STATE-OF-THE-ART PAPER
Left Atrial Size
Physiologic Determinants and Clinical Applications
Walter P. Abhayaratna, MBBS, FRACP*,
James B. Seward, MD, FACC*,
Christopher P. Appleton, MD, FACC ,
Pamela S. Douglas, MD, FACC ,
Jae K. Oh, MD, FACC*,
A. Jamil Tajik, MD, FACC and
Teresa S.M. Tsang, MD, FACC*,*
* Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota
Division of Cardiovascular Diseases, Mayo Clinic, Scottsdale, Arizona
Cardiovascular Medicine Division, Duke University, Durham, North Carolina.
Manuscript received November 18, 2005;
revised manuscript received January 27, 2006,
accepted February 7, 2006.
* Reprint requests and correspondence: Dr. Teresa S. M. Tsang, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905. (Email: tsang.teresa{at}mayo.edu).
 |
Abstract
|
|---|
Left atrial (LA) enlargement has been proposed as a barometer of diastolic burden and a predictor of common cardiovascular outcomes such as atrial fibrillation, stroke, congestive heart failure, and cardiovascular death. It has been shown that advancing age alone does not independently contribute to LA enlargement, and the impact of gender on LA volume can largely be accounted for by the differences in body surface area between men and women. Therefore, enlargement of the left atrium reflects remodeling associated with pathophysiologic processes. In this review, we discuss the normal size and phasic function of the left atrium. Further, we outline the clinically important aspects and pitfalls of evaluating LA size, and the methods for assessing LA function using echocardiography. Finally, we review the determinants of LA size and remodeling, and we describe the evidence regarding the prognostic value of LA size. The use of LA volume for risk stratification is an evolving science. More data are required with respect to the natural history of LA remodeling in disease, the degree of LA modifiability with therapy, and whether regression of LA size translates into improved cardiovascular outcomes.
|
Abbreviations and Acronyms
| | 2D = two-dimensional | | 3D = three-dimensional | | AF = atrial fibrillation | | CHF = congestive heart failure | | LA = left atrial/atrium | | LV = left ventricle/ventricular | | PVar = pulmonary venous flow reversal during atrial systole | | PVd = pulmonary venous flow during early ventricular diastole | | PVs1 = pulmonary venous flow during early ventricular systole | | PVs2 = pulmonary venous flow during late ventricular systole |
|
There is strong evidence that left atrial (LA) enlargement, as determined by echocardiography, is a robust predictor of cardiovascular outcomes. Recently, it has been shown that LA volume provides a more accurate measure of LA size than conventional M-mode LA dimension (1). To optimize the use of LA volume for risk stratification, an understanding of the physiologic determinants of LA size and the methods for accurate quantitation is pivotal. Recent guidelines from the American Society of Echocardiography provide clarification as to which of the multiple methods for LA volume quantitation should be used in clinical practice (2). Such a standardized approach for LA volume assessment will be crucial for reproducible measures and communication of LA size between laboratories. Herein, we present an overview of LA size and function, and describe the physiologic determinants and clinical implications of LA enlargement.
|
LA phasic function and size
|
|---|
The LA mechanical function can be described broadly by three phases within the cardiac cycle (3). First, during ventricular systole and isovolumic relaxation, the LA functions as a "reservoir" that receives blood from pulmonary venous return and stores energy in the form of pressure. Second, during the early phase of ventricular diastole, the LA operates as a "conduit" for transfer of blood into the left ventricle (LV) after mitral valve opening via a pressure gradient, and through which blood flows passively from the pulmonary veins into the left ventricle during LV diastasis. Third, the "contractile" function of the LA normally serves to augment the LV stroke volume by approximately 20% (4). The relative contribution of this "booster pump" function becomes more dominant in the setting of LV dysfunction (5,6).
The size of the LA varies during the cardiac cycle (7–11). Generally, only maximum LA size is routinely measured in clinical practice. However, various LA volumes (8–11) can be used to describe LA phasic function:
- 1 Maximum LA volume occurs just before mitral valve opening.
- 2 Minimum LA volume occurs at mitral valve closure.
- 3 Total LA emptying volume is an estimate of reservoir volume, which is calculated as the difference between maximum and minimum LA volumes.
- 4 LA passive emptying volume is calculated as the difference between maximal LA volume and the LA volume preceding atrial contraction (at the onset of the P-wave on electrocardiography).
- 5 LA active emptying (contractile) volume is calculated as the difference between pre-atrial contraction LA volume and minimum LA volume.
- 6 LA (passive) conduit volume is calculated as the difference between LV stroke volume and the total LA emptying volume.
The relative contribution of LA phasic function to LV filling is dependent upon the LV diastolic properties (12) and therefore varies with age (8). In subjects with normal diastolic function, the relative contribution of the reservoir, conduit, and contractile function of the LA to the filling of the LV is approximately 40%, 35%, and 25%, respectively (12). With abnormal LV relaxation, the relative contribution of LA reservoir and contractile function increases and conduit function decreases. However, as LV filling pressure progressively increases with advancing diastolic dysfunction, the LA serves predominantly as a conduit (12).
|
Assessment of LA size and function
|
|---|
Two-dimensional and Doppler methods have been used increasingly for the assessment of LA size and function, respectively.
LA size assessment.
Measurement of anteroposterior LA linear dimension by M-mode echocardiography (13,14) is simple and convenient but not reliably accurate, given that the LA is not a symmetrically shaped three-dimensional (3D) structure (15). Furthermore, because LA enlargement may not occur in a uniform fashion (16), one-dimensional assessment is likely to be an insensitive assessment of any change in LA size. In contrast to LA dimension, LA volume by two-dimensional (2D) or 3D echocardiography provides a more accurate and reproducible estimate of LA size, when compared with reference standards such as magnetic resonance imaging (MRI) and cine computerized tomography (CT) (17–20), and has a stronger association with cardiovascular outcomes (1,21,22). Accordingly, the American Society of Echocardiography has recommended quantification of LA size by biplane 2D echocardiography using either the method of discs (by Simpson’s rule) or the area-length method (2). Although we have routinely used the area-length method in our laboratory, we have found that the biplane Simpson’s method is comparable in accuracy and reproducibility. Critical elements and common pitfalls for accurate and reproducible measurement of biplane LA volume assessment are detailed in the and outlined in Table 1.
