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J Am Coll Cardiol, 2002; 40:1425-1430
© 2002 by the American College of Cardiology Foundation
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CLINICAL STUDY: CONGESTIVE HEART FAILURE

Determinants and prognostic value of left atrial volume in patients with dilated cardiomyopathy

Andrea Rossi, MD*,*, Mariantonietta Cicoira, MD*, Luisa Zanolla, MD*, Rita Sandrini, MD*, Giorgio Golia, MD*, Piero Zardini, MD* and Maurice Enriquez-Sarano, MD, FACC{dagger}

* Dipartimento di Scienze Biomediche e Chirurgiche, Sezione di Cardiologia, Universita’ di Verona, Verona, Italy
{dagger} Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota, USA

Manuscript received February 4, 2002; revised manuscript received April 30, 2002, accepted June 7, 2002.

* Reprint requests and correspondence: Dr. Andrea Rossi, Divisione Clinicizzata di Cardiologia, Ospedale Maggiore, P.le Stefani 1, 37126 Verona, Italy.
andrea.rossi{at}univr.it


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: We aimed to investigate the determinants of left atrial (LA) volume and its prognostic value in patients with dilated cardiomyopathy (DCM).

BACKGROUND: Enlargement of the LA is a marker of mortality in the general population. Patients with DCM are characterized by a wide range of LA sizes, but the clinical role of this observation has been played down.

METHODS: A complete echocardiographic Doppler examination was performed in 337 patients (age 60 ± 13 years; 84% male) with the diagnosis of DCM. Left atrial maximal volume (LAmax) was measured at left ventricular (LV) end systole (four-chamber view; area–length method). Left ventricular end-diastolic and end-systolic volumes (LVEDV and LVESV) and ejection fraction (EF) were also measured. Mitral regurgitation (MR) was graded using a 5-point scale. Mitral E-wave (E) and A-wave (A) velocities, as well as their ratio (E/A), were measured off-line.

RESULTS: Determinants of LAmax were: atrial fibrillation (r = 0.34, p < 0.0001), LVEDV (r = 0.46, p < 0.0001), EF (r = 0.40, p < 0.0001), MR (r = 0.39, p < 0.0001), and E/A ratio (r = 0.36, p < 0.0001). During follow-up (41 ± 29 months), 77 patients died and 12 underwent heart transplantation. Univariate Cox analysis showed that LAmax (hazard ratio [HR] 1.01, 95% confidence interval [CI] 1.007–1.013, p < 0.0001), LVESV (HR 1.003, CI 1.001–1.005, p = 0.0003), E/A ratio (HR 1.6, CI 1.3–2.005, p < 0.0001), and MR (HR 1.21, CI 1.03–1.44, p = 0.02) were related to the outcome. On bivariate Cox analysis, LAmax predicted the prognosis independently of each determinant. Patients with a larger LA volume (LAmax/m2 >68.5 ml/m2) had a risk ratio of 3.8 compared with those with a smaller LA volume.

CONCLUSIONS: In patients with DCM, LA volume is associated with LV remodeling, diastolic dysfunction, and the degree of MR. The maximal volume of the LA has an independent and incremental prognostic value, compared with all its determinants.

Abbreviations and Acronyms
  AF
  atrial fibrillation
  CI
  confidence interval
  DCM
  dilated cardiomyopathy
  EF
  ejection fraction
  HR
  hazard ratio
  LA
  left atrium/atrial
  LV
  left ventricle/ventricular
  LVEDV and LVESV
  left ventricular end-diastolic and end-systolic volume, respectively
  MR
  mitral regurgitation
  ROC
  receiver-operating characteristic

