REVIEW ARTICLES
Echocardiographic assessment of the left atrial appendage
Yoram Agmon, MDa,
Bijoy K. Khandheria, MDa,
Federico Gentile, MDa and
James B. Seward, MDa
a Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
Manuscript received March 6, 1999;
revised manuscript received June 29, 1999,
accepted September 7, 1999.
Reprint requests and correspondence: Dr. Bijoy K. Khandheria, Mayo Clinic, 200 First St SW, Rochester, Minnesota 55905
 |
Abstract
|
|---|
The left atrial (LA) appendage is a common source of cardiac thrombus formation associated with systemic embolism. Transesophageal echocardiography allows a detailed evaluation of the structure and function of the appendage by two-dimensional imaging and Doppler interrogation of appendage flow. Specific flow patterns, reflecting appendage function, have been characterized for normal sinus rhythm and various abnormal cardiac rhythms. Appendage dysfunction has been associated with LA appendage spontaneous echocardiographic contrast, thrombus formation and thromboembolism. These associations have been studied extensively in patients with atrial fibrillation or atrial flutter, in patients undergoing cardioversion of atrial arrhythmias and in patients with mitral valve disease. The present review summarizes the literature on the echocardiographic assessment of LA appendage structure, function and dysfunction, which has become an integral part of the routine clinical transesophageal echocardiographic examination.
|
Abbreviations and Acronyms
| | AF | = atrial fibrillation | | AFL | = atrial flutter | | LA | = left atrium (-ial) | | LAA | = left atrial appendage | | LV | = left ventricle (-icular) | | SEC | = spontaneous echocardiographic contrast | | SPAF | = Stroke Prevention in Atrial Fibrillation | | TEE | = transesophageal echocardiography |
|
Cardiogenic embolism accounts for  15% of ischemic strokes (1). Left atrial appendage (LAA) thrombi are believed to be the source of embolism in a substantial number of these patients, primarily in association with atrial fibrillation (AF) or rheumatic mitral valve disease (or both). Despite the blind cul-de-sac and multilobed anatomic structure of the LAA (2), thrombus formation is normally prevented by vigorous blood flow in the appendage cavity. Nevertheless, LAA dysfunction in various pathophysiologic states may predispose to local thrombosis and systemic embolization.
Transesophageal echocardiography (TEE) has been used extensively to characterize LAA structure and function in numerous recent studies. Echocardiographic assessment of LAA function was initially described by Suetsugu et al. (3) and by Pollick and Taylor (4) and has become an integral part of the routine TEE examination. The present review summarizes the literature on the anatomy and function of the LAA, as assessed by echocardiography, and the clinical implications of LAA dysfunction.
|
Echocardiographic aspects
|
|---|
The LAA has been imaged primarily in two basic biplane TEE views: 1) the horizontal short-axis view at the base of the heart (5) and 2) the two-chamber longitudinal view of the left atrium (LA) and ventricle (LV) (6). Multiplane TEE (7) allows greater versatility in obtaining these views and enables visualization of the appendage in a continuum of intermediate planes (8). Although the LAA generally is visualized satisfactorily, attempts have been made to improve echocardiographic images and Doppler recordings by injection of transpulmonary contrast agents (9). Transesophageal imaging is necessary for adequate visualization of the LAA, a posterior cardiac structure in proximity to the esophagus. Although the LAA may, at times, be imaged by transthoracic echocardiography (parasternal short-axis view of the base of the heart or apical two-chamber view), the transesophageal approach is mandatory for consistent and precise delineation of the LAA, particularly in the adult population. A recent report has suggested that Doppler interrogation of the LAA is feasible and accurate with transthoracic imaging (10), although this finding needs to be validated in additional studies.
Complete structural and functional assessment of the LAA should consist of two-dimensional imaging of LAA size, morphology and contraction. In addition, LAA function is assessed quantitatively by pulsed-Doppler interrogation of LAA flow. These data are integrated with those from the complete echocardiographic examination, including assessment of LA size, LV systolic and diastolic function and associated valvular disease, primarily mitral valve disease (11).
Two-dimensional imaging of LAA.
LAA area and ejection fraction have been assessed and reported in numerous studies of LAA function (4,12–20). However, measurements of LAA cross-sectional areas are inherently prone to substantial interobserver variability, during both data acquisition and off-line analysis (4,20), primarily because of the complex three-dimensional anatomy of the LAA, which limits accurate definitions of standard tomographic imaging planes of this structure. In our clinical experience, attempts to quantitate LAA size and function by planimetric methods are time-consuming and do not seem to offer any advantage over gross visual estimation of LAA size and function. In contrast, assessment of LAA function by Doppler echocardiography, the main focus of this review, is easily performed, reproducible and highly relevant clinically.
In addition to assessing LAA size and function, two-dimensional imaging is used to determine the presence of LAA spontaneous echocardiographic contrast (SEC) (21), semiquantitative grading of SEC (22), and defining the presence, size and mobility of LAA thrombi (23). The LAA is usually a multilobed structure (2) (Fig. 1). In an autopsy study of 500 normal human hearts, the LAA was bilobed in 54% and multilobed (2 lobes) in 80% of hearts (2). Thus, the LAA should be scanned meticulously in multiple echocardiographic planes, most precisely by multiplane TEE, and the number of lobes determined. A detailed examination of all lobes is necessary for exclusion of LAA thrombi. Owing to the complex structural features of the LAA, the diagnosis of LAA thrombi by TEE is prone to misdiagnosis, both overdiagnosis (false interpretation of prominent pectinate muscles) (2,24) and underdiagnosis (occult thrombi in multilobed appendages) (25).
View larger version (57K):
[in this window]
[in a new window]
|
Figure 1 Pathologic specimens of the LAA displaying its complex and extremely variable configuration, thus emphasizing the need for routine meticulous echocardiographic scanning of the appendage in multiple planes. A, Bilobed LAA (LAA is on right side of picture). B, Single-lobed LAA with an additional "appendix" at its distal end (outside the plane of main LAA body). C, Multilobed LAA (multiple small lobes). D, Multiplane transesophageal echocardiographic demonstration of a multilobed LAA (90° and 135° scanning in D-1 and D-2, respectively). The orifice of the LAA (LA–LAA junction) is marked by a pair of arrows in A to C. (A to C, Courtesy of Dr. W. B. Edwards, Department of Anatomic Pathology, Mayo Clinic.)
|
|
Doppler evaluation of LAA function.
LAA flow is evaluated by pulsed-wave Doppler interrogation of the LAA cavity. The following technical aspects need to be emphasized: - LAA view—The view with the optimal alignment of Doppler with LAA flow, as determined by color flow imaging, should be selected. No differences in Doppler velocities have been noted using various LAA views (8,26).
- Sample volume location—Currently, there is no standard sampling site in the appendage (i.e., sampling at the LAA-LA junction versus sampling at different sites within the LAA cavity). It is unclear whether variations in sampling site location produce significant changes in measured velocities, as demonstrated for other Doppler measurements such as mitral inflow velocities (27). In a recent report, a small trend was observed for lower velocities at the wider orifice of the LAA, in comparison with velocities obtained at the narrower middle portion of the appendage (10). LAA flow should be sampled at the site of maximal flow velocities (determined by color flow imaging), while avoiding wall motion Doppler artifacts, which are commonly observed in the more distal (narrow) portions of the appendage. In practice, technically adequate tracings of maximal LAA flow velocities are commonly recorded within the proximal third of the appendage.