Echocardiographic methods systematically underestimate LA volume when compared with CT (23) or MRI quantitation (19), which in turn underestimates true LA size (11). More recently, magnetic electroanatomic mapping has also been used for assessment of LA volume (24). However, because of its portability and safety, echocardiographic assessment of LA volume is preferable to other imaging methods in clinical practice.
LA volume reference limits.
Reference values for 2D echocardiographic maximum LA volumes have been estimated using data collected on persons free of cardiovascular disease, although few samples have been population based (21,25). Published reference values for maximum and minimum LA volumes are 22 ± 6 ml/m2 (26) and 9 ± 4 ml/m2 (27), respectively. In a study of LA function, mean total LA emptying volume was 13.5 ± 4.3 ml/m2 (representing 37 ± 13% of LV stroke volume), fractional emptying of the LA was 65 ± 9%, and conduit volume was 23 ± 8 ml/m2 (28).
Assessment of LA function by echocardiography.
Pulsed-wave Doppler evaluation of transmitral and pulmonary venous blood flow velocity can be used for assessment of LA function, in addition to its widespread use for the evaluation of LV diastolic function and filling pressure (29–31). The normal pulmonary venous flow pattern reflects flow from the pulmonary veins to the LA during early ventricular systole (PVs1; seen distinctly in about 30% of transthoracic echocardiography studies [32]), late ventricular systole and isovolumic relaxation (PVs2), early ventricular diastole (PVd), and reversal of flow from the left atrium to pulmonary veins during atrial systole (PVar). Apart from flow in late ventricular systole (reflected by PVs2), which represents propagation of the right ventricular pressure pulse through the pulmonary circulation (33), blood flow in the pulmonary veins is determined by events that regulate phasic LA pressure (34). The magnitude and velocity-time integral of the PVs waves reflect LA reservoir function and are determined by LV systolic function and LA relaxation (PVs1), LA compliance (PVs1 and PVs2), and right ventricular stroke volume (PVs2) (33). Peak velocity and velocity-time integral of PVd is an index of LA conduit function (35) and is dependent on factors that influence LA afterload: LV relaxation and early filling (12) and mechanical obstruction from the mitral valve apparatus (36). During LA contraction, blood is ejected from the LA into the LV and the pulmonary veins. Thus, assessment of transmitral (peak A-wave velocity, A-wave velocity-time integral, and atrial filling fraction) (6,37) and pulmonary venous blood flow (PVar) (38) provides additive information for the evaluation of LA booster pump function. More recently, global and regional atrial contractile function has been evaluated with pulse wave and color tissue Doppler imaging (8), but the incremental clinical utility of this assessment remains to be determined. Further, new echocardiographic techniques, such as with automated border detection using acoustic quantification, are being developed to facilitate evaluation of LA size and function (8).
|
Determinants of LA size and remodeling
|
|---|
Demographic and anthropometric influences.
Body size is a major determinant of LA size. To adjust for this influence, LA size should be indexed to a measure of body size, most commonly to body surface area (21,25). It remains to be clarified if this approach attenuates obesity-related variations in LA volume, which may be prognostically significant (39). Gender differences in LA size are nearly completely accounted for by variation in body size (8,21,40,41). In persons free of cardiovascular disease, indexed LA volume is independent of age from childhood onward (42). Indeed, age-related LA enlargement is a reflection of the pathophysiologic perturbations that often accompany advancing age rather than a consequence of chronologic aging (9). The relation of LA size to race or ethnicity has not been sufficiently studied.
Atrial structural remodeling.
Many conditions are associated with LA remodeling and dilatation. The atria will enlarge in response to two broad conditions: pressure and volume overload. The relationship between increased LA size and increased filling pressures has been validated against invasive measures in subjects with (43,44) and without (30,45) mitral valve disease. Left atrial enlargement due to pressure overload is usually secondary to increased LA afterload, in the setting of mitral valve disease or LV dysfunction. Case reports have suggested that LA dilatation can also occur in response to pressure overload resulting from fibrosis and/or calcification of the LA. This condition, known as "stiff LA syndrome" (46,47), causes a reduction of LA compliance, a marked increase in LA and pulmonary pressures, and right heart failure. Chronic volume overload associated with conditions such as valvular regurgitation, arteriovenous fistulas, and high output states including chronic anemia and athletic heart (48,49), can also contribute to generalized chamber enlargement. Both volume and pressure overload can increase atrial size. However, pressure overload is uniformly accompanied by abnormal myocyte relaxation, while volume overload is characteristically associated with normal myocardial relaxation physiology.
LA volume as an expression of LV filling pressures.
In subjects without primary atrial pathology or congenital heart or mitral valve disease, increased LA volume usually reflects elevated ventricular filling pressures. During ventricular diastole, the LA is exposed to the pressures of the LV. With increased stiffness or noncompliance of the LV, LA pressure rises to maintain adequate LV filling (50), and the increased atrial wall tension leads to chamber dilatation and stretch of the atrial myocardium. Thus, LA volume increases with severity of diastolic dysfunction (22,51). The structural changes of the LA may express the chronicity of exposure to abnormal filling pressures (22,45) and provide predictive information beyond that of diastolic function grade (52), which is determined from evaluating multiple load-dependent parameters and therefore reflective of the instantaneous LV diastolic function and filling pressures. In this way, analogous to the relationship between hemoglobin A1C and random glucose levels, LA volume reflects an average effect of LV filling pressures over time, rather than an instantaneous measurement at the time of study (53). Thus, Doppler and tissue Doppler assessment of instantaneous filling pressure is better suited for monitoring hemodynamic status in the short term, whereas LA volume is useful for monitoring long-term hemodynamic control.
