromboembolism, would be realized.

The index of suspicion is heightened by identifying the risk factors for developing AF. Congestive heart failure, valvular heart disease, advancing age, and diabetes mellitus have been identified in the Framingham Heart Study as predictors of the future development of AF.¹⁰ Given the wide prevalence of hypertension and ischemic heart disease in the community, these two comorbid conditions are the two most commonly seen in patients with AF.⁸

The history and physical examination of a patient suspected of AF is directed at: (1) establishing the diagnosis; (2) excluding precipitating factors; and (3) determining the impact that AF has. AF is defined as an irregularly irregular rhythm. Both the pulse and precordial auscultation would demonstrate the irregularity if the patient is in AF. In addition to irregularity, the intensity of the first heart sound varies with variation in the R-R intervals, and the fourth heart sound, if it had been previously heard, is now lost with loss of atrial contractility. Physical examination would help uncover diseases associated with AF such as hyperthyroidism, exacerbation of chronic obstructive pulmonary disease, or mitral stenosis. The clinical evaluation should also aim to uncover the impact AF has had on the patient. Elevated jugular venous pressure, rales over the lung fields, hepatomegaly, and lower-extremity edema are all consistent with congestive heart failure.

AF is diagnosed electrocardiographically. No P waves can be seen; instead, they are replaced by fine or course undulation of the baseline reflecting the rapid, chaotic depolarization of the atria. The ventricular rate is usually rapid, unless the patient is on drugs that modulate AV conduction or has intrinsic AV conduction disease. Regularization of the ventricular rate should always alert the clinician to the possibility that the patient has complete AV block and the regular rhythm is a junctional escape. AF can be detected in a variety of ways: standard electrocardiography, electrocardiographic telemetry in a monitored setting, 24-hour Holter monitor, loop monitor, and long-term implantable loop monitors. The increasing use of cardiac implantable electronic devices (pacemakers and ICDs) has provided an added opportunity to detect subclinical atrial arrhythmias and assess their significance. The detection of atrial tachyarrhythmias with such devices, lasting longer than 6 minutes, has been shown to be associated with a 2.5-fold increase in the incidence of ischemic stroke or systemic embolism.11

THE CLASSIFICATION OF AF

AF can exist and present in one of several clinical scenarios classified according to its duration and susceptibility to revert back to normal sinus rhythm (SR). The classification has important impact on management. A patient who presents for the first time in AF, particularly in the context of an intercurrent illness known for its association with AF such as thyrotoxicosis, pneumonia, or pericarditis, is diagnosed with “first-diagnosed AF”.¹² This is not uncommonly seen after cardiothoracic surgery or in the context of alcohol intoxication. The implication is that management is directed toward restoring normal SR when appropriate and not labeling the patient as having AF unless there is a recurrence. Recurrent AF lasting < 7 days is labeled paroxysmal, whereas AF lasting > 7 days, is labeled persistent.^8,12 The importance lies in that AF lasting > 48 hours is less likely to revert to SR spontaneously. In addition, the outcome of catheter ablation for AF that is paroxysmal carries a higher success rate than persistent AF.¹³ If a patient in whom the decision was made to pursue a rhythm-control strategy has been in AF > 12 months, the AF is classified as longstanding persistent.^8,12 If, on the other hand, the patient and clinician decided to assume a rate-control policy, AF is classified as permanent.^8,12 AF in the setting of rheumatic mitral stenosis, mechanical or bioprosthetic valve, or following mitral valve repair is associated with a high risk of thromboembolism and is classified as valvular AF.⁸ None of the novel oral anticoagulants have been approved for use in this setting.

EVALUATION

The initial evaluation should aim at determining the consequences AF has had on the patient. This would include symptoms of shortness of breath, altered mental status, chest discomfort, and/or hypotension. These symptoms are markers of hemodynamic instability and would prompt immediate intervention to restore SR (see below).^14,15 In a stable patient, the history should be directed toward the classification of AF (see above), past medical therapies directed toward AF, comorbidities, and potential causes of AF.

After determining the impact AF is having on the patient, the most important next step is assessing the future risk of thromboembolism. The role played by AF in the genesis of stroke, particularly in the elderly, has long been appreciated.¹⁶ Furthermore, strokes associated with AF tend to be associated with greater disability, higher recurrence rate and mortality.17 It has long been appreciated that the risk of thromboembolism is not uniform. Recently, several algorithms have been adopted to help determine what the risk is and to better help guide therapy.^18,19 The most current guidelines have supplanted the stroke risk classification schema represented by the acronym CHADS₂ with the newer stroke risk classification schema represented by the acronym CHA₂DS₂-VASc.⁸ One point is assigned to heart failure (LVEF < 40%) one point for hypertension (H), one point for age > 65 and 2 for age > 75 (A), one point for diabetes (D), 2 points for history of stroke/thromboembolism, one point for vascular disease (VA) and one point for female gender (Sc). Patients with AF whose score is > 1 should be considered for oral anticoagulation.⁸ The current guidelines recommend using the CHA₂DS₂-VASc score in determining the risk of thromboembolism.⁸ The CHA₂DS₂-VASc scoring does not take into account patients with hypertrophic cardiomyopathy. Patients with hypertrophic cardiomyopathy develop AF at a rate of 2% per year and have a 17× increase in the risk of thromboembolism; anticoagulation should be initiated as soon as the inception of this arrhythmia is appreciated^20,21 (Table 13.1).

