Jack Z, a 75-year-old man with well-controlled hypertension, diabetes controlled by diet, and atrial fibrillation (AF) presents to the family medicine clinic to establish care with you after moving to the community from out of town.
The patient describes a 1-year history of AF. He provides you with an echocardiography report from 6 months ago that shows no evidence of structural heart disease. He takes lisinopril, to control blood pressure; an anticoagulant; a betablocker; and amiodarone for rhythm control. Initially, he took flecainide, which was ineffective for rhythm control, before being switched to amiodarone. He had 2 cardioversion procedures, each time after episodes of symptoms. He does not smoke or drink alcohol.
Mr. Z describes worsening palpitations and shortness of breath over the past 9 months. Symptoms now include episodes of exertional fatigue, even when he is not having palpitations. Prior to the episodes of worsening symptoms, he tells you that he lived a "fairly active" life, golfing twice a week.
The patient's previous primary care physician had encouraged him to talk to his cardiologist about "other options" for managing AF, because levels of his liver enzymes had started to rise (a known adverse effect of amiodarone (1)) when measured 3 months ago. He did not undertake that conversation, but asks you now about other treatments for AF.
Atrial fibrillation is the most common sustained cardiac arrhythmia, characterized by discordant electrical activation of the atria due to structural or electrophysiological abnormalities, or both. The disorder is associated with an increased rate of stroke and heart failure and is independently associated with a 1.5- to 2-fold risk of all-cause mortality. (2) In this article, we review the pathophysiology of AF; management, including the role of, and indications for, catheter ablation; and patient- and disease-related factors associated with ablation (including odds of success, complications, risk of recurrence, and continuing need for thromboprophylaxis) that family physicians should consider when contemplating referral to a cardiologist or electrophysiologist for catheter ablation for AF.
What provokes AF?
AF is thought to occur as a result of an interaction among 3 phenomena:
* enhanced automaticity of abnormal atrial tissue
* triggered activity of ectopic foci within 1 or more pulmonary veins, lying within the left atrium
* re-entry, in which there is propagation of electrical impulses from an ectopic beat through another pathway.
In patients who progress from paroxysmal to persistent AF (see "Subtypes," below), 2 distinct pathways, facilitated by the presence of abnormal tissue, continuously activate one another, thus maintaining the arrhythmia. Myocardial tissue in the pulmonary veins is responsible for most ectopic electrical impulses in patients with drug-refractory AF (see "Rhythm control").
* Subtypes. For the purpose of planning treatment, AF is classified as:
* Paroxysmal. Terminates spontaneously or with intervention [less than or equal to] 7 days after onset.
* Persistent. Continuous and sustained for > 7 days.
* Longstanding persistent. Continuous for > 12 months.
* Permanent. The patient and physician accept that there will be no further attempt to restore or maintain sinus rhythm.
Goals of treatment