Left atrial size as an expression of diastolic function and filling pressures has not been fully evaluated in specific conditions. Most studies of LA size and outcomes have excluded patients with atrial fibrillation (AF). The relationship between AF and LA volume is complex (54). It has been difficult to establish the causal relationship between AF and LA structural remodeling. In patients with AF and cardiac disease, structural LA alterations may be related to the underlying cardiac pathophysiology rather than solely the arrhythmia itself (55,56). Experimental animal studies have documented that sustained atrial tachyarrhythmias induce electrical, contractile and structural remodeling (57). In some cases, it appears that LA structural remodeling may be related to high ventricular rate and increased ventricular filling pressures rather than to the atrial tachyarrhythmia itself (58,59). However, in other individuals, the size of the LA varies widely for given LV relaxation and filling properties, suggesting a hysteresis between LA size and filling pressures. Few studies have assessed the impact of sustained AF on atrial structure in patients with lone AF (60).
|
LA size for the prediction of cardiovascular outcomes
|
|---|
There is considerable data confirming the relationship between increased LA size, principally maximal but also minimal (30,61), and the development of adverse cardiovascular outcomes in subjects without a history of AF or significant valvular disease (62–75) (Table 2).
AF.
Atrial fibrillation is the most common of the serious cardiac arrhythmias and is associated with increased morbidity and mortality in the community. Prospective data from the large population-based studies have established a relationship between M-mode anteroposterior LA diameter and the risk of developing AF (76,77). In the Framingham study, a 5-mm incremental increase in anteroposterior LA diameter was associated with a 39% increased risk for subsequent development of AF (76). In the Cardiovascular Health Study, subjects in sinus rhythm with an anteroposterior LA diameter >5.0 cm had approximately four times the risk of developing AF during the subsequent period of surveillance (77). More recently, LA volume has been shown to predict AF in patients with cardiomyopathy (68,69) and first-diagnosed nonvalvular AF in a random sample of elderly Olmsted County residents who had undergone investigation with a clinically indicated echocardiogram (62,63). The relationship between LA volume and LA dimension was nonlinear (68), and it has been confirmed that LA volume represented a superior measure over LA diameter for predicting outcomes including AF (62,68,75) and provided prognostic information that was incremental to clinical risk factors (62).
Stroke.
Stroke is the leading cause of severe long-term disability and the third largest contributor to mortality in the U.S. (78). Despite the strong association between AF and ischemic stroke, 85% of strokes occur in patients who are in apparent sinus rhythm (78). In the general population, LA size has been determined to be a predictor of stroke and death (79). Increased LA volume has also been shown to predict the onset of first stroke in clinic-based elderly persons who were in sinus rhythm and did not have a history of ischemic neurologic events, AF, or valvular heart disease (70). Even after censoring for the development of documented AF, an indexed LA volume  32 ml/m2 was associated with an increased stroke risk (hazard ratio [HR] 1.67, 95% confidence interval [CI] 1.08 to 2.58) over 4.3 ± 2.7 years, independent of age and other clinical risk factors for cerebrovascular disease.
Heart failure.
As previously discussed, LA volume is a barometer of LV filling pressure and reflects the burden of diastolic dysfunction in subjects without AF or significant valvular disease (22). Elevation of filling pressure is uniformly found in the presence of symptomatic congestive heart failure (CHF). Because the majority of individuals in the community with LV dysfunction (systolic or "isolated" diastolic) are in a preclinical phase of the disease (80), methods to quantify the risk of progression to symptomatic heart failure would be clinically useful. Evidence for a prognostic role for LA volume to predict incident CHF is emerging (73,74). In a large prospective, population-based study, subjects with incident CHF during follow-up had slightly higher baseline LA linear diameters (39 mm vs. 37 mm for women [p < 0.01], 41 mm vs. 39 mm for men [p < 0.01]) (81). In a study of older adults referred for echocardiography, LA volume 32 ml/m2 was associated with increased incidence of CHF, independent of age, myocardial infarction, diabetes mellitus, hypertension, LV hypertrophy, and mitral inflow velocities (HR 1.97, 95% CI 1.4 to 2.7) (73). Furthermore, in subjects with an LV ejection fraction 50% at baseline and within four weeks of incident CHF, there was an increase of 8 ml/m2 in LA volume from baseline to CHF diagnosis, reflecting the added burden of diastolic dysfunction during the period of transition from preclinical to clinical status.
Mortality.
The relationship between LA size and death has been demonstrated in high-risk groups, such as patients with dilated cardiomyopathy (64), LV dysfunction (82), atrial arrhythmias (83), acute myocardial infarction (66,71), and patients undergoing valve replacement for aortic stenosis (84) and mitral regurgitation (85). The LA diameter has also been shown to independently predict death in the general population (81). However, in other population-based studies, the relationship between LA size and death has been attenuated when LV mass (79), LV hypertrophy (86), or diastolic function (51) has been considered. Thus, owing to the intimate relationship between LA volume, LV mass/hypertrophy, and diastolic dysfunction, the incremental value of each parameter for the prediction of death is diminished when considering the others.
Although a dilated LA is associated with a number of adverse outcomes, there is increasing evidence suggesting that LA size is potentially modifiable with medical therapy (87–96), but whether LA size reduction translates to improved outcomes remains to be established.
|
Conclusions
|
|---|
Left atrial enlargement carries important clinical and prognostic implications. Left atrial volume is superior to LA diameter as a measure of LA size, and should be incorporated into routine clinical evaluation. Future studies are warranted to further our understanding of the natural history of LA remodeling, the extent of reversibility of LA enlargement with medical therapy, and the impact of such changes on outcomes. The utility of LA volume and function for monitoring cardiovascular risk and for guiding therapy is an evolving science and may prove to have a very important public health impact.
|
Appendix
|
|---|
For the measurement of LA volume by echocardiography, please see the online version of this article.