In patients with dilated cardiomyopathy (DCM), a wide range of left atrial (LA) sizes has been observed (1,2). The prognostic impact of this observation has recently been analyzed in the Studies Of Left Ventricular Dysfunction (SOLVD) population (3). Patients with a reduced left ventricular (LV) ejection fraction (EF) had an increased risk proportional to the increase in the size of the LA, which was independent of EF, age, or symptomatic status. However, it is unclear whether the prognostic power of the enlarged LA might be the result of LV diastolic dysfunction or the presence of mitral regurgitation (MR) or atrial fibrillation (AF). This is noteworthy because all of these pathophysiologic variables contribute to both enlarging the atrial chamber (4–6) and influencing the prognosis in patients with a reduced EF (1,2,7,8). Although atrial enlargement has long been known to be associated with an increased mortality rate in the general population (9), the pathophysiologic determinants of atrial size have rarely been investigated, particularly in patients with ventricular diseases. It has recently been demonstrated that the size of the LA is better described by volume rather than diameter (10). However, unidimensional measurement is still the method used worldwide to quantify atrial size, so that the potential clinical information provided by atrial volume is largely hidden. The aims of the present study were to analyze the degree of LA remodeling and the pathophysiologic determinants of LA volume in patients with LV systolic dysfunction and to verify the prognostic power of atrial volume in relation to its determinants.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 References
 
Patients were recruited from those routinely referred to the Outpatient Clinic of Verona Hospital with a diagnosis of DCM. Consecutive patients who had a complete echocardiographic Doppler examination in the echocardiographic laboratory of our institution within one month of clinical evaluation (beginning of follow-up) formed the study population. The exclusion criteria were: 1) significant organic mitral or aortic valve disease; 2) the presence of clinical or echocardiographic features of amyloidosis or constrictive pericarditis; and 3) a recent myocardial infarction (<6 months). The duration of the disease was taken to be the number of years of awareness of cardiac impairment.

Twenty-six gender- and age-matched subjects in sinus rhythm, with no history of cardiac disease and with entirely normal echocardiographic findings, who had been referred to the echocardiographic laboratory to rule out pericardial disease or for systolic murmurs, were enrolled as a control group.

Follow-up information was obtained from clinical records, death certificates, and correspondence. The composite end point of follow-up was death or heart transplantation. Patients who died of noncardiac causes were censored at the time of death.

Echocardiography.   Left atrial maximal volume (LAmax) was measured at LV end systole, and LA minimal volume (LAmin) at LV end diastole from the apical four-chamber view (area–length method). Left ventricular end-diastolic and end-systolic volumes (area–length method) and EF were measured off-line from the apical four-chamber view. Mitral E-wave (E) and A-wave (A) velocities, E/A ratio, and E-wave deceleration time (DTE) were also measured off-line. This last variable was measured as the interval (in milliseconds) from peak early mitral filling to an extrapolation of the deceleration to 0 m/s. All measurements were obtained from the mean of 3 beats for patients in sinus rhythm and 5 beats for those with AF. A restrictive mitral inflow pattern was defined as an E/A >2 or between 1 and 2 and DTE <140 ms in patients in sinus rhythm or a DTE <140 ms in patients with AF. Mitral regurgitation was semiquantitatively assessed by color flow Doppler echocardiography. Five regurgitant grades were routinely determined and recorded directly in the study data base (0 = no regurgitation; 1 = mild; 2 = mild to moderate; 3 = moderate; 4 = moderate to severe; 5 = severe).

Statistical analysis
Continuous data are presented as the mean value ± SD. Comparisons of all measurements between normal subjects and patients with DCM were made using the unpaired t test. Determinants of LAmax were evaluated using linear regression analysis. Multivariate analysis was used to identify the independent relationship between each variable and LA volume. Ejection fraction was not used in the multivariate model, so as to avoid multi-collinearity, because it is both statistically and pathophysiologically related to left ventricular end-diastolic and end-systolic volume (LVEDV and LVESV). The E-wave DT and velocity were also not used in the model because of their strong relation to the E/A ratio. The relation of specific variables to mortality was investigated univariately using the Cox proportional hazards model. To assess the independence of the predictive value of LAmax from that of its determinants, bivariate models were used.

The prognostic power of LA parameters (LAmax, LAmax/m2, LAmin, LAmin/m2) significantly related to the outcome was compared using the log-likelihood ratio test.

Receiving-operator characteristics (ROC) curves were constructed to compare different predictive values at particular time points. Differences between curves were assessed with the z-statistic. The best prognostic cut-off value for survival status, defined as that which gave the highest product of sensitivity and specificity, was used to dichotomize patients for Kaplan-Meier survival analysis. To perform these analyses, two different statistical programs were employed: Statview 5.0 (Abacus Concepts, SAS Institute, Cary, North Carolina) and MedCalc 5.0 (Mariakerke, Belgium). A p value <0.05 was considered statistically significant.


