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Dr. Pollick is Director, Non-Invasive Cardiology, Good Samaritan Hospital, and Associate Clinical Professor, UCLA School of Medicine.
Correspondence to: Charles Pollick, MD, Los Angeles Cardiology Associates, 1245 Wilshire Blvd, Suite 703, Los Angeles, CA 90017; e-mail: Cpollick{at}lacard.com
It has been estimated that 2.2 million Americans have atrial fibrillation (AF).1 The incidence of AF rises progressively with age from 0.5% for the 50- to 59-year age group to almost 9% for the 80- to 89-year age group.2 The risk of stroke in patients with AF depends on associated etiology; it is 17-fold with rheumatic heart disease and four- to fivefold in nonrheumatic patients compared to similar age cohorts in sinus rhythm.3 Age is an independent risk factor.4 5 In "lone" AF (no associated valve disease, hypertension, cardiomyopathy, or ischemic heart disease), the risk of stroke at age < 60 years is negligible, but in patients > 80 years old, it climbs to 3% per year.5 In the Framingham study (which looked at nonrheumatic AF that included valve disease and hypertension), the annual incidence of stroke in patients > 80 years old was reported to be as high as 7%.4 The presumed cause of stroke in the majority of these patients is embolization of thrombus from the left atrial appendage (LAA): the pathologic association of AF with LAA thrombus has been acknowledged for just over 30 years.6 The cerebral infarct caused by AF is frequently large, often produced by the occlusion of a major cerebral artery, resulting in a severe or fatal stroke.7 In a series of hospitalized patients with stroke associated with AF, 71% died or had a severe permanent neurologic deficit.8
The current era of echocardiographic assessment and management of AF began in 1986, when Aschenberg et al9 reported the detection of LAA thrombus by transesophageal echocardiography (TEE). In 1991, after being motivated by a case report10 that demonstrated the dynamic nature of LAA contraction, we reported our findings in a group of 82 patients.11 We revealed that the LAA was not a static pouch, but rather a highly dynamic structure with a characteristic pattern of emptying and filling in sinus rhythm. LAA emptying velocities were significantly reduced in the presence of LAA thrombus, and we proposed that poor LAA contraction was the likely cause of thrombus formation in patients with sinus rhythm and AF. One of the reviewers of our study was skeptical of our findings. The reviewer contended that the LAA was not contracting and proposed that our findings represented movement of an akinetic LAA moving in and out of the echocardiographic plane as the heart moved within the chest during the cardiac cycle. Indeed, prior to our report there had been no echocardiographic or angiographic studies demonstrating LAA contraction, although the contractile nature of the LAA was common knowledge among cardiac surgeons. Our findings that the LAA is a dynamic structure, however, have been confirmed in approximately 30 peer-reviewed manuscripts (discovered by a MEDLINE search) that have appeared since 1991. In a recent report, Kamp et al12 went one step further beyond the recognition that poor LAA contraction is associated with spontaneous contrast and thrombus formation, and reported that poor LAA contraction is also a predictor of thromboembolic events in AF.
The article by Tsai et al in this issue of CHEST (see page 309) adds another piece to this interesting puzzle. They have provided a follow-up of patients with nonrheumatic AF: virtually 50% of patients without spontaneous contrast in the LAA at the outset developed this 13 months later with concomitant reduction of LAA velocities. These findings are somewhat at odds with the clinical data from the Framingham study,13 which shows a clustering of stroke close to the onset of AF: almost 25% of patients have AF noted for the first time during hospitalization for stroke. There is, however, an approximately 5% recurring annual incidence of stroke thereafter.13 The Framingham data13 taken together with the observations by Tsai et al suggest two reactions of the LAA to AF. Just as Zipes16 has previously postulated that AF produces an atrial cardiomyopathy that has implications for perpetuation of AF; in some patients, LAA stunning may produce an "acute myopathy" of the LAA and cause thrombus to form. In other patients, the LAA musculature may gradually fatigue and a "delayed myopathy" may develop that creates the susceptible environment for thrombus formation. This delayed LAA "myopathy" may be responsible for the continued risk of stroke in patients with AF. The higher incidence of stroke in elderly patients with AF may be a function of the longer duration of AF and delayed LAA "myopathy," rather than age per se. The finding that AF-induced LAA "myopathy" may develop gradually over time has important implications relative to anticoagulation. It suggests that a "one-time" decision regarding anticoagulation in patients with AF is not justified. Perhaps such patients should have TEE performed at 1- or 2-year intervals to monitor LAA function; if and when a LAA "myopathy" develops, eg, when LAA emptying velocities fall < 20 cm/s, then warfarin should be started. Serial TEE may also be justified in patients with sinus rhythm and demand ventricular pacing in whom deterioration of LAA function has been recently reported.15
A recent study16 and editorial17 have emphasized the role of TEE in the decision-making process concerning anticoagulation in AF. The TEE appearance of poor LAA function, spontaneous contrast, or thrombus are indications for warfarin.15 The current paper by Tsai et al underscores the importance of assessing the LAA at regular intervals, as a one-time decision seems inappropriate, given the decline in LAA function over time leading to the development of a delayed LAA "myopathy," and the known persistent risk of stroke in patients with AF.
References
This article has been cited by other articles:
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  O. M. Wazni, H.-M. Tsao, S.-A. Chen, H.-H. Chuang, W. Saliba, A. Natale, and A. L. Klein Cardiovascular Imaging in the Management of Atrial Fibrillation J. Am. Coll. Cardiol., November 21, 2006; 48(10): 2077 - 2084. [Abstract] [Full Text] [PDF]
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 C. Stollberger, B. Schneider, and J. Finsterer Elimination of the Left Atrial Appendage To Prevent Stroke or Embolism?: Anatomic, Physiologic, and Pathophysiologic Considerations Chest, December 1, 2003; 124(6): 2356 - 2362. [Abstract] [Full Text] [PDF]
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