- Doppler sample size and machine gains—These are set to visualize a spectral Doppler signal with a clear envelope, typical of the normal laminar appendage flow. Initially, filters are set at low values to enable visualization of low velocity flow, characteristic of early diastolic LAA flow in sinus rhythm and LAA flow in a subset of patients with AF.
|
LAA flow patterns in various cardiac rhythms
|
|---|
Distinct LAA flow patterns have been observed in sinus rhythm, AF, atrial flutter (AFL) and cardiac pacing. Previously published values of LAA flow velocities in small groups of volunteers and patients without cardiac disease are presented in Table 1 (15,26,28). Values of LAA velocities in a large population-based study have been reported recently (29).
Sinus rhythm.
Discrete Doppler flow signals have been described in patients in sinus rhythm (Fig. 2). - LAA contraction, resulting in a late diastolic, positive (i.e., toward the TEE transducer) Doppler outflow signal, shortly following the onset of the ECG P wave. This signal coincides with two-dimensional and color flow imaging of LAA contraction and outflow (4) and is related temporally to late diastolic mitral flow (mitral A wave) (30). Measurements of contraction velocities, which are easily reproducible, correlate with two-dimensional measurements of LAA ejection fraction (15).
- LAA filling, an early systolic, negative (i.e., away from the TEE transducer) Doppler inflow signal, immediately following LA contraction (4,28). The physiologic processes underlying LAA filling have not been studied in detail as have their counterpart ventricular processes, and the relative roles of active (LAA relaxation) versus passive (e.g., elastic recoil) processes resulting in LAA filling are poorly defined (hence, the preferred general term "LAA filling"). Although not studied systematically in various patient populations, there is generally a gross correlation between LAA contraction and filling velocities.
- Systolic reflection waves, following LAA contraction and filling. A variable number of alternating LAA outflow and inflow signals of diminishing amplitude are commonly recorded (14,31), resulting from passive outward and inward flow waves following the initial high velocity flows of appendage contraction and filling. The velocities of these reflection waves correlate with the preceding LAA contraction and filling velocities (14) and usually are observed in subjects with high LAA contraction velocities (31).
- Early diastolic LAA flow, a low velocity outflow signal following early diastolic mitral flow (mitral E wave) and pulmonary venous diastolic flow signals (28,32). Initially, it was proposed that early diastolic LAA flow results from compression of the LAA medial wall by the superior motion of the base of the LV during diastole (4). However, a more plausible explanation is passive emptying of the appendage, paralleling LA emptying during rapid ventricular filling in early diastole. Following early diastolic LAA outflow, a low velocity LAA filling signal is infrequently detected (Fig. 2B) and is related to continuous filling of the LA and LAA from pulmonary venous flow during mid-diastole. LAA diastolic filling flow may be observed more commonly in subjects with relatively slow heart rates (28). As shown in Table 1, early LAA diastolic velocities are significantly lower than velocities during active LAA contraction and are of undetermined significance. However, it is possible that passive early diastolic LAA flow may gain significance in the presence of LAA contractile dysfunction (33).
View larger version (32K):
[in this window]
[in a new window]
|
Figure 2 A, Diagram of LAA flow in sinus rhythm. 1, LAA contraction; 2, LAA filling; 3, systolic reflection waves (positive and negative); 4, early diastolic LAA outflow (see text for details). B, Pulsed-Doppler tracing of LAA flow in sinus rhythm (flow signals 1 to 4 as in A).
|
|
Effect of heart rate
The effect of heart rate on LAA has not been studied sufficiently in patients with sinus rhythm. Fusion of LAA early diastolic and contraction velocities, resulting in higher total velocities, has been observed in young healthy volunteers with sinus tachycardia (28).
Atrial fibrillation.
Active LAA flow is commonly observed in patients with AF, with alternating positive and negative sawtooth-appearing flow signals of variable amplitude and regularity (Fig. 3A). Mean LAA flow velocities have greater physiologic significance than peak velocities. These should be averaged for each cardiac cycle and then averaged for several cycles. Characteristically, flow signals have lower velocities during ventricular systole (LAA contraction in the presence of a closed mitral valve) than during diastole (34). In addition to flow resulting from active appendage contraction, a discrete early diastolic outflow signal, similar to that in sinus rhythm, is observed occasionally (22), although commonly it is difficult to identify this signal clearly and to differentiate it from fibrillatory flow signals.
View larger version (132K):
[in this window]
[in a new window]
|
Figure 3 A, Pulsed-Doppler tracing of LAA flow in AF. Note the rapid fibrillatory flow waves, which are of higher velocity during ventricular diastole than systole (arrows; see text for details). B, Pulsed-Doppler tracing of LAA flow in AFL (with a 2:1 ventricular response). Flutter flow waves are, in general, slower and of higher velocity than fibrillatory flow waves.
|
|
Generally, flow velocities during AF are lower than those during sinus rhythm (12,32,35). However, flow velocities in patients with AF are highly variable, with high velocity flows on one end of the spectrum (velocities similar to, or even exceeding, those observed in sinus rhythm), and minimal to absent flow on the other end (12). This represents the wide continuum of LAA contractile dysfunction in patients with AF, from relatively preserved contraction to complete paralysis of the appendage.
Effect of heart rate
The effect of ventricular response rate in AF on LAA flow velocities has been studied by comparing cardiac cycles with long and short RR intervals. Because LAA flow velocities in AF are higher in diastole than in systole, longer cardiac cycles are associated with higher mean LAA velocities because of prolongation of diastole (34). Similarly, an inverse correlation has been observed between LAA ejection fraction and ventricular response rate during AF (36). Therefore, high ventricular response rates during AF may be associated with further impairment of LAA flow.
ECG correlation
Generally, the correlation between ECG fibrillatory wave amplitude in nonrheumatic AF and LAA velocities is not clear. A lack of any significant correlation has been reported in two studies (35,37). In a single study, an association has been noted between coarse AF (greatest amplitude of fibrillatory waves in ECG lead V1 1 mm) and low LAA contraction velocities and LAA ejection fraction (38). These nonconclusive findings probably result from the multiple factors associated with the ECG manifestations of AF, and thus explain the lack of association between ECG AF pattern and the risk of embolic events (37).
Atrial flutter.
In patients with AFL, a more consistent high velocity, relatively regular sawtooth flow pattern is the rule (39–41) (Fig. 3B). The rate of LAA contraction typically is slower in AFL than in AF (40). Flow velocities generally are approximately twice the velocities observed in AF (39,41), although there is significant overlap in the velocities of these arrhythmias.
ECG correlation
An intermediate ECG pattern of atrial activity, atrial "fibrillation-flutter," is associated with a velocity profile resembling that of AF, with lower velocities than those observed in pure AFL (39). Similarly, LAA flow velocities are higher in patients with pure AFL than in those with AFL and intermittent episodes of AF (42).
Cardiac pacing.
The effect of atrioventricular asynchrony on LAA flow pattern has been studied in patients with implanted cardiac pacemakers. In the absence of associated AF, ventricular-demand pacing (VVI pacing mode) is accompanied by atrioventricular dissociation or retrograde ventriculoatrial conduction (43). In patients with atrioventricular dissociation, LAA contraction occurs intermittently during ventricular diastole, resulting in relatively high LAA flow velocities, whereas LAA contraction against a closed mitral valve, during ventricular systole, is associated with low velocities (44). In the presence of ventriculoatrial conduction, LAA contraction uniformly occurs during ventricular systole, resulting in low velocity LAA flow (45). Restoration of atrioventricular synchrony by dual-chamber pacing (DDD pacing mode) is associated with higher LAA flow velocities (46).
|
Pathophysiology of LAA function
|
|---|
General aspects.