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
A total of 337 patients (294 men and 43 women; age 60 ± 13 years) formed the study population. Table 1 shows the clinical and echocardiographic characteristics of the patients. The etiology of their cardiomyopathy was idiopathic in 25% and ischemic in the remaining 75%.


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  		Table 1 Clinical and Echocardiographic Characteristics of 337 Patients With Dilated Cardiomyopathy

 
Left atrial remodeling and determinants of LA volume.   Patients with DCM showed a larger LAmax (131 ± [SD] 65 ml, SEM 4.1; range 25 to 481) compared with normal control subjects (59 ± [SD] 19 ml, SEM 3.8; p < 0.0001); however, a wide range was observed. The frequency of LA remodeling was high: 75% of patients with DCM had a LAmax higher (by >1 SD of the mean value) than that of control subjects. In contrast, no differences in the E-wave velocity (0.61 ± [SD] 0.2, SEM 0.015 vs. 0.64 ± [SD] 0.2, SEM 0.04; p = 0.6), A-wave velocity (0.59 ± [SD] 0.3, SEM 0.015 vs. 0.67 ± [SD] 0.2, SEM 0.039; p = 0.08), E/A ratio (1.19 ± [SD] 0.9, SEM 0.060 vs. 0.98 ± [SD] 0.3, SEM 0.058; p = 0.2), or DTE (200 ± [SD] 75, SEM 4.86 vs. 215 ± [SD] 47, SEM 9.4; p = 0.3) were observed between patients and control subjects. The determinants of LA volume were defined by means of linear regression analysis (Table 2).


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  		Table 2 Echocardiographic Determinants of Left Atrial Maximal Volume in the Study Population (Univariate Analysis)

 
The LAmax increased with LV enlargement, increasing severity of MR, degree of diastolic dysfunction, and presence of AF. Multivariate analysis showed that LAmax was independently related to age and the degree of MR and more strongly related to the LVEDV and E/A ratio (Table 3).


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  		Table 3 Echocardiographic Determinants of Left Atrial Maximal Volume in the Study Population (Multivariate Analysis)

 
In 102 patients for whom the duration of the disease was available, LAmax normalized by body surface area (LAmax/m2) showed a positive relation to the duration of the disease (p = 0.007), independently of age (p = 0.0005), in a multivariate model.

Survival analysis
During follow-up (median 41 ± 29 months), 77 patients died and 12 underwent heart transplantation. Five patients died of noncardiac causes and, accordingly their follow-up, were censored at the time of death. Cox univariate analysis showed several clinical and echocardiographic markers of prognosis in our population (Table 4). The maximal volume of the LA was a strong predictor of mortality (hazard ratio [HR] 1.01, 95% confidence interval [CI] 1.007 to 1.013; p < 0.0001). However, most of the variables identified as determinants of LAmax—namely, ventricular volumes, MR, and markers of diastolic function—showed clinically important predictive power, as well.


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  		Table 4 Predictors of Death in the Study Population (Cox Univariate Analysis)

 
Bivariate Cox models were subsequently used to assess the independence of the prognostic value of LAmax from that of each of its determinants (Table 5). Bivariate analysis was preferred to avoid multi-collinearity, because most of the determinants of LAmax are strongly related to each other.


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  		Table 5 Predictors of Death in the Study Population (Cox Bivariate Models)

 
Although the presence of AF did not influence the prognosis in our population, we performed a subgroup analysis of patients with chronic AF. This group consisted of 39 patients (mean age 63 ± 8 years, mean EF 26 ± 9%) who were followed up for 51 ± 29 months; 14 patients died. In this group, LAmax maintained its predictive power (HR 1.01, CI 1.003 to 1.018; p = 0.008), but EF did not have any impact on the prognosis. Likewise, the predictive value of LAmax was confirmed in patients without MR (grade <1) (HR 1.01, CI 1.006 to 1.017; p < 0.0001) and with MR (HR 1.008, CI 1.004 to 1.013; p = 0.0008).

