Older Man With Atrial Fibrillation
A new patient with a history of atrial fibrillation (AF) and heart failure presents for an initial visit. The 72-year-old man denies exertional chest pain and paroxysmal nocturnal dyspnea. He is able to perform all his routine daily activities and can even climb 2 flights of stairs without dyspnea—although with more vigorous effort, he does become short of breath. He occasionally experiences pedal edema at the end of the day, but the condition resolves by morning.
He has long-standing hypertension, which for the past 2 years has finally been well controlled with an angiotensin-converting enzyme inhibitor and diuretics. He has organic heart disease, manifested by episodes of AF and echocardiographic findings of atrial enlargement of 5 cm, left ventricular hypertrophy (LVH), and an ejection fraction of 45%. His AF has been treated with rhythm control, by both electric and pharmacological means. At his last office visit, he was in sinus rhythm. Results of pharmacological stress testing have been negative for ischemia.
Heart rate is 115 beats per minute; blood pressure, 122/78 mm Hg. Results of examination of the head, ears, eyes, nose, and throat are normal; there are no distended neck veins. Chest is clear; heart rhythm is irregularly irregular, with no S3 gallop and no murmurs. No edema is noted. The remainder of the physical findings are normal.
LABORATORY AND IMAGING STUDIES
Results of a complete blood cell count and a chemistry panel are within normal limits. An ECG confirms AF and also demonstrates voltage criteria for LVH.
CORRECT ANSWER: B
AF is the most common sustained cardiac arrhythmia encountered in practice. AF is a serious condition: it causes palpitations, exertional dyspnea, and even frank congestive heart failure (related to the diminished effective cardiac output). In addition, it can result in stroke and peripheral embolization. Thus, AF is an independent risk factor for excess mortality: in persons with AF, the risk of death is doubled.1
Rhythm control versus rate control. In recent decades, the standard of care for initial therapy in patients with newly diagnosed AF was to attempt to restore normal sinus rhythm using cardioversion and a variety of antiarrhythmic drugs.1 The alleged benefits of this "rhythm-control" approach included fewer symptoms, improved cardiac output and exercise tolerance, lower stroke incidence, and diminished need for anticoagulant prophylaxis. It was also suggested that this approach improved survival.
However, recent major studies have shifted the treatment paradigm toward the more easily effected "rate control." Large trials in both the United States2 and Europe3 showed no survival advantage of rhythm control over rate control. Moreover, a secondary finding in these studies was less morbidity in the rate-control group; this outcome was apparently associated with less use of cardiac medications in this group. The results of these studies also suggested that patients treated with rhythm control are likely to continue to have random episodic AF, which requires continued anticoagulant prophylaxis—thereby negating one of the major purported advantages of rhythm control. The studies concluded that quality of life, risk of stroke, and overall mortality were equivalent for both the rate-control and rhythm-control strategies.2,3
Lenient versus strict rate control. A new study further defines the optimal rate control strategy.4 Van Gelder and colleagues4 found that in patients with AF, lenient rate control (resting heart rate of less than 110 beats per minute) was as effective as strict rate control (resting heart rate of less than 80 beats per minute and heart rate during moderate exercise of less than 110 beats per minute) at preventing cardiovascular morbidity and mortality. In addition, lenient rate control was more easily achieved.
Thus, choice B—reduction of heart rate to less than 110 beats per minute at rest—is the best option for this patient. For now, it is a strategy that seems both reasonable and safe.5 A variety of drugs—β-blockers, calcium channel blockers, and digoxin—can be used to control heart rate. Along with rate control, however, anticoagulation with warfarin( to an international normalized ratio between 2.0 and 3.0 is indicated.
Choices A and C are not correct because current data demonstrate that they are too aggressive. As mentioned above, the stroke incidence with rhythm control is equivalent to that seen with rate control, probably because of undocumented episodes of AF with rhythm control.
Choice D is not correct because it would lower the heart rate below what the data indicate is necessary. In addition, the 2010 study showed that with a target resting heart rate of 80 beats per minute, there was a high incidence (25%) of drug-related adverse effects.4 Thus, the more aggressive protocol described in choice D, with its even lower target rate, would likely further increase the number of adverse effects.
Outcome of this case. A resting heart rate of under 110 beats per minute was easily achieved using a β-blocker alone. The patient is doing well 6 months after initiation of therapy: he has dyspnea (minimal) only with significant activity.
1. Benjamin EJ, Wolf PA, D'Agostino RB, et al. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98:946-952.
2. 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;347:1825-1833.
3. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347:1834-1840.
4. Van Gelder IC, Groenveld HF, Crijns HJ, et al; RACE II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010;362:1363-1373.
5. Dorian P. Rate control in atrial fibrillation. N Engl J Med. 2010;362:1439-1441.