|
References
|
|---|
1. Lester SJ, Ryan EW, Schiller NB, Foster E. Best method in clinical practice and in research studies to determine left atrial size Am J Cardiol 1999;84:829-832.[CrossRef][Web of Science][Medline]2. Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantificationa report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440-1463.[CrossRef][Web of Science][Medline] 3. Pagel PS, Kehl F, Gare M, Hettrick DA, Kersten JR, Warltier DC. Mechanical function of the left atriumnew insights based on analysis of pressure-volume relations and Doppler echocardiography. Anesthesiology 2003;98:975-994.[CrossRef][Web of Science][Medline] 4. Mitchell JH, Shapiro W. Atrial function and the hemodynamic consequences of atrial fibrillation in man Am J Cardiol 1969;23:556-567.[CrossRef][Web of Science][Medline] 5. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic functionnew insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12:426-440.[Abstract] 6. Thomas L, Levett K, Boyd A, Leung DY, Schiller NB, Ross DL. Compensatory changes in atrial volumes with normal agingis atrial enlargement inevitable?. J Am Coll Cardiol 2002;40:1630-1635.[Abstract/Free Full Text] 7. Braunwald E, Frahm C. Studies on Starling’s law of the heart, IVobservations on the hemodynamic functions of the left atrium in man. Circulation 1961;24:633-642.[Abstract/Free Full Text] 8. Spencer KT, Mor-Avi V, Gorcsan IJ, et al. Effects of aging on left atrial reservoir, conduit, and booster pump functiona multi-institution acoustic quantification study. Heart 2001;85:272-277.[Abstract/Free Full Text] 9. Thomas L, Levett K, Boyd A, Leung DYC, Schiller NB, Ross DL. Changes in regional left atrial function with agingevaluation by Doppler tissue imaging. Eur J Echocardiogr 2003;4:92-100.[CrossRef][Medline] 10. Nikitin NP, Witte KKA, Thackray SDR, Goodge LJ, Clark AL, Cleland JGF. Effect of age and sex on left atrial morphology and function Eur J Echocardiogr 2003;4:36-42.[CrossRef][Medline] 11. Jarvinen V, Kupari M, Hekali P, Poutanen VP. Assessment of left atrial volumes and phasic function using cine magnetic resonance imaging in normal subjects Am J Cardiol 1994;73:1135-1138.[CrossRef][Web of Science][Medline] 12. Prioli A, Marino P, Lanzoni L, Zardini P. Increasing degrees of left ventricular filling impairment modulate left atrial function in humans Am J Cardiol 1998;82:756-761.[CrossRef][Web of Science][Medline] 13. Hirata T, Wolfe SB, Popp RL, Helmen CH, Feigenbaum H. Estimation of left atrial size using ultrasound Am Heart J 1969;78:43-52.[CrossRef][Web of Science][Medline] 14. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiographyresults of a survey of echocardiographic measurements. Circulation 1978;58:1072-1083.[Abstract/Free Full Text] 15. Schabelman S, Schiller N, Anschuetz R, Silverman N, Glantz S. Comparison of four two-dimensional echocardiographic views for measuring left atrial size(abstr) Am J Cardiol 1978;41:391. 16. Lemire F, Tajik AJ, Hagler DJ. Asymmetric left atrial enlargement; an echocardiographic observation Chest 1976;69:779-781.[Free Full Text] 17. Kircher B, Abbott JA, Pau S, et al. Left atrial volume determination by biplane two-dimensional echocardiographyvalidation by cine computed tomography. Am Heart J 1991;121:864-871.[CrossRef][Web of Science][Medline] 18. Himelman RB, Cassidy MM, Landzberg JS, Schiller NB. Reproducibility of quantitative two-dimensional echocardiography Am Heart J 1988;115:425-431.[CrossRef][Web of Science][Medline] 19. Rodevan O, Bjornerheim R, Ljosland M, Maehle J, Smith HJ, Ihlen H. Left atrial volumes assessed by three- and two-dimensional echocardiography compared to MRI estimates Int J Card Imaging 1999;15:397-410.[CrossRef][Web of Science][Medline] 20. Poutanen T, Jokinen E, Sairanen H, Tikanoja T. Left atrial and left ventricular function in healthy children and young adults assessed by three dimensional echocardiography Heart 2003;89:544-549.[Abstract/Free Full Text] 21. Pritchett AM, Jacobsen SJ, Mahoney DW, Rodeheffer RJ, Bailey KR, Redfield MM. Left atrial volume as an index of left atrial sizea population-based study. J Am Coll Cardiol 2003;41:1036-1043.[Abstract/Free Full Text] 22. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden Am J Cardiol 2002;90:1284-1289.[CrossRef][Web of Science][Medline] 23. Vandenberg BF, Weiss RM, Kinzey J, et al. Comparison of left atrial volume by two-dimensional echocardiography and cine-computed tomography Am J Cardiol 1995;75:754-757.[CrossRef][Web of Science][Medline] 24. Patel VV, Ren JF, Jeffery ME, Plappert TJ, St John Sutton MG, Marchlinski FE. Comparison of left atrial volume assessed by magnetic endocardial catheter mapping versus transthoracic echocardiography Am J Cardiol 2003;91:351-354.[Medline] 25. Vasan RS, Larson MG, Levy D, Evans JC, Benjamin EJ. Distribution and categorization of echocardiographic measurements in relation to reference limits: the Framingham Heart Study: formulation of a height- and sex-specific classification and its prospective validation Circulation 1997;96:1863-1873.[Abstract/Free Full Text] 26. Schiller N, Foster E. Analysis of left ventricular systolic function Heart 1996;75(Suppl 2):17-26.[Abstract/Free Full Text] 27. Triposkiadis F, Tentolouris K, Androulakis A, et al. Left atrial mechanical function in the healthy elderlynew insights from a combined assessment of changes in atrial volume and transmitral flow velocity. J Am Soc Echocardiogr 1995;8:801-809.[CrossRef][Medline] 28. Gutman J, Wang YS, Wahr D, Schiller NB. Normal left atrial function determined by 2-dimensional echocardiography Am J Cardiol 1983;51:336-340.