Managing newly diagnosed atrial fibrillation: Rate, rhythm, and risk

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ABSTRACTThe treatment of atrial fibrillation focuses on controlling the heart rate, preventing thromboembolic events, and, depending on the symptoms, restoring and maintaining sinus rhythm. In most cases, the rate or rhythm can be quickly controlled, and a long-term plan can be started that will minimize the impact of this disorder on the life of the patient.


  • When atrial fibrillation is newly diagnosed, reversible causes and commonly associated processes should be sought.
  • Agents to control the heart rate, eg, beta-blockers or nondihydropyridine calcium channel blockers, are often started and titrated intravenously and then changed to oral dosing.
  • The benefit of rhythm control has not been firmly established. Although we try cardioversion at least once when atrial fibrillation is first diagnosed, rhythm control is generally reserved for patients whose symptoms persist despite rate control, or for patients in whom the heart rate cannot be controlled.
  • The need for short-term or long-term anticoagulation must be estimated.



Three general concerns dictate the management of atrial fibrillation:

  • Controlling the heart rate
  • Controlling symptoms
  • Preventing thromboembolic events, including stroke.

When seeing a patient with newly diagnosed atrial fibrillation, these same three concerns should be kept in mind, but several additional issues must be addressed:

  • Reversible causes of atrial fibrillation must be ruled out
  • The true time of onset of the atrial fibrillation and the frequency of the episodes should be ascertained, if possible
  • A careful estimation of the patient’s symptom burden should be made.

Atrial fibrillation is common and has a huge impact in terms of the morbidity, death, and costs associated with it. It affects more than 2.2 million Americans.1 Approximately 1 in 10 people over the age of 80 has atrial fibrillation, and for those over the age of 40, the lifetime risk of developing it is one in four.2 Framingham data suggest that the risk of death is approximately twice as high for patients with atrial fibrillation compared with a similar cohort without.3–5


Does the patient have a reversible cause of atrial fibrillation?

Atrial fibrillation is thought to be due to triggers that initiate it and to a myocardial substrate that supports it. While it may develop in the absence of other heart disease, it is often associated with hypertension, diabetes, obesity, structural heart disease (including congenital heart disease), obstructive sleep apnea, advanced age, and alcohol abuse.

Therefore, once atrial fibrillation has been diagnosed, the history, examination, and diagnostic workup should be directed toward looking for potentially reversible causes and for frequently associated comorbidities. Common reversible causes include:

Hyperthyroidism. The laboratory evaluation should include a thyrotropin (thyroid-stimulating hormone, or TSH) level.

Alcohol use, especially binge drinking.

Obstructive sleep apnea, if suspected on the basis of the history or the body habitus.

Structural heart disease such as valvular heart disease or congenital heart defects may also predispose to atrial fibrillation. Therefore, listen carefully to the heart and obtain a transthoracic echocardiogram if one has not already been done or if you suspect a change in valvular disease or systolic function since the most recent study.

How long has the patient been in atrial fibrillation?

The duration of the atrial fibrillation often affects the treatment strategy. Therefore, when the diagnosis has been made, it is important to try to estimate how long the patient has been in atrial fibrillation.

Often, we must settle for an estimate, as the patient’s recollection may be vague. However, in some cases, the symptoms are pronounced or electrocardiographic or telemetric data are available, allowing the time of onset to be clearly defined.

In addition, it is helpful to know if the patient has had prior episodes that were never brought to medical attention. To this end, elicit the patient’s spectrum of symptoms and encourage him or her to think back months or years and try to recall other times when similar symptoms might have occurred.

How do the symptoms affect the patient’s quality of life?

The clinician must also estimate the extent to which the symptoms affect the patient’s quality of life. This is best done when the heart rate is under control. If the patient still has significant symptoms despite adequate rate control, then a rhythm control strategy should probably be pursued.


Control the heart rate with a beta-blocker, a calcium channel blocker, or digoxin

Many patients present during their first episode of atrial fibrillation with a rapid ventricular rate, especially if they are not already taking a drug to slow conduction through the atrioventricular node. If the symptoms are particularly profound, one should try to get the heart rate under control quickly.

Oral agents take time to be absorbed and are not always easy to titrate. Intravenous beta-blockers such as metoprolol (Lopressor) and labetalol (Normodyne, Trandate) or intravenous diltiazem (Cardizem) can slow the heart rate quickly and can be titrated. Once the heart rate is controlled, the oral form can be started, to allow weaning from the intravenous agent. In acute management, we seek a heart rate of less than about 100 to 110 beats per minute.

If the patient’s blood pressure is marginal, loading with intravenous digoxin may be considered. The dosage is 0.5 mg intravenously, then 0.25 mg intravenously in the first 6 hours and another 0.25 mg intravenously in another 6 hours. In patients with renal insufficiency the dosage should be less, or digoxin should be avoided altogether. Often, the blood pressure will improve once the heart rate is decreased, allowing other agents to be initiated. However, if the patient is frankly hypotensive with chest pain, shortness of breath, or a diminished level of consciousness, then emergency electrical cardioversion is indicated even if anticoagulation has not yet been started (more about anticoagulation below).

Oral forms of these same agents are the workhorses for heart rate control in the outpatient setting. Oral beta-blockers and nondihydropyridine calcium channel blockers (ie, diltiazem or verapamil [Calan, Verelan]) are the first-line agents, because when digoxin is used alone, it is relatively poor at controlling the heart rate, especially when the patient is not at rest.

The choice between these agents should be dictated by whether the patient has comorbidities such as coronary artery disease, heart failure, or reactive airway disease. Nondihydropyridine calcium channel blockers are relatively contraindicated in patients with heart failure, while beta-blockers can exacerbate reactive airway disease.6

It is also important to document that the heart rate is adequately controlled outside the hospital or outpatient clinic, where the patient is typically sitting or supine. This can be done with a 6-minute walk, exercise test, or Holter monitor once rate-controlling agents have been titrated.7


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