Clinical associations
Age-associated changes in LAA velocities have been described in 50 subjects with normal hearts (15). Aging was associated with a progressive linear decline in all LAA flow variables (LAA contraction and filling velocities and early diastolic LAA flow) (15). A possible effect of various systemic diseases (e.g., hypertension) on LAA function has not been determined.
Echocardiographic correlates
1) LA/LAA size: in patients with sinus rhythm, there is no clear association between LA size and LAA flow velocities (4). However, concomitant LAA enlargement and low LAA contraction velocities are common in patients with mitral stenosis who are in sinus rhythm (13). In patients with AF, larger LA and LAA sizes commonly are associated with lower LAA flow velocities (14,22,47), both in patients with (13) and in those without (48) associated rheumatic mitral disease. This is most pronounced in patients with near absence of LAA flow, in whom significant dilation of the LA and LAA is the rule. Of note, significant LAA dilation resulting from any cause may potentially further impair LAA function by increasing LAA wall stress.
2) LAA flow versus mitral and pulmonary venous flow: the following correlations were observed between LAA flow velocities and mitral inflow and pulmonary venous flow velocities in the presence of sinus rhythm: a) lack of correlation (14,32) or even a negative correlation (15) between LAA contraction velocities and mitral inflow A velocities, b) lack of correlation between LAA and pulmonary venous flow velocities (15), and c) significant positive correlation between early diastolic LAA outflow and both mitral E velocities and pulmonary venous diastolic velocities, all of which decline progressively with aging due to age-related slowing of LV relaxation (15).
LAA function versus global LA function
Various methods developed to evaluate LA contractile function are time-consuming and, thus, not routinely used in clinical practice. Hence, it is tempting to apply LAA flow variables as clinically applicable surrogates for global LA function (20,49), although the validity of such an approach is questionable. The LAA and main LA cavity are derived embryologically from different sources. The trabecular LAA is a remnant of the embryonic LA, whereas the smooth LA cavity is derived from an outgrowth of the pulmonary veins (50). Therefore, it is conceivable that LAA function may dissociate from global LA function. The following arguments support this: - Dissociation of LAA and LA function has been anecdotally reported during sinus rhythm in patients with preserved global LA function (manifested as normal mitral inflow A velocities), but low or absent LAA flow velocities, in association with LAA thrombus formation, spontaneous echocardiographic contrast and clinical embolic events (35). Dissociation of LA and LAA mechanical activity has been described recently in patients after cardioversion, in whom organized LA mechanical activity may be present along with disorganized LAA contraction (51). A contrasting phenomenon has been described in patients in whom effective LAA contraction was restored early after cardioversion, in the absence of effective global LA activity (absent mitral A waves) (52).
- As noted above, a lack of correlation (14,32) or even a negative correlation (15) between LAA contraction velocities and mitral inflow A velocities has been observed in patients with sinus rhythm. However, this apparent dissociation between LA and LAA function may result from the multiple determinants of mitral A velocities, which are independent of LA contractility (LV diastolic characteristics and loading conditions), rather than a true functional dissociation between LA and LAA function.
- Relatively preserved LAA function with high velocity LAA flow is commonly observed during AF in patients without evidence of atrial activity in mitral inflow. Although functional dissociation between the LA and LAA is a possible explanation, it is more likely that for a similar degree of residual contractility, the small-sized appendage is able to generate significant flow during AF, whereas the larger main LA cavity is not.
- Despite the above observations, clinical experience suggests that evaluation of LAA function may serve as a clinically applicable surrogate of overall LA function.
|
LAA function and cardiac hemodynamics
|
|---|
LAA contractility.
LAA contractility is the primary determinant of LAA end-diastolic outflow. However, similar to ventricular physiology, loading conditions may affect LAA function and flow. These interactions were assessed by observations of the effects of LA (and, hence, LAA) pressures, concomitant mitral valve disease and LV hemodynamics on LAA function.
LA pressure.
LA pressure is a major determinant of LAA flow. In a combined Doppler and catheterization study of 31 patients with various myocardial (nonvalvular) diseases, Tabata et al. (16) demonstrated an inverse correlation between LAA contraction velocities and mean pulmonary capillary wedge pressure. Similarly, treatment of heart failure, resulting in a decrease in LA filling pressures, is accompanied by an improvement in LAA function (19). In a canine model, preload elevation by volume infusion, resulting in an increase in LA pressures in the normal physiologic range, was associated with subtle increases in LAA contraction velocities (53). Hence, mildly increasing LA pressures may enhance LAA function, as a possible reflection of LAA preload reserve, whereas more significant increases in LA pressures may result in LAA contractile dysfunction due to afterload elevation.
Of interest, recent studies have suggested that the LAA plays a role as a beneficial modulator of LA pressure. The LAA is more compliant than the main LA cavity (54). Accordingly, surgical LAA clamping (55) or appendectomy (56) decreases overall LA compliance, resulting in a shift of the LA pressure-volume relation upward and to the left.
Mitral valve disease.
Hemodynamically significant mitral stenosis increases the resistance to both active and passive LAA emptying, resulting in an overall lowering of LAA flow velocities, regardless of the specific rhythm. Hwang et al. (13) have demonstrated a marked decrease in LAA contraction velocities in patients with mitral stenosis, compared with patients without rheumatic heart disease, both in sinus rhythm and in AF. In addition to overall impairment of LAA function, mitral stenosis specifically limits the normal augmentation of LAA flow during diastole in patients with AF, a phenomenon related to the severity of the stenosis (57). In the presence of AF, patients with severe mitral stenosis typically demonstrate low-to-absent LAA velocities. This is in contrast to nonrheumatic AF, which is associated with a wide spectrum of flow velocities, with both "high velocity" (velocities 25 cm/s) and "low velocity" (velocities <25 cm/s, i.e., a flow profile similar to flow in rheumatic AF) flow variants (26). These effects of mitral stenosis on LAA function are probably the result of the severe hemodynamic impairment in patients with mitral stenosis (significant elevation of LA pressures). Direct LA and LAA involvement in the rheumatic inflammatory process, and an atrial myopathy resulting from chronic LA pressure elevation, are additional possibilities. Similar changes in LAA function have been observed in the presence of mitral valve prostheses (58), resulting from the prolonged effects of the presurgical valvular disease on LAA function as well as inherent prosthetic valve stenosis.
The hemodynamic effects of mitral stenosis on LAA function are further understood by analyzing the effect of percutaneous balloon mitral valvotomy on LAA function. TEE studies early after percutaneous balloon mitral valvotomy have demonstrated recovery of LAA function within 24 to 72 h after the procedure, both in patients with sinus rhythm and those with AF (17,59,60). The augmentation of LAA velocities following balloon valvotomy is related directly to the hemodynamic relief of the valvular stenosis (i.e., the decrease in transmitral pressure gradient) (17).
Few data are available about the effects of mitral regurgitation on LAA function. Hemodynamically significant mitral regurgitation is predicted to impair LAA function via LA and LAA dilatation and increased filling pressures. This finding has been observed (55), although inconsistently (32), in small-sized studies. Despite a possible deleterious effect of mitral regurgitation on LAA function, mitral regurgitation has an overall protective effect against thromboembolism (61) by prevention of LA stasis.