[CrossRef][Web of Science][Medline] 29. Appleton CP, Gonzalez MS, Basnight MA. Relationship of left atrial pressure and pulmonary venous flow velocitiesimportance of baseline mitral and pulmonary venous flow velocity patterns studied in lightly sedated dogs. J Am Soc Echocardiogr 1994;7:264-275.[Medline] 30. Appleton CP, Galloway JM, Gonzalez MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction J Am Coll Cardiol 1993;22:1972-1982.[Abstract] 31. Basnight MA, Gonzalez MS, Kershenovich SC, Appleton CP. Pulmonary venous flow velocityrelation to hemodynamics, mitral flow velocity and left atrial volume, and ejection fraction. J Am Soc Echocardiogr 1991;4:547-558.[Medline] 32. Jensen JL, Williams FE, Beilby BJ, et al. Feasibility of obtaining pulmonary venous flow velocity in cardiac patients using transthoracic pulsed wave Doppler technique J Am Soc Echocardiogr 1997;10:60-66.[CrossRef][Web of Science][Medline] 33. Smiseth OA, Thompson CR, Lohavanichbutr K, et al. The pulmonary venous systolic flow pulse—its origin and relationship to left atrial pressure J Am Coll Cardiol 1999;34:802-809.[Abstract/Free Full Text] 34. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity componentsnew insights from studies in lightly sedated normal dogs. J Am Coll Cardiol 1997;30:1562-1574.[Abstract] 35. Castello R, Pearson AC, Lenzen P, Labovitz AJ. Evaluation of pulmonary venous flow by transesophageal echocardiography in subjects with a normal heartcomparison with transthoracic echocardiography. J Am Coll Cardiol 1991;18:65-71.[Abstract] 36. Chen YT, Kan MN, Lee AY, Chen JS, Chiang BN. Pulmonary venous flowits relationship to left atrial and mitral valve motion. J Am Soc Echocardiogr 1993;6:387-394.[Medline] 37. Manning WJ, Leeman DE, Gotch PJ, Come PC. Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation J Am Coll Cardiol 1989;13:617-623.[Abstract] 38. Nakatani S, Garcia MJ, Firstenberg MS, et al. Noninvasive assessment of left atrial maximum dP/dt by a combination of transmitral and pulmonary venous flow J Am Coll Cardiol 1999;34:795-801.[Abstract/Free Full Text] 39. Vasan RS, Levy D, Larson MG, Benjamin EJ. Interpretation of echocardiographic measurementsa call for standardization. Am Heart J 2000;139:412-422.[CrossRef][Web of Science][Medline] 40. Wang Y, Gutman JM, Heilbron D, Wahr D, Schiller NB. Atrial volume in a normal adult population by two-dimensional echocardiography Chest 1984;86:595-601.[Abstract/Free Full Text] 41. Knutsen KM, Stugaard M, Michelsen S, Otterstad JE. M-mode echocardiographic findings in apparently healthy, nonathletic Norwegians aged 20–70 years. Influence of age, sex and body surface area J Intern Med 1989;225:111-115.[Web of Science][Medline] 42. Pearlman JD, Triulzi MO, King ME, Abascal VM, Newell J, Weyman AE. Left atrial dimensions in growth and developmentnormal limits for two-dimensional echocardiography. J Am Coll Cardiol 1990;16:1168-1174.[Abstract] 43. Kennedy JW, Yarnall SR, Murray JA, Figley MM. Quantitative angiocardiography. IV. Relationships of left atrial and ventricular pressure and volume in mitral valve disease Circulation 1970;41:817-824.[Abstract/Free Full Text] 44. Pape LA, Price JM, Alpert JS, Ockene IS, Weiner BH. Relation of left atrial size to pulmonary capillary wedge pressure in severe mitral regurgitation Cardiology 1991;78:297-303.[Medline] 45. Simek CL, Feldman MD, Haber HL, Wu CC, Jayaweera AR, Kaul S. Relationship between left ventricular wall thickness and left atrial sizecomparison with other measures of diastolic function. J Am Soc Echocardiogr 1995;8:37-47.[CrossRef][Medline] 46. Mehta S, Charbonneau F, Fitchett DH, Marpole DG, Patton R, Sniderman AD. The clinical consequences of a stiff left atrium Am Heart J 1991;122:1184-1191.[CrossRef][Web of Science][Medline] 47. Pilote L, Huttner I, Marpole D, Sniderman A. Stiff left atrial syndrome Can J Cardiol 1988;4:255-257.[Web of Science][Medline] 48. Hoogsteen J, Hoogeveen A, Schaffers H, Wijn PF, van der Wall EE. Left atrial and ventricular dimensions in highly trained cyclists Int J Cardiovasc Imaging 2003;19:211-217.[CrossRef][Web of Science][Medline] 49. Lai ZY, Chang NC, Tsai MC, Lin CS, Chang SH, Wang TC. Left ventricular filling profiles and angiotensin system activity in elite baseball players Int J Cardiol 1998;67:155-160.[Medline] 50. Greenberg B, Chatterjee K, Parmley WW, Werner JA, Holly AN. The influence of left ventricular filling pressure on atrial contribution to cardiac output Am Heart J 1979;98:742-751.[CrossRef][Web of Science][Medline] 51. Pritchett AM, Mahoney DW, Jacobsen SJ, Rodeheffer RJ, Karon BL, Redfield MM. Diastolic dysfunction and left atrial volumea population-based study. J Am Coll Cardiol 2005;45:87-92.[Abstract/Free Full Text] 52. Soufer R, Wohlgelernter D, Vita NA, et al. Intact systolic left ventricular function in clinical congestive heart failure Am J Cardiol 1985;55:1032-1036.[CrossRef][Web of Science][Medline] 53. Douglas PS. The left atriuma biomarker of chronic diastolic dysfunction and cardiovascular disease risk. J Am Coll Cardiol 2003;42:1206-1207.[Free Full Text] 54. Thamilarasan M, Klein AL. Factors relating to left atrial enlargement in atrial fibrillation"chicken or the egg" hypothesis. (comment) Am Heart J 1999;137:381-383.[CrossRef][Web of Science][Medline] 55. Mary-Rabine L, Albert A, Pham TD, et al. The relationship of human atrial cellular electrophysiology to clinical function and ultrastructure Circ Res 1983;52:188-199.[Abstract/Free Full Text] 56. Thiedemann KU, Ferrans VJ. Left atrial ultrastructure in mitral valvular disease Am J Pathol 1977;89:575-604.