When the overall population was classified into two groups according to the presence or absence of a restrictive mitral filling pattern, LAmax significantly predicted the outcome in both groups (HR 1.006, CI 1.001 to 1.012, p = 0.03 and HR 1.01, CI 1.005 to 1.017, p = 0.0003, respectively).

The log-likelihood ratio test showed that LAmax/m2 was a more powerful predictor of survival than LAmax (p < 0.0001), LAmin (p < 0.0001), and LAmin/m2 (p = 0.02).

The best cut-off value for LAmax/m2 in the overall population, regardless of the duration of follow-up, was calculated using ROC analysis. The value of 68.5 ml/m2 predicted survival with 65% sensitivity (95% CI 55.8 to 73.9) and 76% specificity (CI 65.6 to 88.4). Patients with a higher LAmax/m2 value had a 3.8 times higher risk of an adverse outcome than patients with a smaller LA. The ROC area under the curve (AUC) for LAmax/m2, as a continuous variable, was higher than that for LVESV/m2 over the whole follow-up period, reaching statistical significance at 12 months (p = 0.009) (Fig. 1).



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  		Figure 1 The receiver-operating characteristic (ROC) areas under the curve (AUC) of left atrial maximal volume/m2 (line with triangles) and left ventricular end-systolic volume/m2 (line with squares) of patients with dilated cardiomyopathy for prediction of death at 12 to 72 months.

 
Kaplan-Meier curves were constructed using a cut-off value for LAmax/m2 of 68.5 ml/m2. Survival analysis was performed for the subgroup of patients with particularly severe systolic dysfunction (EF <30%). The presence of a large LA volume predicted a worse outcome, compared with patients with a smaller LA (Fig. 2).



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  		Figure 2 Kaplan-Meier survival curves of a subgroup of patients with severe systolic dysfunction (ejection fraction <30%), taken from the overall study population and classified into two groups according to the best cut-off value of left atrial maximal volume (LAmax)/m2 (68.5 ml/m2), as obtained from the receiver-operating characteristic curves (see text for details).

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The present study showed that LA remodeling is frequent, in patients with DCM. Left atrial volume is mainly determined by the degree of LV dilation, diastolic dysfunction, and the extent of MR. On survival analysis, LA volume is found to be a powerful prognostic marker, adding important clinical information, independent of any of its determinants.

In patients with chronic heart failure due to DCM, diastolic dysfunction is an important hallmark of the severity of the disease. The degree of diastolic impairment correlates with symptoms and prognosis more closely than does EF (1,2,11–13). However, the predictive power of diastolic markers has been frequently but not uniformly confirmed (14). This is probably due to the strong load dependency of mitral parameters, which can dramatically change after blood volume depletion (15). It has been shown that the predictive power of mitral inflow can be enhanced when analyzed in relation to loading modification (16). The role of LA size as a diastolic marker is well known (17–19), and, accordingly, we found a strong relation between atrial volume and diastolic markers. Interestingly, the predictive value of atrial volume is stronger and independent of echocardiographic Doppler diastolic parameters. This might be related to a lower load dependency due to increased fibrosis and reduced elastic recoil in a chronically enlarged atrium (20–22). Furthermore, LA size has been shown to reflect prognosis in patients who have cardiac disease with prevalent diastolic function, such as aortic stenosis and restrictive cardiomyopathy (23–25).

Functional MR is a major confounding factor in the hemodynamic of patients with LV systolic dysfunction (26,27). Mitral regurgitant volume is a key determinant of atrial volume (5), which may reflect the severity, duration, and prognosis of MR (28). However, in our study, the predictive role of LA volume proved to be more powerful than MR, independent of the degree of MR, and it was confirmed in both the group of patients with and the group without MR.

The relationship between atrial dilation, AF, and LV dysfunction is intriguing, and it may contribute to overshadowing of the predictive power of atrial size. However, in our study, AF had no prognostic power, and, more interestingly, the predictive value of LA volume was confirmed in the subgroup of patients with AF.

In our opinion, LA enlargement represents a strong predictive marker, because the atrial chamber is a window allowing comprehensive evaluation of several factors associated with a bad prognosis, which are often difficult to document separately. Atrial size might also reflect marked hemodynamic atrial overload in specific phases during the course of chronic heart disease, such as during exercise, giving evidence of temporal hemodynamic impairment (MR or diastolic dysfunction) which otherwise would remain silent (29). An appealing suggestion is that LA volume stores information on the history of the disease (30), highlighting its duration (31). Accordingly, in our study, LA volume correlated weakly but significantly with the duration of the disease.