LV function.
LV systolic (62–64) and/or diastolic dysfunction may affect LAA contraction, primarily through its effect on LAA filling pressures (19). Thus, in addition to the potential for LV thrombi, LV dysfunction may predispose to LAA thrombus formation. Furthermore, impaired LV relaxation is associated with a concomitant decline in both mitral inflow E waves and LAA early diastolic flow. This has been observed in relation to aging (14,15) and LV hypertrophy (14). Similarly, in an animal study, early diastolic LAA velocities were determined independently by the time constant of LV relaxation (tau) (53). The possible clinical role of LV dysfunction as a determinant of LAA function is suggested by clinical and echocardiographic data from the Stroke Prevention in Atrial Fibrillation (SPAF) study, in which clinical heart failure and echocardiographic evidence of LV dysfunction (65) were independent predictors of thromboembolic events.
|
Clinical implications of LAA dysfunction
|
|---|
Many studies have suggested that determination of LAA function by echocardiography allows the identification of patients with AF or AFL who are at high risk for the development of LA or LAA thrombi and thromboembolic complications. Assessment of LAA function has also revealed the phenomenon of postcardioversion LAA dysfunction ("stunning"), responsible for the prothrombotic state following cardioversion. In addition, a few recent studies have suggested a role for LAA function assessment in predicting the immediate and, possibly, the long-term success of conversion of AF.
|
AF and AFL
|
|---|
LAA dysfunction and LAA SEC, thrombi and embolic events.
LA and LAA SEC, resulting from local blood stasis, is associated with a high incidence of thrombus formation and thromboembolic events (21,22,66). LAA dysfunction, associated with AF of various causes, is commonly accompanied by SEC (26,47,48,66,67). In the SPAF III TEE substudy of high-risk AF patients, LAA contraction velocities of  20 cm/s were associated with SEC in 75% of patients, significantly less than the 58% frequency noted in the higher velocity group. Similarly, Mügge et al. (26) demonstrated SEC in a significantly higher proportion of patients with LAA velocities <25 cm/s. By semiquantitative analysis, the degree of LAA SEC is negatively associated with LAA velocities (22).
Significant LAA dysfunction is similarly associated with LAA thrombus formation (22,47), although anticoagulation therapy may weaken this association. LAA velocities are significant predictors of thrombus formation, independent of various hemostatic variables indicating platelet or coagulation activation (68). Almost uniformly, the presence of LAA thrombus is accompanied by extreme LAA dysfunction, manifested as a low-to-absent LAA flow velocity profile (47,48). In SPAF III, LAA thrombi were more prevalent in the low (20 cm/s) than in the higher LAA velocity groups (17% vs. 5%, respectively) (66). From a practical echocardiographic standpoint, assessment of LAA function may assist in the accurate diagnosis of intra-appendage masses and "pseudomasses" (24). Significant impairment of LAA function supports a diagnosis of LAA thrombus, whereas normal function suggests an alternative diagnosis.
Many studies have shown retrospectively an association between LAA dysfunction and previous systemic embolic events, primarily cerebral embolism (26,69–72). Recently, the SPAF III trial has demonstrated prospectively the role of LAA dysfunction as a risk factor for future embolic events (66). The relative risk of ischemic stroke was 2.6 times greater in patients with LAA flow velocities <20 cm/s than in those with higher LAA velocities. Furthermore, LAA flow velocities progressively decline with increasing clinically defined risk of thromboembolism (73). In general, the above associations of LAA dysfunction and SEC, thrombus formation and thromboembolism are stronger in rheumatic than in nonrheumatic AF (13,26), and in AF than in AFL (39,41), relating to greater degrees of LAA dysfunction in rheumatic heart disease and in AF, respectively.
The clinical implications of the preceding observations relating LAA dysfunction to thromboembolic risk have not been defined clearly. Although patients with AF can be stratified according to thromboembolic risk by assessment of LAA function, the clinical impact of risk stratification on patient therapy has not been determined.
Effect of cardioversion on LAA function.
Initially, it was proposed that resumption of LA mechanical activity after cardioversion may result in systemic embolization of preformed LA thrombi, thus explaining the occurrence of thromboembolic events in the immediate postcardioversion period. However, several recent studies have supported an opposing mechanism, in which cardioversion of AF produces transient worsening of LA mechanical function ("stunning") (74), thus predisposing to thromboembolism. This observation has been extended to the LAA by numerous studies that uniformly have demonstrated the phenomenon of postcardioversion LAA stunning (18,41,52,75–82). LAA stunning is manifested echocardiographically as a "paradoxical" reduction in LAA flow velocities, compared with the precardioversion LAA velocities in AF, despite the reversion to a regular sinus rhythm LAA flow pattern. LAA dysfunction after cardioversion is commonly associated with new or worsening SEC (52,75,77,78), thus predisposing to thromboembolism (75).
Initially described in association with direct-current external cardioversion (52,75), post-AF LAA stunning has also been observed in spontaneous cardioversion (76), pharmacologic cardioversion (77) and low energy internal atrial defibrillation (78). This supports the hypothesis that conversion to sinus rhythm itself, rather than the method of cardioversion, is responsible for LAA stunning. The lack of LAA dysfunction after direct-current endocardial or external shocks in patients with sinus rhythm (80) and the absence of correlation between the electrical energy used for cardioversion and the degree of LAA stunning (82) further support the above observations. Although well-described echocardiographically, the pathophysiologic basis of LAA stunning has not been defined.
Postcardioversion LAA stunning is also observed after cardioversion of AFL (41). Because of higher initial LAA flow velocities in AFL, postcardioversion LAA velocities are greater following cardioversion of AFL than of AF despite a similar absolute reduction in LAA velocities (41). Therefore, new or worsening SEC after cardioversion is less common in AFL (41), explaining the relatively low incidence of embolic episodes following cardioversion of AFL. LAA stunning has been observed following radiofrequency ablation of chronic AFL (79), further emphasizing the role of cardioversion itself rather than the technique in the pathogenesis of LAA stunning.
The time course of resolution of LAA stunning is variable and dependent on several patient, cardiac and arrhythmia characteristics, as suggested for overall LA function assessed by transthoracic echocardiography (74). Because TEE is an invasive procedure, sequential TEE data assessing recovery of LAA function are limited. Significant improvement has been observed in LAA function within 7 to 30 days (18,78,79,81) after cardioversion, although the determinants of the time-course of LAA recovery are incompletely defined. The clinical implication of postcardioversion LAA stunning is straightforward, emphasizing the need for well-controlled anticoagulation therapy in the postcardioversion period in the absence of demonstrable LA or LAA thrombi before cardioversion. The possible role of TEE assessment of LAA function, as a guide to the duration of postcardioversion anticoagulation, has not been determined to date (to our knowledge).
Prediction of cardioversion success.