[Abstract] 57. Allessie M, Ausma J, Schotten U. Electrical, contractile and structural remodeling during atrial fibrillation Cardiovasc Res 2002;54:230-246.[Abstract/Free Full Text] 58. Schoonderwoerd BA, Ausma J, Crijns HJ, Van Veldhuisen DJ, Blaauw EH, Van Gelder IC. Atrial ultrastructural changes during experimental atrial tachycardia depend on high ventricular rate J Cardiovasc Electrophysiol 2004;15:1167-1174.[CrossRef][Web of Science][Medline] 59. Schoonderwoerd BA, Van Gelder IC, van Veldhuisen DJ, et al. Electrical remodeling and atrial dilation during atrial tachycardia are influenced by ventricular raterole of developing tachycardiomyopathy. J Cardiovasc Electrophysiol 2001;12:1404-1410.[CrossRef][Web of Science][Medline] 60. Frustaci A, Chimenti C, Bellocci F, Morgante E, Russo MA, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation Circulation 1997;96:1180-1184.[Abstract/Free Full Text] 61. Fatema K, Abhayaratna WP, Barnes ME, et al. Minimal left atrial volume as a predictor of first atrial fibrillation/flutter in an elderly cohort(abstr) Circulation 2005;112:585A. 62. Tsang TS, Barnes ME, Bailey KR, et al. Left atrial volumeimportant risk marker of incident atrial fibrillation in 1,655 older men and women. Mayo Clin Proc 2001;76:467-475.[Abstract] 63. Tsang TS, Gersh BJ, Appleton CP, et al. Left ventricular diastolic dysfunction as a predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women J Am Coll Cardiol 2002;40:1636-1644.[Abstract/Free Full Text] 64. Rossi A, Cicoira M, Zanolla L, et al. Determinants and prognostic value of left atrial volume in patients with dilated cardiomyopathy J Am Coll Cardiol 2002;40:1425-1430.[Abstract/Free Full Text] 65. Tsang TS, Barnes ME, Gersh BJ, et al. Prediction of risk for first age-related cardiovascular events in an elderly populationthe incremental value of echocardiography. J Am Coll Cardiol 2003;42:1199-1205.[Abstract/Free Full Text] 66. Moller JE, Hillis GS, Oh JK, et al. Left atrial volumea powerful predictor of survival after acute myocardial infarction. Circulation 2003;107:2207-2212.[Abstract/Free Full Text] 67. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Risks for atrial fibrillation and congestive heart failure in patients 65 years of age with abnormal left ventricular diastolic relaxation Am J Cardiol 2004;93:54-58.[CrossRef][Web of Science][Medline] 68. Tani T, Tanabe K, Ono M, et al. Left atrial volume and the risk of paroxysmal atrial fibrillation in patients with hypertrophic cardiomyopathy J Am Soc Echocardiogr 2004;17:644-648.[CrossRef][Web of Science][Medline] 69. Losi MA, Betocchi S, Aversa M, et al. Determinants of atrial fibrillation development in patients with hypertrophic cardiomyopathy Am J Cardiol 2004;94:895-900.[CrossRef][Web of Science][Medline] 70. Barnes ME, Miyasaka Y, Seward JB, et al. Left atrial volume in the prediction of first ischemic stroke in an elderly cohort without atrial fibrillation Mayo Clin Proc 2004;79:1008-1014.[Abstract/Free Full Text] 71. Beinart R, Boyko V, Schwammenthal E, et al. Long-term prognostic significance of left atrial volume in acute myocardial infarction J Am Coll Cardiol 2004;44:327-334.[Abstract/Free Full Text] 72. Sabharwal N, Cemin R, Rajan K, Hickman M, Lahiri A, Senior R. Usefulness of left atrial volume as a predictor of mortality in patients with ischemic cardiomyopathy Am J Cardiol 2004;94:760-763.[CrossRef][Web of Science][Medline] 73. Takemoto Y, Barnes ME, Seward JB, et al. Usefulness of left atrial volume in predicting first congestive heart failure in patients 65 years of age with well-preserved left ventricular systolic function Am J Cardiol 2005;96:832-836.[CrossRef][Web of Science][Medline] 74. Gottdiener JS, Kitzman DW, Aurigemma GP, Arnold AM, Manolio TA. Left atrial volume, geometry, and function in systolic and diastolic heart failure of persons 65 years of age (the Cardiovascular Health Study) Am J Cardiol 2006;97:83-89.[CrossRef][Web of Science][Medline] 75. Tsang TS, Abhayaratna WP, Barnes ME, et al. Prediction of cardiovascular outcomes with left atrial sizeis volume superior to area or diameter?. J Am Coll Cardiol 2006;47:1018-1023.[Abstract/Free Full Text] 76. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study Circulation 1994;89:724-730.[Abstract/Free Full Text] 77. Psaty BM, Manolio TA, Kuller LH, et al. Incidence of and risk factors for atrial fibrillation in older adults Circulation 1997;96:2455-2461.[Abstract/Free Full Text] 78. American Heart Association Heart Disease and Stroke Statistics—2005 Update. Dallas, TX: American Heart Association; 2003. 79. Benjamin EJ, D’Agostino RB, Belanger AJ, Wolf PA, Levy D. Left atrial size and the risk of stroke and death. The Framingham Heart Study Circulation 1995;92:835-841.[Abstract/Free Full Text] 80. Redfield MM, Jacobsen SJ, Burnett Jr. JC, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the communityappreciating the scope of the heart failure epidemic. JAMA 2003;289:194-202.[Abstract/Free Full Text] 81. Gardin JM, McClelland R, Kitzman D, et al. M-mode echocardiographic predictors of six- to seven-year incidence of coronary heart disease, stroke, congestive heart failure, and mortality in an elderly cohort (the Cardiovascular Health Study) Am J Cardiol 2001;87:1051-1057.[CrossRef][Web of Science][Medline] 82. Giannuzzi P, Temporelli PL, Bosimini E, et al. Independent and incremental prognostic value of Doppler-derived mitral deceleration time of early filling in both symptomatic and asymptomatic patients with left ventricular dysfunction J Am Coll Cardiol 1996;28:383-390.