Source: Modified from the guidelines for the management of AF: the Task Force for the Management of AF of the European Society of Cardiology (ESC) and Lip et al.^12,19

The risk of thromboembolism and its alleviation with anticoagulants should be counterbalanced with the risk of bleeding. A widely adopted scoring schema is the HAS-BLED bleeding risk score.²² The risk is assessed based upon the following risk factors: hypertension (defined as systolic > 160 mm Hg), abnormal renal function (≥ 2.3 mg/dL or on hemodialysis), or liver function (cirrhosis, bilirubin > 2× upper limit of normal or ALT/AST > 3× upper limit of normal) abnormalities (1 point for each), stroke (1 point), bleeding (1 point), labile INR (within therapeutic range < 60% of the time) (1 point), elderly (age > 65) (1 point), drugs (predisposing to bleeding such as ASA and NSAIDs), or alcohol (> 8 drinks a week) (1 point for each)^12,22 (Table 13.2).

A score ≥ 3 indicates the need to exercise caution upon anticoagulation. Source: Modified from Pisters et al.²²

The role obstructive sleep apnea plays in the genesis of AF and in reducing the efficacy of established therapy is increasingly appreciated; therefore, its presence or absence should be determined.^23,24 AF is commonly associated with hyperthyroidism and if not treated, conventional therapy for AF is less likely to succeed.¹⁴ While the incidence of hyperthyroidism in patients with AF is low, it is important to recognize that patients with subclinical hyperthyroidism are as likely to develop AF as those who have overt hyperthyroidism.¹⁴ This observation justifies excluding hyperthyroidism in patients presenting with AF, particularly the elderly, in whom symptoms and signs of hyperthyroidism are often subtle or absent.¹⁵

MANAGEMENT OF AF

Acute Management

The first step in the management of AF is determining the impact the arrhythmia has on the patient. Cardioversion should be considered if the patient is deemed hemodynamically unstable; if suffering from ischemic chest pain, acute pulmonary edema, acute alteration in mental status, or hypotension, cardioversion should be performed.¹⁵ If the duration of AF is unknown or if greater than 48 hours, cardioversion may lead to acute thromboembolism.²⁵ A transesophageal echocardiogram would help exclude a left atrial appendage clot.²⁶ If the patient’s condition does not allow a transesophageal echocardiogram to be performed, anticoagulation should immediately be implemented and continued for no less than 4 weeks.⁸ A recent study has demonstrated that patients with AF of < 48 hours’ duration suffering from heart failure and diabetes mellitus carry a 9.8% risk of thromboembolism postcardioversion.²⁷ This high-risk patient population should also be anticoagulated at the time of the cardioversion and for the subsequent 4 weeks.⁸

A distinct group of patients are those with AF and preexcitation (Wolff-Parkinson-White syndrome) given the risk of progression from AF to ventricular fibrillation and sudden death.²⁸ Patients who are hemodynamically unstable should be cardioverted immediately.¹⁴ In stable patients, drugs that have the potential to block AV node conduction, in turn increasing conduction down the bypass tract, including nondihydropyridine calcium channel blockers, amiodarone, adenosine, and digoxin, are contraindicated.⁸ Intravenous drugs such as ibutilide and procainamide can help slow conduction down the bypass tract and convert AF to SR.⁸

Rate Control

The rapid ventricular rate associated with AF is the most important determinant of symptoms and hemodynamic instability. One of the first goals that should be achieved in hemodynamically stable patients who do not require immediate cardioversion is rate control. An unchecked, rapid ventricular rate can lead to heart failure and the development of a tachymyopathy. The most frequently used agents are β-adrenergic blockers followed by nondihydropyridine calcium channel blockers. Care should be exercised when using β-adrenergic blockers in patients with chronic obstructive pulmonary disease and nondihydropyridine calcium channel blockers in patients with decompensated heart failure and impaired systolic function. The role played by digoxin has become progressively more limited with the advent of newer agents. The desired effect takes time to be realized, the potential for interaction with other agents exists, and the therapeutic window is narrow. A few studies have associated the use of digoxin with increased mortality.29,30 Digoxin may play a role in rate control of AF in sedentary patients with heart failure.¹² Oral and intravenous amiodarone can be used, in the absence of preexcitation, for rate control when other agents are not working or marginally depressed blood pressure precludes the further administration of β-adrenergic blockers or nondihydropyridine calcium channel blockers.⁸

The long-term goal of rate control is alleviation of symptoms and preventing the development of heart failure. Toward that goal, the aim is a resting heart rate of < 80 bpm, although, in the absence of heart failure or symptoms, a more liberal resting target heart rate (< 110 bpm) can be considered.^8,12,31 If rate control cannot be achieved or the patient remains symptomatic, restoration of SR can be pursued as an option if it had not been considered previously, as a method of “rate control.” The last option to consider is ablating the AV node and implanting a permanent pacemaker. This option should only be pursued after all other options have failed due to the irreversible nature of this undertaking.⁸ This option should be reserved for older individuals. The pacemaker may be implanted in advance of the ablation to insure that normal pacemaker function is established well before the patient is rendered pacemaker-dependent. There is a small but real risk of sudden cardiac death following this procedure attributed to polymorphic ventricular tachyarrhythmias and dispersion of ventricular repolarization.³² Postablation, the pacing rate is set at 90 bpm with monthly decrement in the pacing rate until 60 bpm is reached.³³ Given our current appreciation of the deleterious effect of exclusive right ventricular pacing in patients with impaired left ventricular systolic function, biventricular pacing should be used when AV node ablation is considered in this patient population.^34,35

ANTICOAGULATION

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