Recent studies have suggested that the success of cardioversion of AF to sinus rhythm (spontaneous, drug-induced or electrical) may be predicted by assessing LAA function before cardioversion. LAA velocities during AF may predict both the short-term success of cardioversion (18,70,83,84) and the long-term maintenance of sinus rhythm (85), although this is not a uniform short-term (64,85) or long-term (64,83) observation. Velocities greater than approximately 20 cm/s are associated with a higher rate of short-term success in converting to sinus rhythm (83,84). The association between LAA velocities and successful cardioversion is probably related to the association of LAA velocities and LA and/or LAA size (70,84,85), LA filling pressures and the duration of AF (67,70,84,85), all of which are predictors of cardioversion success.
|
Sinus rhythm
|
|---|
A few studies have considered the effects of LAA dysfunction in patients with rheumatic mitral disease in sinus rhythm in whom LA and LAA SEC is associated with low LAA flow velocities (13,86). However, the role of LAA dysfunction in patients with sinus rhythm and no associated rheumatic valvular disease is not clear and has been reported only anecdotally (35,87). The role of LAA dysfunction in sinus rhythm as a predictor of future embolic events, and possibly the future development of AF, needs to be addressed in large prospective trials.
|
References
|
|---|
1. Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol. 1986;43:71–84[Abstract/Free Full Text]
2. Veinot JP, Harrity PJ, Gentile F, et al. Anatomy of the normal left atrial appendage: a quantitative study of age-related changes in 500 autopsy hearts; implications for echocardiographic examination. Circulation. 1997;96:3112–3115[Abstract/Free Full Text]
3. Suetsugu M, Matsuzaki M, Toma Y, et al. Detection of mural thrombi and analysis of blood flow velocities in the left atrial appendage using transesophageal two-dimensional echocardiography and pulsed Doppler flowmetry [Japanese]. J Cardiol. 1988;18:385–394[Medline]
4. Pollick C, Taylor D. Assessment of left atrial appendage function by transesophageal echocardiography: implications for the development of thrombus. Circulation. 1991;84:223–231[Abstract/Free Full Text]
5. Seward JB, Khandheria BK, Oh JK, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. Mayo Clin Proc. 1988;63:649–680[Medline]
6. Seward JB, Khandheria BK, Edwards WD, Oh JK, Freeman WK, Tajik AJ. Biplanar transesophageal echocardiography: anatomic correlations, image orientation, and clinical applications. Mayo Clin Proc. 1990;65:1193–1213[Medline]
7. Seward JB, Khandheria BK, Freeman WK, et al. Multiplane transesophageal echocardiography: image orientation, examination technique, anatomic correlations, and clinical applications. Mayo Clin Proc. 1993;68:523–551[Medline]
8. Chan SK, Kannam JP, Douglas PS, Manning WJ. Multiplane transesophageal echocardiographic assessment of left atrial appendage anatomy and function. Am J Cardiol. 1995;76:528–530[CrossRef][Medline]
9. Yao SS, Ilercil A, Meisner JS, Strom JA, Shirani J. Improved Doppler echocardiographic assessment of the left atrial appendage by peripheral vein injection of sonicated albumin microbubbles. Am Heart J. 1997;133:400–405[CrossRef][Medline]
10. Carranza C, Abufhele A, Cartes F, Forero A. Transthoracic versus transesophageal two-dimensional echo Doppler evaluation of flow velocity in the left atrial appendage. Echocardiography. 1997;14:357–361[Medline]
11. Fatkin D, Feneley M. Stratification of thromboembolic risk of atrial fibrillation by transthoracic echocardiography and transesophageal echocardiography: the relative role of left atrial appendage function, mitral valve disease, and spontaneous echocardiographic contrast. Prog Cardiovasc Dis. 1996;39:57–68[CrossRef][Medline]
12. Li YH, Lai LP, Shyu KG, et al. Clinical implications of left atrial appendage function: its influence on thrombus formation. Int J Cardiol. 1994;43:61–66[CrossRef][Medline]
13. Hwang JJ, Li YH, Lin JM, et al. Left atrial appendage function determined by transesophageal echocardiography in patients with rheumatic mitral valve disease. Cardiology. 1994;85:121–128[Medline]
14. Fatkin D, Feneley MP. Patterns of Doppler-measured blood flow velocity in the normal and fibrillating human left atrial appendage. Am Heart J. 1996;132:995–1003[CrossRef][Medline]
15. Tabata T, Oki T, Fukuda N, et al. Influence of aging on left atrial appendage flow velocity patterns in normal subjects. J Am Soc Echocardiogr. 1996;9:274–280[CrossRef][Medline]
16. Tabata T, Oki T, Fukuda N, et al. Influence of left atrial pressure on left atrial appendage flow velocity patterns in patients in sinus rhythm. J Am Soc Echocardiogr. 1996;9:857–864[CrossRef][Medline]
17. Porte JM, Cormier B, Iung B, et al. Early assessment by transesophageal echocardiography of left atrial appendage function after percutaneous mitral commissurotomy. Am J Cardiol. 1996;77:72–76[CrossRef][Medline]
18. Tabata T, Oki T, Iuchi A, et al. Evaluation of left atrial appendage function by measurement of changes in flow velocity patterns after electrical cardioversion in patients with isolated atrial fibrillation. Am J Cardiol. 1997;79:615–620[CrossRef][Medline]
19. Ito T, Suwa M, Kobashi A, Yagi H, Hirota Y, Kawamura K. Influence of altered loading conditions on left atrial appendage function in vivo. Am J Cardiol. 1998;81:1056–1059[CrossRef][Medline]
20. Ito T, Suwa M, Hirota Y, Otake Y, Moriguchi A, Kawamura K. Influence of left atrial function on Doppler transmitral and pulmonary venous flow patterns in dilated and hypertrophic cardiomyopathy: evaluation of left atrial appendage function by transesophageal echocardiography. Am Heart J. 1996;131:122–130[CrossRef][Medline]
21. Black IW, Hopkins AP, Lee LC, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. J Am Coll Cardiol. 1991;18:398–404[Abstract]
22. Fatkin D, Kelly RP, Feneley MP. Relations between left atrial appendage blood flow velocity, spontaneous echocardiographic contrast and thromboembolic risk in vivo. J Am Coll Cardiol. 1994;23:961–969[Abstract]
23. Mügge A, Daniel WG, Hausmann D, Gödke J, Wagenbreth I, Lichtlen PR. Diagnosis of left atrial appendage thrombi by transesophageal echocardiography: clinical implications and follow-up. Am J Card Imaging. 1990;4:173–179
24. Seward JB, Khandheria BK, Oh JK, Freeman WK, Tajik AJ. Critical appraisal of transesophageal echocardiography: limitations, pitfalls, and complications. J Am Soc Echocardiogr. 1992;5:288–305[Medline]
25. Herzog E, Sherrid M. Bifid left atrial appendage with thrombus: source of thromboembolism. J Am Soc Echocardiogr. 1998;11:910–915[CrossRef][Medline]
26. Mügge A, Kuhn H, Nikutta P, Grote J, Lopez JA, Daniel WG. Assessment of left atrial appendage function by biplane transesophageal echocardiography in patients with nonrheumatic atrial fibrillation: identification of a subgroup of patients at increased embolic risk. J Am Coll Cardiol. 1994;23:599–607[Abstract]
27. Appleton CP, Jensen JL, Hatle LK, Oh JK. Doppler evaluation of left and right ventricular diastolic function: a technical guide for obtaining optimal flow velocity recordings. J Am Soc Echocardiogr. 1997;10:271–292[CrossRef][Medline]
28. Kortz RA, Delemarre BJ, van Dantzig JM, Bot H, Kamp O, Visser CA. Left atrial appendage blood flow determined by transesophageal echocardiography in healthy subjects. Am J Cardiol. 1993;71:976–981[CrossRef][Medline]
29. Agmon Y, Khandheria BK, Meissner I, et al. Age-associated changes in left atrial appendage function: a population-based transesophageal echocardiographic study (abstr). J Am Coll Cardiol. 1998;31(Suppl A):163A