These observations might help to explain the difference in AUCs between atrial and ventricular volumes in short-term follow-up (12 months). The low predictive value of LVESV/m2 at this time point might depend on improvement of LV function, which, in some cases, occurs spontaneously (32) or after pharmacologic or surgical therapy in the early phase of the disease. The excellent prognosis associated with ventricular recovery (32) might confound the predictive power of the dysfunctional ventricle at baseline.

It is possible that in patients with DCM, atrial enlargement could also be due to concomitant atrial myopathic disease (33) caused by a more widespread primary pathologic process. Finally, the prognostic role of LA size might be partly related to natriuretic peptide levels (e.g., atrial natriuretic peptide) (34), which have been demonstrated to have diagnostic (35) and prognostic power (36) in patients with LV systolic dysfunction.

Others studies have included LA size in the survival analysis. In particular, two studies (1,2) showed that LA size predicted the outcome independent of the restrictive mitral pattern, New York Heart Association functional class and EF, but they confirmed that the restrictive pattern had a higher predictive power than did atrial size. A possible explanation might be the difference between their patient cohorts and ours. Both studies analyzed populations of patients with very severe diastolic dysfunction, with a prevalence of a restrictive pattern of 42% and 46%, respectively. The narrow range of these pathophysiologic variables raises the question as to whether those cohorts can adequately represent the whole spectrum of the disease. In contrast, our population was characterized by a wider range of systolic dysfunction, and only a 22% prevalence rate of a restrictive pattern, indicating a less severe disease state.

Furthermore, in the study by Pinamonti et al. (2), the overall population had a relatively young mean age (39 ± 15 years). This casts doubt on the accuracy of mitral parameters in describing restrictive physiology, because of the strong age dependence of the mitral pattern.


   Footnotes
 
Dr. Cicoira was supported by a grant from the Italian Society of Cardiology for Cardiovascular Research. Dr. Enriquez-Sarano was supported in part by Grant HL-64928 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