[Abstract] 83. Cabin HS, Clubb KS, Hall C, Perlmutter RA, Feinstein AR. Risk for systemic embolization of atrial fibrillation without mitral stenosis Am J Cardiol 1990;65:1112-1116.[CrossRef][Web of Science][Medline] 84. Rossi A, Tomaino M, Golia G, et al. Usefulness of left atrial size in predicting postoperative symptomatic improvement in patients with aortic stenosis Am J Cardiol 2000;86:567-570.[CrossRef][Web of Science][Medline] 85. Reed D, Abbott RD, Smucker ML, Kaul S. Prediction of outcome after mitral valve replacement in patients with symptomatic chronic mitral regurgitation. The importance of left atrial size Circulation 1991;84:23-34.[Abstract/Free Full Text] 86. Laukkanen JA, Kurl S, Eranen J, Huttunen M, Salonen JT. Left atrium size and the risk of cardiovascular death in middle-aged men Arch Intern Med 2005;165:1788-1793.[Abstract/Free Full Text] 87. Sanders P, Morton JB, Kistler PM, Vohra JK, Kalman JM, Sparks PB. Reversal of atrial mechanical dysfunction after cardioversion of atrial fibrillationimplications for the mechanisms of tachycardia-mediated atrial cardiomyopathy. Circulation 2003;108:1976-1984.[Abstract/Free Full Text] 88. Raitt MH, Kusumoto W, Giraud G, McAnulty JH. Reversal of electrical remodeling after cardioversion of persistent atrial fibrillation J Cardiovasc Electrophysiol 2004;15:507-512.[Web of Science][Medline] 89. Hornero F, Rodriguez I, Buendia J, et al. Atrial remodeling after mitral valve surgery in patients with permanent atrial fibrillation J Card Surg 2004;19:376-382.[CrossRef][Web of Science][Medline] 90. Trikas A, Papathanasiou S, Tousoulis D, et al. Left atrial function, cytokines and soluble apoptotic markers in mitral stenosiseffects of valvular replacement. Int J Cardiol 2005;99:111-115.[Medline] 91. Kumagai K, Nakashima H, Urata H, Gondo N, Arakawa K, Saku K. Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation J Am Coll Cardiol 2003;41:2197-2204.[Abstract/Free Full Text] 92. Shinagawa K, Derakhchan K, Nattel S. Pharmacological prevention of atrial tachycardia induced atrial remodeling as a potential therapeutic strategy Pacing Clin Electrophysiol 2003;26:752-764.[CrossRef][Medline] 93. Tsao HM, Wu MH, Huang BH, et al. Morphologic remodeling of pulmonary veins and left atrium after catheter ablation of atrial fibrillationinsight from long-term follow-up of three-dimensional magnetic resonance imaging. J Cardiovasc Electrophysiol 2005;16:7-12.[CrossRef][Web of Science][Medline] 94. Thomas L, Boyd A, Thomas SP, Schiller NB, Ross DL. Atrial structural remodelling and restoration of atrial contraction after linear ablation for atrial fibrillation Eur Heart J 2003;24:1942-1951.[Abstract/Free Full Text] 95. Yalcin F, Aksoy FG, Muderrisoglu H, Sabah I, Garcia MJ, Thomas JD. Treatment of hypertension with perindopril reduces plasma atrial natriuretic peptide levels, left ventricular mass, and improves echocardiographic parameters of diastolic function Clin Cardiol 2000;23:437-441.[Web of Science][Medline] 96. Tsang TS, Barnes ME, Abhayaratna WP, et al. Effects of quinapril on left atrial structural remodeling and arterial stiffness Am J Cardiol 2006;97:916-920.[CrossRef][Web of Science][Medline]
This article has been cited by other articles:
|
|
|
|
 
A. D'Andrea, R. Scarafile, L. Riegler, G. Salerno, R. Gravino, R. Cocchia, F. Castaldo, F. Allocca, G. Limongelli, G. Di Salvo, et al.
Right atrial size and deformation in patients with dilated cardiomyopathy undergoing cardiac resynchronization therapy
Eur J Heart Fail,
December 1, 2009;
11(12):
1169 - 1177.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. A. Marsan, L. F Tops, P. Nihoyannopoulos, E. R Holman, and J. J Bax
Real-time three dimensional echocardiography: current and future clinical applications
Heart,
November 15, 2009;
95(22):
1881 - 1890.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Belohlavek, P. Jiamsripong, A. M. Calleja, E. M. McMahon, C. L. Maarouf, T. A. Kokjohn, T. L. Chaffin, L. J. Vedders, Z. Garami, T. G. Beach, et al.
Patients With Alzheimer Disease Have Altered Transmitral Flow: Echocardiographic Analysis of the Vortex Formation Time
J. Ultrasound Med.,
November 1, 2009;
28(11):
1493 - 1500.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. H. Cuthbertson, B. L. Croal, D. Rae, P. H. Gibson, J. D. McNeilly, R. R. Jeffrey, W. C. Smith, G. J. Prescott, K. G. Buchan, H. El-Shafei, et al.
N-terminal pro-B-type natriuretic peptide levels and early outcome after cardiac surgery: a prospective cohort study
Br. J. Anaesth.,
November 1, 2009;
103(5):
647 - 653.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Aune, M. Baekkevar, J. Roislien, O. Rodevand, and J. E. Otterstad
Normal reference ranges for left and right atrial volume indexes and ejection fractions obtained with real-time three-dimensional echocardiography
Eur J Echocardiogr,
August 1, 2009;
10(6):
738 - 744.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Caso, R. Ancona, G. Di Salvo, S. Comenale Pinto, M. Macrino, V. Di Palma, A. D'Andrea, A.R. Martiniello, S. Severino, and R. Calabro
Atrial reservoir function by strain rate imaging in asymptomatic mitral stenosis: prognostic value at 3 year follow-up
Eur J Echocardiogr,
August 1, 2009;
10(6):
753 - 759.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. S.P. Lam, B. A. Borlaug, G. C. Kane, F. T. Enders, R. J. Rodeheffer, and M. M. Redfield
Age-Associated Increases in Pulmonary Artery Systolic Pressure in the General Population
Circulation,
May 26, 2009;
119(20):
2663 - 2670.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Yoshida, S. Nakao, A. Goda, Y. Naito, M. Matsumoto, M. Otsuka, M. Shimoshikiryo, A. Eguchi, M. Lee-Kawabata, T. Tsujino, et al.