30. Okamoto M, Hashimoto M, Sueda T, Yamada T, Karakawa S, Kajiyama G. Time interval determination from left atrial appendage ejection flow in patients with mitral stenosis. J Clin Ultrasound. 1997;25:97–102[CrossRef][Medline]
31. Zeppellini R, Schon F, Gheno G, et al. Left atrial appendage systolic forward flow. Am J Cardiol. 1995;75:204–206[CrossRef][Medline]
32. Jue J, Winslow T, Fazio G, Redberg RF, Foster E, Schiller NB. Pulsed Doppler characterization of left atrial appendage flow. J Am Soc Echocardiogr. 1993;6:237–244[Medline]
33. Lin JM, Lin JL, Tseng YZ. Left atrial appendage blood flow in a case of persistent atrial standstill. Int J Cardiol. 1996;57:97–99[CrossRef][Medline]
34. Noda T, Arakawa M, Miwa H, et al. Effects of heart rate on flow velocity of the left atrial appendage in patients with nonvalvular atrial fibrillation. Clin Cardiol. 1996;19:295–300[Medline]
35. Pozzoli M, Febo O, Torbicki A, et al. Left atrial appendage dysfunction: a cause of thrombosis? Evidence by transesophageal echocardiography-Doppler studies. J Am Soc Echocardiogr. 1991;4:435–441[Medline]
36. Akosah KO, Funai JT, Porter TR, Jesse RL, Mohanty PK. Left atrial appendage contractile function in atrial fibrillation: influence of heart rate and cardioversion to sinus rhythm. Chest. 1995;107:690–696[Abstract/Free Full Text]
37. Stroke Prevention in Atrial Fibrillation InvestigatorsBlackshear JL, Safford RE, Pearce LA. F-amplitude, left atrial appendage velocity, and thromboembolic risk in nonrheumatic atrial fibrillation. Clin Cardiol. 1996;19:309–313[Medline]
38. Li YH, Hwang JJ, Tseng YZ, Kuan P, Lien WP. Clinical significance of fibrillatory wave amplitude: a clue to left atrial appendage function in nonrheumatic atrial fibrillation. Chest. 1995;108:359–363[Abstract/Free Full Text]
39. Santiago D, Warshofsky M, Li Mandri G, et al. Left atrial appendage function and thrombus formation in atrial fibrillation-flutter: a transesophageal echocardiographic study. J Am Coll Cardiol. 1994;24:159–164[Abstract]
40. Grimm RA, Chandra S, Klein AL, et al. Characterization of left atrial appendage Doppler flow in atrial fibrillation and flutter by Fourier analysis. Am Heart J. 1996;132:286–296[CrossRef][Medline]
41. Grimm RA, Stewart WJ, Arheart K, Thomas JD, Klein AL. Left atrial appendage "stunning" after electrical cardioversion of atrial flutter: an attenuated response compared with atrial fibrillation as the mechanism for lower susceptibility to thromboembolic events. J Am Coll Cardiol. 1997;29:582–589[Abstract]
42. Omran H, Jung W, Rabahieh R, et al. Left atrial appendage function in patients with atrial flutter. Heart. 1997;78:250–254[Abstract/Free Full Text]
43. Bhagwat AR, Hoit BD. Diagnosis of retrograde ventriculoatrial conduction by left atrial appendage Doppler flow analysis. Pacing Clin Electrophysiol. 1996;19:1257–1259[CrossRef][Medline]
44. Lin JM, Lin JL, Chen JJ, Li YH, Huang JJ, Tseng YZ. Left atrial appendage blood flow determined by transesophageal echocardiography in patients with complete atrioventricular block. Cardiology. 1996;87:71–75[Medline]
45. Asanuma T, Tanabe K, Yoshitomi H, et al. Left atrial appendage function in patients with single-chamber ventricular pacing. Am J Cardiol. 1995;76:840–842[CrossRef][Medline]
46. Simantirakis EN, Parthenakis FI, Chrysostomakis SI, Zuridakis EG, Igoumenidis NE, Vardas PE. Left atrial appendage function during DDD and VVI pacing. Heart. 1997;77:428–431[Abstract/Free Full Text]
47. Garcia-Fernandez MA, Torrecilla EG, San Roman D, et al. Left atrial appendage Doppler flow patterns: implications on thrombus formation. Am Heart J. 1992;124:955–961[CrossRef][Medline]
48. Li YH, Lai LP, Shyu KG, Hwang JJ, Kuan P, Lien WP. Clinical implications of left atrial appendage flow patterns in nonrheumatic atrial fibrillation. Chest. 1994;105:748–752[Abstract/Free Full Text]
49. Ito T, Suwa M, Otake Y, Moriguchi A, Hirota Y, Kawamura K. Left ventricular Doppler filling pattern in dilated cardiomyopathy: relation to hemodynamics and left atrial function. J Am Soc Echocardiogr. 1997;10:518–525[CrossRef][Medline]
50. Sadler TW. Langman’s Medical Embryology, 6th ed. Baltimore: Williams & Wilkins; 1990. p. 179–227
51. Bellotti P, Spirito P, Lupi G, Vecchio C. Left atrial appendage function assessed by transesophageal echocardiography before and on the day after elective cardioversion for nonvalvular atrial fibrillation. Am J Cardiol. 1998;81:1199–1202[CrossRef][Medline]
52. Grimm RA, Stewart WJ, Maloney JD, et al. Impact of electrical cardioversion for atrial fibrillation on left atrial appendage function and spontaneous echo contrast: characterization by simultaneous transesophageal echocardiography. J Am Coll Cardiol. 1993;22:1359–1366[Abstract]
53. Hoit BD, Shao Y, Gabel M. Influence of acutely altered loading conditions on left atrial appendage flow velocities. J Am Coll Cardiol. 1994;24:1117–1123[Abstract]
54. Hondo T, Okamoto M, Yamane T, et al. The role of the left atrial appendage: a volume loading study in open-chest dogs. Jpn Heart J. 1995;36:225–234[Medline]
55. Tabata T, Oki T, Yamada H, et al. Role of left atrial appendage in left atrial reservoir function as evaluated by left atrial appendage clamping during cardiac surgery. Am J Cardiol. 1998;81:327–332[CrossRef][Medline]
56. Hoit BD, Shao Y, Tsai LM, Patel R, Gabel M, Walsh RA. Altered left atrial compliance after atrial appendectomy: influence on left atrial and ventricular filling. Circ Res. 1993;72:167–175[Abstract/Free Full Text]
57. Lin JM, Hsu KL, Hwang JJ, Li YH, Tseng YZ. Interference of mitral valve stenosis with left ventricular diastole and left atrial appendage flow. Cardiology. 1996;87:537–544[Medline]
58. Lee TM, Chou NK, Su SF, et al. Left atrial spontaneous echo contrast in asymptomatic patients with a mechanical valve prosthesis. Ann Thorac Surg. 1996;62:1790–1795[Abstract/Free Full Text]
59. Lin JM, Hsu KL, Hwang JJ, Li YH, Tseng YZ. Effects of percutaneous mitral valvuloplasty on left atrial appendage flow velocity. Am J Cardiol. 1995;76:609–611[CrossRef][Medline]
60. Sarikamis C, Bozat T, Akkaya V. Persistence of left atrial spontaneous echocardiographic contrast after percutaneous mitral valvulotomy: a study in the Turkish population. J Heart Valve Dis. 1997;6:160–165[Medline]
61. Blackshear JL, Pearce LA, Asinger RW, et al. Mitral regurgitation associated with reduced thromboembolic events in high-risk patients with nonrheumatic atrial fibrillation. Am J Cardiol. 1993;72:840–843[CrossRef][Medline]
62. Siostrzonek P, Koppensteiner R, Gossinger H, et al. Hemodynamic and hemorheologic determinants of left atrial spontaneous echo contrast and thrombus formation in patients with idiopathic dilated cardiomyopathy. Am Heart J. 1993;125:430–434[CrossRef][Medline]
63. Lin JM, Hsu KL, Hwang JJ, Tseng YZ. Influence of left ventricular diastole on left atrial appendage blood flow in patients with nonrheumatic atrial fibrillation. Cardiology. 1997;88:563–568[Medline]
64. Perez Y, Duval AM, Carville C, et al. Is left atrial appendage flow a predictor for outcome of cardioversion of nonvalvular atrial fibrillation? A transthoracic and transesophageal echocardiographic study. Am Heart J. 1997;134:745–751[CrossRef][Medline]
65. The Stroke Prevention in Atrial Fibrillation Investigators. Predictors of thromboembolism in atrial fibrillation: I. Clinical features of patients at risk. II. Echocardiographic features of patients at risk. Ann Intern Med 1992;116:1–5; 6–12.
66. Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography. Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med. 1998;128:639–647[Abstract/Free Full Text]
67. Rubin DN, Katz SE, Riley MF, Douglas PS, Manning WJ. Evaluation of left atrial appendage anatomy and function in recent-onset atrial fibrillation by transesophageal echocardiography. Am J Cardiol. 1996;78:774–778[CrossRef][Medline]
68. Heppell RM, Berkin KE, McLenachan JM, Davies JA. Haemostatic and haemodynamic abnormalities associated with left atrial thrombosis in non-rheumatic atrial fibrillation. Heart. 1997;77:407–411[Abstract/Free Full Text]
69. Verhorst PM, Kamp O, Visser CA, Verheugt FW. Left atrial appendage flow velocity assessment using transesophageal echocardiography in nonrheumatic atrial fibrillation and systemic embolism. Am J Cardiol. 1993;71:192–196[CrossRef][Medline]
70. Mitusch R, Garbe M, Schmucker G, Schwabe K, Stierle U, Sheikhzadeh A. Relation of left atrial appendage function to the duration and reversibility of nonvalvular atrial fibrillation. Am J Cardiol. 1995;75:944–947[CrossRef][Medline]
71. Shively BK, Gelgand EA, Crawford MH. Regional left atrial stasis during atrial fibrillation and flutter: determinants and relation to stroke. J Am Coll Cardiol. 1996;27:1722–1729[Abstract]
72. Li YH, Hwang JJ, Lin JL, Tseng YZ, Lien WP. Importance of left atrial appendage function as a risk factor for systemic thromboembolism in patients with rheumatic mitral valve disease. Am J Cardiol. 1996;78:844–847[Medline]
73. Zabalgoitia M, Halperin JL, Pearce LA, Blackshear JL, Asinger RW, Hart RG. Transesophageal echocardiographic correlates of clinical risk of thromboembolism in nonvalvular atrial fibrillation: Stroke Prevention in Atrial Fibrillation III Investigators. J Am Coll Cardiol. 1998;31:1622–1626[Abstract/Free Full Text]
74. Manning WJ, Silverman DI. Atrial anatomy and function postcardioversion: insights from transthoracic and transesophageal echocardiography. Prog Cardiovasc Dis. 1996;39:33–46[CrossRef][Medline]
75. Fatkin D, Kuchar DL, Thorburn CW, Feneley MP. Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complications. J Am Coll Cardiol. 1994;23:307–316[Abstract]
76. Grimm RA, Leung DY, Black IW, Stewart WJ, Thomas JD, Klein AL. Left atrial appendage "stunning" after spontaneous conversion of atrial fibrillation demonstrated by transesophageal Doppler echocardiography. Am Heart J. 1995;130:174–176[CrossRef][Medline]
77. Falcone RA, Morady F, Armstrong WF. Transesophageal echocardiographic evaluation of left atrial appendage function and spontaneous contrast formation after chemical or electrical cardioversion of atrial fibrillation. Am J Cardiol. 1996;78:435–439[CrossRef][Medline]
78. Omran H, Jung W, Rabahieh R, et al. Left atrial chamber and appendage function after internal atrial defibrillation: a prospective and serial transesophageal echocardiographic study. J Am Coll Cardiol. 1997;29:131–138[Abstract]
79. Sparks PB, Jayaprakash S, Vohra JK, et al. Left atrial "stunning" following radiofrequency catheter ablation of chronic atrial flutter. J Am Coll Cardiol. 1998;32:468–475[Abstract/Free Full Text]
80. Sparks PB, Kulkarni R, Vohra JK, et al. Effect of direct current shocks on left atrial mechanical function in patients with structural heart disease. J Am Coll Cardiol. 1998;31:1395–1399[Abstract/Free Full Text]
81. Ito T, Suwa M, Otake Y, et al. Assessment of left atrial appendage function after cardioversion of atrial fibrillation: relation to left atrial mechanical function. Am Heart J. 1998;135:1020–1026[CrossRef][Medline]
82. Harjai K, Mobarek S, Abi-Samra F, et al. Mechanical dysfunction of the left atrium and the left atrial appendage following cardioversion of atrial fibrillation and its relation to total electrical energy used for cardioversion. Am J Cardiol. 1998;81:1125–1129[CrossRef][Medline]
83. Tanabe K, Yoshitomi H, Asanuma T, Okada S, Shimada T, Morioka S. Prediction of outcome of electrical cardioversion by left atrial appendage flow velocities in atrial fibrillation. Jpn Circ J. 1997;61:19–24[CrossRef][Medline]
84. Manabe K, Oki T, Tabata T, et al. Transesophageal echocardiographic prediction of initially successful electrical cardioversion of isolated atrial fibrillation: effects of left atrial appendage function. Jpn Heart J. 1997;38:487–495[Medline]
85. Verhorst PM, Kamp O, Welling RC, Van Eenige MJ, Visser CA. Transesophageal echocardiographic predictors for maintenance of sinus rhythm after electrical cardioversion of atrial fibrillation. Am J Cardiol. 1997;79:1355–1359[CrossRef][Medline]
86. Li YH, Hwang JJ, Ko YL, et al. Left atrial spontaneous echo contrast in patients with rheumatic mitral valve disease in sinus rhythm: implication of an altered left atrial appendage function in its formation. Chest. 1995;108:99–103[Abstract/Free Full Text]
87. Kamalesh M, Copeland TB, Sawada S. Severely reduced left atrial appendage function: a cause of embolic stroke in patients in sinus rhythm? J Am Soc Echocardiogr. 1998;11:902–904[CrossRef][Medline]
This article has been cited by other articles:
|
|
|
|
 
J. Hur, Y. J. Kim, H.-J. Lee, J.-W. Ha, J. H. Heo, E.-Y. Choi, C.-Y. Shim, T. H. Kim, J. E. Nam, K. O. Choe, et al.
Left Atrial Appendage Thrombi in Stroke Patients: Detection with Two-Phase Cardiac CT Angiography versus Transesophageal Echocardiography
Radiology,
June 1, 2009;
251(3):
683 - 690.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Jungwirth and G. B. Mackensen
Real-Time 3-Dimensional Echocardiography in the Operating Room
Seminars in Cardiothoracic and Vascular Anesthesia,
December 1, 2008;
12(4):
248 - 264.