  1. 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]
  2. Pinamonti B, Di Lenarda A, Sinagra G, Camerini F. Restrictive ventricular filling pattern in dilated cardiomyopathy assessed by Doppler echocardiography: clinical, echocardiographic and hemodynamic correlation and prognostic implication. J Am Coll Cardiol. 1993;22:808–815[Abstract]
  3. SOLVD InvestigatorsQuinones MA, Greenberg BH, Kopelen HA, et al. Echocardiographic predictors of clinical outcome in patients with left ventricular dysfunction enrolled in the SOLVD registry and trials: significance of left ventricular hypertrophy. J Am Coll Cardiol. 2000;35:1237–1244[Abstract/Free Full Text]
  4. Appleton CP, Galloway JM, Gonzales MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressure 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]
  5. Rossi A, Golia G, Gasparini G, Prioli MA, Anselmi M, Zardini P. Left atrial filling volume can be used to reliably estimate the regurgitant volume in mitral regurgitation. J Am Coll Cardiol. 1999;33:212–217[Abstract/Free Full Text]
  6. Sanfilippo AJ, Abascal VM, Sheehan M, et al. Atrial enlargement as a consequence of atrial fibrillation: a prospective echocardiographic study. Circulation. 1990;82:792–797[Abstract/Free Full Text]
  7. Blondheim DS, Jacobs LE, Kotler MN, Costacurta GA, Parry WR. Dilated cardiomyopathy with mitral regurgitation: decreased survival despite a low frequency of ventricular thrombus. Am Heart J. 1991;122:763–771[CrossRef][Medline]
  8. V-HeFT VA Cooperative Studies GroupCarson PE, Johnson GR, Dunkman WB, Fletcher RD, Farell L, Cohn JN. The influence of atrial fibrillation on prognosis: the influence of atrial fibrillation on prognosis in mild to moderate heart failure: the V-HeFT studies. Circulation. 1993;87(Suppl VI):VI102–110
  9. 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]
  10. 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][Medline]
  11. Grossman W, McLaurin LP, Rolett EL. Alteration in left ventricular relaxation and diastolic compliance in congestive cardiomyopathy. Cardiovasc Res. 1979;13:514–522[Medline]
  12. Packer M. Abnormalities of diastolic function as a potential cause of exercise intolerance in chronic heart failure. Circulation. 1990;81(Suppl III):III78–86
  13. Xie GY, Berk MR, Smith M, Gurley JC, DeMaria A. Prognostic value of Doppler transmitral flow patterns in patients with congestive heart failure. J Am Coll Cardiol. 1994;24:132–139[Abstract]
  14. Rihal CS, Nishimura RA, Hatle LK, Bailey KR, Tajik AJ. Systolic and diastolic dysfunction in patients with clinical diagnosis of dilated cardiomyopathy: relation to symptoms and prognosis. Circulation. 1994;90:2772–2779[Abstract/Free Full Text]
  15. Hurrel PG, Nishimura RA, Ilstrup DM, Appleton CP. Utility of preload alteration in assessment of left ventricular filling pressure by Doppler echocardiography: a simultaneous catheterization and Doppler echocardiographic study. J Am Coll Cardiol. 1997;30:459–467[Abstract]
  16. Pozzoli M, Traversi E, Cioffi G, Stenner R, Sanarico M, Tavazzi L. Loading manipulations improves the prognostic value of Doppler evaluation of mitral flow in patients with chronic heart failure. Circulation. 1997;95:1222–1230[Abstract/Free Full Text]
  17. Simek LC, Feldman MD, Haber HL, Wu CC, Jayaweera AR, Kaul S. Relationship between left ventricular wall thickness and left atrial size: comparison with other measures of diastolic function. J Am Soc Echocardiogr. 1995;8:37–47[CrossRef][Medline]
  18. Appleton CP, Galloway JM, Gonzales MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressure 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]
  19. Matsuda M, Matsuda Y. Mechanism of left atrial enlargement related to ventricular diastolic impairment in hypertension. Clin Cardiol. 1996;19:954–959[Medline]
  20. Pepi M, Marenzi GC, Agostoni PG, et al. Sustained cardiac diastolic changes elicited by ultrafiltration in patients with moderate congestive heart failure: pathophysiological correlates. Br Heart J. 1993;70:135–140[Abstract/Free Full Text]
  21. Hoit BD, Shao Y, Liang-Miin T, Patel R, Gabel M, Walsh RA. Altered left atrial compliance after atrial appendectomy: influence of atrial and ventricular filling. Circ Res. 1993;72:167–175[Abstract/Free Full Text]
  22. Kihara Y, Sasayama S, Miyazaki S. Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs. Circ Res. 1988;62:543–553[Abstract/Free Full Text]
  23. 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][Medline]
  24. Rossi A, Tomaino M, Golia G, Anselmi M, Fucá G, Zardini P. Echocardiographic prediction of clinical outcome in medically treated patients with aortic stenosis. Am Heart J. 2000;140:766–771[CrossRef][Medline]
  25. Ammash NM, Seward JB, Bailey KR, Edwards WD, Tajik AJ. Clinical profile and outcome of idiopathic restrictive cardiomyopathy. Circulation. 2000;101:2490–2496[Abstract/Free Full Text]
  26. Enriquez-Sarano M, Rossi A, Seward JB, Tajik AJ. Determinants of pulmonary hypertension in left ventricular dysfunction. J Am Coll Cardiol. 1997;29:153–159[Abstract]
  27. Rossi A, Cicoira M, Golia G, Anselmi M, Zardini P. Mitral regurgitation and left ventricular diastolic dysfunction similarly affect mitral and pulmonary vein flow Doppler parameters: the advantage of end-diastolic markers. J Am Soc Echocardiogr. 2001;14:562–568[CrossRef][Medline]
  28. Reed D, Abbott RD, Smucker MI, 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]
  29. Stoddart MF, Prince CR, Dillon S, Longaker RA, Morris GT, Liddell NE. Exercise-induced mitral regurgitation is a predictor of morbid events in subjects with mitral valve prolapse. J Am Coll Cardiol. 1995;25:693–699[Abstract]
  30. Hoit BD, Shao Y, Liang-Miin T, Patel R, Gabel M, Walsh RA. Altered left atrial compliance after atrial appendectomy: influence of atrial and ventricular filling. Circ Res. 1993;72:167–175[Abstract/Free Full Text]
  31. Pizzarello RA, Turnier J, Padmanabhan TV, Goldman MA, Tortolani AJ. Left atrial size, pressure and V wave height in patients with isolated, severe, pure mitral regurgitation. Cathet Cardiovasc Diagn. 1984;62:543–553
  32. Cicoira M, Zanolla L, Latina L, et al. Frequency, prognosis and predictors of improvement of systolic left ventricular function in patients with "classic" clinical diagnosis of idiopathic dilated cardiomyopathy. Eur J Heart Fail. 2001;3:323–330[CrossRef][Medline]
  33. Triposkiadis F, Pitsavos C, Boudoulas H, Trikas A, Toutouzas P. Left atrial myopathy in idiopathic dilated cardiomyopathy. Am Heart J. 1994;128:308–315[CrossRef][Medline]
  34. Rossi A, Enriquez-Sarano M, Burnett JC, Lerman A, Abel MD, Seward JB. Natriuretic peptide levels in atrial fibrillation: a prospective hormonal and Doppler-echocardiography study. J Am Coll Cardiol. 2000;35:1256–1262[Abstract/Free Full Text]
  35. Lerman A, Gibbons RJ, Rodeheffer RJ, et al. Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left ventricular dysfunction. Lancet. 1993;341:1105–1109[CrossRef][Medline]
  36. Hall C, Rouleau JL, Moye L, et al. N-terminal proatrial natriuretic factor: an independent predictor of long-term prognosis after myocardial infarction. Circulation. 1994;89:1934–1942[Abstract/Free Full Text]