Value of assessment of left atrial volume and diameter in patients with heart failure but with normal left ventricular ejection fraction and mitral flow velocity pattern
Eur J Echocardiogr,
March 1, 2009;
10(2):
278 - 281.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. F. Nagueh, C. P. Appleton, T. C. Gillebert, P. N. Marino, J. K. Oh, O. A. Smiseth, A. D. Waggoner, F. A. Flachskampf, P. A. Pellikka, and A. Evangelisa
Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography
Eur J Echocardiogr,
March 1, 2009;
10(2):
165 - 193.
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. P. Flagg, O. Cazorla, M. S. Remedi, T. E. Haim, M. A. Tones, A. Bahinski, R. E. Numann, A. Kovacs, J. E. Schaffer, C. G. Nichols, et al.
Ca2+-Independent Alterations in Diastolic Sarcomere Length and Relaxation Kinetics in a Mouse Model of Lipotoxic Diabetic Cardiomyopathy
Circ. Res.,
January 2, 2009;
104(1):
95 - 103.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Boccanelli, G. F. Mureddu, G. Cacciatore, F. Clemenza, A. Di Lenarda, A. Gavazzi, M. Porcu, R. Latini, D. Lucci, A. P. Maggioni, et al.
Anti-remodelling effect of canrenone in patients with mild chronic heart failure (AREA IN-CHF study): final results
Eur J Heart Fail,
January 1, 2009;
11(1):
68 - 76.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Jarnert, A. Melcher, K. Caidahl, H. Persson, L. Ryden, and M. J. Eriksson
Left atrial velocity vector imaging for the detection and quantification of left ventricular diastolic function in type 2 diabetes
Eur J Heart Fail,
November 1, 2008;
10(11):
1080 - 1087.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A D'Andrea, G De Corato, R Scarafile, S Romano, L Reigler, C Mita, F Allocca, G Limongelli, G Gigantino, B Liccardo, et al.
Left atrial myocardial function in either physiological or pathological left ventricular hypertrophy: a two-dimensional speckle strain study
Br. J. Sports Med.,
August 1, 2008;
42(8):
696 - 702.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Marui, Y. Saji, T. Nishina, E. Tadamura, S. Kanao, T. Shimamoto, N. Sasahashi, T. Ikeda, and M. Komeda
Impact of left atrial volume reduction concomitant with atrial fibrillation surgery on left atrial geometry and mechanical function.
J. Thorac. Cardiovasc. Surg.,
June 1, 2008;
135(6):
1297 - 1305.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F Antonini-Canterin, C C Beladan, B A Popescu, C Ginghina, A C Popescu, R Piazza, E Leiballi, B Zingone, and G L Nicolosi
Left atrial remodelling early after mitral valve repair for degenerative mitral regurgitation
Heart,
June 1, 2008;
94(6):
759 - 764.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Williams
The Year in Hypertension
J. Am. Coll. Cardiol.,
May 6, 2008;
51(18):
1803 - 1817.
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Watz, B. Waschki, C. Boehme, M. Claussen, T. Meyer, and H. Magnussen
Extrapulmonary Effects of Chronic Obstructive Pulmonary Disease on Physical Activity: A Cross-sectional Study
Am. J. Respir. Crit. Care Med.,
April 1, 2008;
177(7):
743 - 751.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Farzaneh-Far and N. B. Schiller
Left atrial dimension in stress echocardiography.
J. Am. Coll. Cardiol.,
January 29, 2008;
51(4):
514 - 515.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Casaclang-Verzosa, B. J. Gersh, and T. S.M. Tsang
Structural and functional remodeling of the left atrium: clinical and therapeutic implications for atrial fibrillation.
J. Am. Coll. Cardiol.,
January 1, 2008;
51(1):
1 - 11.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. P. Sengupta, V. K. Krishnamoorthy, W. P. Abhayaratna, J. Korinek, M. Belohlavek, T. M. Sundt III, K. Chandrasekaran, F. Mookadam, J. B. Seward, A. J. Tajik, et al.
Disparate patterns of left ventricular mechanics differentiate constrictive pericarditis from restrictive cardiomyopathy.
J. Am. Coll. Cardiol. Img.,
January 1, 2008;
1(1):
29 - 38.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. A. Groh, O. A. Binns, H. G. Burton III, S. W. Ely, and A. M. Johnson
Ultrasonic Cardiac Ablation for Atrial Fibrillation During Concomitant Cardiac Surgery: Long-Term Clinical Outcomes
Ann. Thorac. Surg.,
December 1, 2007;
84(6):
1978 - 1983.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. D'Andrea, P. Caso, S. Romano, R. Scarafile, L. Riegler, G. Salerno, G. Limongelli, G. Di Salvo, P. Calabro, L. Del Viscovo, et al.
Different effects of cardiac resynchronization therapy on left atrial function in patients with either idiopathic or ischaemic dilated cardiomyopathy: a two-dimensional speckle strain study
Eur. Heart J.,
November 2, 2007;
28(22):
2738 - 2748.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. F Tops, E. E van der Wall, M. J Schalij, and J. J Bax
Multi-modality imaging to assess left atrial size, anatomy and function
Heart,
November 1, 2007;
93(11):
1461 - 1470.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Marui, K. Tambara, E. Tadamura, Y. Saji, N. Sasahashi, T. Ikeda, T. Nishina, and M. Komeda
A novel approach to restore atrial function after the maze procedure in patients with an enlarged left atrium
Eur. J. Cardiothorac. Surg.,
August 1, 2007;
32(2):
308 - 312.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Messika-Zeitoun, M. Bellamy, J.-F. Avierinos, J. Breen, C. Eusemann, A. Rossi, T. Behrenbeck, C. Scott, J. A. Tajik, and M. Enriquez-Sarano
Left atrial remodelling in mitral regurgitation--methodologic approach, physiological determinants, and outcome implications: a prospective quantitative Doppler-echocardiographic and electron beam-computed tomographic study
Eur. Heart J.,
July 2, 2007;
28(14):
1773 - 1781.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
LA phasic function and...