[Abstract]
[PDF]
|
|
|
|
|
|
|
J. Hur, Y. J. Kim, J. E. Nam, K. O. Choe, E.-Y. Choi, C.-Y. Shim, and B. W. Choi
Thrombus in the Left Atrial Appendage in Stroke Patients: Detection with Cardiac CT Angiography--A Preliminary Report
Radiology,
October 1, 2008;
249(1):
81 - 87.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. M. Lacomis, O. Goitein, C. Deible, P. L. Moran, G. Mamone, S. Madan, and D. Schwartzman
Dynamic multidimensional imaging of the human left atrial appendage
Europace,
December 1, 2007;
9(12):
1134 - 1140.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Writing Committee Members, V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, et al.
ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society
Europace,
September 1, 2006;
8(9):
651 - 745.
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al.
ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society
J. Am. Coll. Cardiol.,
August 15, 2006;
48(4):
e149 - e246.
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al.
ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society
Circulation,
August 15, 2006;
114(7):
e257 - e354.
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. K. Mohrs, B. Nowak, S. E. Petersen, M. Welsner, C. Rubel, A. Magedanz, H.-U. Kauczor, and T. Voigtlaender
Thrombus Detection in the Left Atrial Appendage Using Contrast-Enhanced MRI: A Pilot Study
Am. J. Roentgenol.,
January 1, 2006;
186(1):
198 - 205.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Donal, H. Yamada, C. Leclercq, and D. Herpin
The Left Atrial Appendage, a Small, Blind-Ended Structure: A Review of Its Echocardiographic Evaluation and Its Clinical Role
Chest,
September 1, 2005;
128(3):
1853 - 1862.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Bernhardt, H. Schmidt, C. Hammerstingl, B. Luderitz, and H. Omran
Patients With Atrial Fibrillation and Dense Spontaneous Echo Contrast at High Risk: A Prospective and Serial Follow-Up Over 12 Months With Transesophageal Echocardiography and Cerebral Magnetic Resonance Imaging
J. Am. Coll. Cardiol.,
June 7, 2005;
45(11):
1807 - 1812.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Erdogan, M. T. Goren, R. Diz-Kucukkaya, and M. Inanc
Assessment of Cardiac Structure and Left Atrial Appendage Functions in Primary Antiphospholipid Syndrome: A Transesophageal Echocardiographic Study
Stroke,
March 1, 2005;
36(3):
592 - 596.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
I. A. Paraskevaidis, T. Dodouras, D. Tsiapras, and D. T. Kremastinos
Prediction of Successful Cardioversion and Maintenance of Sinus Rhythm in Patients With Lone Atrial Fibrillation
Chest,
February 1, 2005;
127(2):
488 - 494.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G Corrado, S Beretta, L Sormani, G Tadeo, G Foglia-Manzillo, L.M Tagliagambe, and M Santarone
Prevalence of atrial thrombi in patients with atrial fibrillation/flutter and subtherapeutic anticoagulation prior to cardioversion
Eur J Echocardiogr,
August 1, 2004;
5(4):
257 - 261.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
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]
|
|
|
|
|
|
|
S Illien, S Maroto-Jarvinen, G von der Recke, C Hammerstingl, H Schmidt, S Kuntz-Hehner, B Luderitz, and H Omran
Atrial fibrillation: relation between clinical risk factors and transoesophageal echocardiographic risk factors for thromboembolism
Heart,
February 1, 2003;
89(2):
165 - 168.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Antonielli, A. Pizzuti, A. Palinkas, M. Tanga, N. o. Gruber, C. Michelassi, A. Varga, A. Bonzano, N. Gandolfo, L.a. Halmai, et al.
Clinical value of left atrial appendage flow for prediction of long-term sinus rhythm maintenance in patients with nonvalvular atrial fibrillation
J. Am. Coll. Cardiol.,
May 1, 2002;
39(9):
1443 - 1449.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Shimizu, Y. Murakami, S.-i. Inoue, Y. Ohta, K. Nakamura, H. Katoh, T. Sakne, N. Takahashi, S. Ohata, T. Sugamori, et al.
High Plasma Brain Natriuretic Polypeptide Level as a Marker of Risk for Thromboembolism in Patients With Nonvalvular Atrial Fibrillation
Stroke,
April 1, 2002;
33(4):
1005 - 1010.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Agmon, B. K. Khandheria, F. Gentile, and J. B. Seward
Clinical and Echocardiographic Characteristics of Patients With Left Atrial Thrombus and Sinus Rhythm: Experience in 20 643 Consecutive Transesophageal Echocardiographic Examinations
Circulation,
January 1, 2002;
105(1):
27 - 31.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Palinkas, E. Antonielli, E. Picano, A. Pizzuti, A. Varga, B. Nyuzo, J.M. Alegret, A. Bonzano, M. Tanga, A. Coppolino, et al.
Clinical value of left atrial appendage flow velocity for predicting of cardioversion success in patients with non-valvular atrial fibrillation
Eur. Heart J.,
December 1, 2001;
22(23):
2201 - 2208.
[Abstract]
[PDF]
|
|
|
|
|
|
|
V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al.
ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology
Circulation,
October 23, 2001;
104(17):
2118 - 2150.
[Full Text]
[PDF]
|
|
|
|
|
|
|
Guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology
Eur. Heart J.,
October 2, 2001;
22(20):
1852 - 1923.
[PDF]
|
|
|
|
|
|
|
V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al.
ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary: A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology
J. Am. Coll. Cardiol.,
October 1, 2001;
38(4):
1231 - 1265.
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al.
ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology
J. Am. Coll. Cardiol.,
October 1, 2001;
38(4):
1266 - 1266.
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Schmidt, G. von der Recke, S. Illien, T. Lewalter, R. Schimpf, C. Wolpert, H. Becher, B. Luderitz, and H. Omran
Prevalence of left atrial chamber and appendage thrombi in patients with atrial flutter and its clinical significance
J. Am. Coll. Cardiol.,
September 1, 2001;
38(3):
778 - 784.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. L. Klein, R. D. Murray, and R. A. Grimm
Role of transesophageal echocardiography-guided cardioversion of patients with atrial fibrillation
J. Am. Coll. Cardiol.,
March 1, 2001;
37(3):
691 - 704.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. G. Hart and J. L. Halperin
Atrial Fibrillation and Stroke : Concepts and Controversies
Stroke,
March 1, 2001;
32(3):
803 - 808.
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. S. Go, E. M. Hylek, K. A. Phillips, L. H. Borowsky, L. E. Henault, Y. Chang, J. V. Selby, and D. E. Singer
Implications of Stroke Risk Criteria on the Anticoagulation Decision in Nonvalvular Atrial Fibrillation : The Anticoagulation and Risk Factors In Atrial Fibrillation (ATRIA) Study
Circulation,
July 4, 2000;
102(1):
11 - 13.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Echocardiographic aspects