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W. P. Abhayaratna, J. B. Seward, C. P. Appleton, P. S. Douglas, J. K. Oh, A. J. Tajik, and T. S.M. Tsang
Left Atrial Size: Physiologic Determinants and Clinical Applications
J. Am. Coll. Cardiol., June 20, 2006; 47(12): 2357 - 2363.
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T. S.M. Tsang, W. P. Abhayaratna, M. E. Barnes, Y. Miyasaka, B. J. Gersh, K. R. Bailey, S. S. Cha, and J. B. Seward
Prediction of Cardiovascular Outcomes With Left Atrial Size: Is Volume Superior to Area or Diameter?
J. Am. Coll. Cardiol., March 7, 2006; 47(5): 1018 - 1023.
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 Eur Heart JHome page
M. Osranek, F. Bursi, K. R. Bailey, B. R. Grossardt, R. D. Brown Jr, S. L. Kopecky, T. S. Tsang, and J. B. Seward
Left atrial volume predicts cardiovascular events in patients originally diagnosed with lone atrial fibrillation: three-decade follow-up
Eur. Heart J., December 1, 2005; 26(23): 2556 - 2561.
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A. Bollmann
First comes diagnosis then comes treatment: an underappreciated paradigm in atrial fibrillation management
Eur. Heart J., December 1, 2005; 26(23): 2487 - 2489.
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 CirculationHome page
S. J. Kernis, V. T. Nkomo, D. Messika-Zeitoun, B. J. Gersh, T. M. Sundt III, K. V. Ballman, C. G. Scott, H. V. Schaff, and M. Enriquez-Sarano
Atrial Fibrillation After Surgical Correction of Mitral Regurgitation in Sinus Rhythm: Incidence, Outcome, and Determinants
Circulation, October 19, 2004; 110(16): 2320 - 2325.
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P. de Groote, J. Dagorn, B. Soudan, N. Lamblin, E. McFadden, and C. Bauters
B-type natriuretic peptide and peak exercise oxygen consumption provide independent information for risk stratification in patients with stable congestive heart failure
J. Am. Coll. Cardiol., May 5, 2004; 43(9): 1584 - 1589.
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A. Khan, G. W. Moe, N. Nili, E. Rezaei, M. Eskandarian, J. Butany, and B. H. Strauss
The cardiac atria are chambers of active remodeling and dynamic collagen turnover during evolving heart failure
J. Am. Coll. Cardiol., January 7, 2004; 43(1): 68 - 76.
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