|Year : 2019 | Volume
| Issue : 4 | Page : 186-192
A clinical study of prognostic significance of left atrial volume index in patients with acute coronary syndrome
Praveen Nagula, Subba Reddy Venkata Yerrabandi, Adikesava Naidu Otikunta, Suneetha Karumuri
Department of Cardiology, Osmania Medical College/General Hospital, Hyderabad, Telangana, India
|Date of Web Publication||11-Mar-2020|
Dr. Praveen Nagula
Osmania Medical College/General Hospital, Afzal Gunj, Hyderabad - 500 012, Telangana
Source of Support: None, Conflict of Interest: None
Background: The aim of the study is to determine the relationship of left atrial volume index (LAVI) with the clinical presentation, comorbidities, and adverse events in acute coronary syndrome (ACS) patients at admission and during their follow-up. Methods: A total of 160 ACS patients enrolled have been divided into Group A (LAVI > 34 ml/m2) and Group B ( LAVI ≤ 34 ml/m2). The symptoms and the LAVI have been assessed at 1, 6, and 12 months of follow-up. The primary end point was cardiovascular (CV) mortality. The secondary end point is the occurrence of major adverse CV events, i.e., repeat hospitalization postdischarge for heart failure, reinfarction, atrial fibrillation, or ischemic stroke. Results: Overall, the median age at presentation was 55 years. There was no sex predilection for increased LAVI or an association with conventional risk factors. The echocardiographic E wave velocity divided by propagation velocity had a positive correlation with the LAVI (r = 0.321, P = 0.0036). The relative risk of morbidity with an increased LAVI was 2.74. The hazard ratio for adverse events in patients with increased LAVI was 2.81. The total number of deaths was 21 (16 and 5 in Group A and B). The LAVI was found to be the independent predictor of mortality than left ventricular ejection fraction on multivariate regression analysis. The receiver operating characteristic curve analysis had an area under the curve of 0.801 for increased LAVI. Conclusion: The LAVI is an independent predictor of adverse events and mortality during the initial hospital stay and at follow-up in ACS patients.
Keywords: Acute coronary syndrome, Gensini score, left atrial volume index, left ventricular ejection fraction
|How to cite this article:|
Nagula P, Venkata Yerrabandi SR, Otikunta AN, Karumuri S. A clinical study of prognostic significance of left atrial volume index in patients with acute coronary syndrome. J Indian coll cardiol 2019;9:186-92
|How to cite this URL:|
Nagula P, Venkata Yerrabandi SR, Otikunta AN, Karumuri S. A clinical study of prognostic significance of left atrial volume index in patients with acute coronary syndrome. J Indian coll cardiol [serial online] 2019 [cited 2020 Apr 6];9:186-92. Available from: http://www.joicc.org/text.asp?2019/9/4/186/280347
| Introduction|| |
Atherosclerotic cardiovascular disease (ASCVD), a chronic inflammatory disorder, is often asymptomatic and has a slow progression during the lifetime of an individual. It can manifest as coronary heart disease (CHD), stroke, peripheral artery disease, and aortic aneurysm. The CHD is the most common form of heart disease encountered in the adults, accounting for 50% of the ASCVD.,
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those of ST-segment elevation myocardial infarction (STEMI) to presentation in non-STEMI (NSTEMI) or unstable angina (UA). It is one of the major causes of cardiovascular (CV) mortality in the world, both in developing and developed countries. The role of echocardiography includes diagnosing, detecting the complications, and assessing the prognosis of this cardiac disorder.
The left ventricular (LV) function is an important prognostic marker for patients with ACS. The left atrial volume (LAV) is a robust predictor of the CV outcomes and has upcoming evidence supporting its role.
The present study intends to determine the relationship of the LA volume index (LAVI) in the patients with ACS at admission with the clinical presentation and the comorbidities. The relationship of increased LAVI with the occurrence of the adverse events during the hospital stay and at follow-up, thereby its role as a prognostic marker, is also evaluated.
| Methods|| |
It is a prospective cohort study. The ethical committee clearance has been obtained before the initiation of the study. The study duration is from January 2014 to December 2015 (24 months) including the follow-up period at the Department of Cardiology, Osmania General Hospital, Hyderabad. All the patients were included after a detailed informed consent (either signed or right thumb impression). A cutoff of LAVI ≤ 34ml/m2 was considered as normal as per the 2015 American Society of Echocardiography Chamber Quantification guidelines.
Patients with age >18 years and with a diagnosis of ACS at admission and not having any of the exclusion criteria were included in the study.
Patients with chronic stable angina (angina being present on exertion and relieved by rest or sublingual nitroglycerine), with a previous history of percutaneous transluminal coronary angioplasty or coronary bypass grafting, with a diagnosis of significant valvular heart disease (i.e., moderate mitral stenosis, mitral regurgitation, aortic stenosis with aortic jet velocity of >2.5 m/s, aortic regurgitation) irrespective of the etiology, with chronic kidney disease (eGFR <60 ml/m2), with a previous diagnosis of cardiomyopathy, with chronic atrial fibrillation, cor pulmonale, malignancy, and anemia (hemoglobin <12 g/dl in males and <11 g/dl in females) were excluded from the study.
The primary end point was CV death. The secondary endpoint is the occurrence of major adverse CV events (MACEs), i.e., repeat hospitalization for heart failure (HF), in-stent restenosis, reinfarction, target vessel revascularization, repeat revascularization, atrial fibrillation, or ischemic stroke.
A total of 160 consecutive ACS (after analysis of 565 patients with a diagnosis of chest pain seen at the outpatient department) who satisfied the inclusion criteria were enrolled in the study and followed up for 1 year from the date of enrollment. Each patient who has fulfilled the inclusion criteria was analyzed clinically in detail. The baseline electrocardiogram (ECG) was taken in each patient, and if thrombolysis has been done, another ECG was taken postthrombolysis. The anthropometry (height, weight, body mass index, and body surface area) and the biochemical parameters (hemoglobin, total leukocyte count, differential cell count, blood urea, serum creatinine, random blood sugar, serum electrolytes, lipid profile, blood grouping, and viral markers) were analyzed at the time of admission.
The ACS is a term encompassing the diagnosis of UA, NSTEMI, and STEMI. The patients without persistent >20 min ST-segment elevation in two or more contiguous leads but with the biomarker evidence of myocardial necrosis are classified as having NSTEMI, whereas in the patients without such evidence of myocardial necrosis, UA is diagnosed a condition generally carrying a better prognosis. Patients satisfying the criteria of III universal definition of STEMI were categorized as having STEMI.,
Each patient was assessed clinically and echocardiographically at 1, 6, and 12 months. The echo parameters were compared with the initial values and correlated with the newly diagnosed comorbidities or clinical features.
Assessment by echocardiography
The two-dimensional echocardiography was done with PHILIPS iE33 (Philips Medical Systems, Andover, MA, USA) within 48 h of admission, and the patient was assigned to Group A or Group B based on the LAVI value attained: those with LAVI > 34 ml/m2 as Group A and those with LAVI ≤ 34 ml/m2 as Group B. The patients underwent echocardiography done by a cardiologist who is blinded to the study protocol.
The LV systolic function was assessed by Simpson's disc volumetric method. The presence of regional wall motion abnormality (RWMA) if any was noted concerning the arterial territory involved and was graded as being hypokinetic, akinetic, and dyskinetic visually. The diastolic function parameters were assessed simultaneously and were correlated with the LAVI.
The mitral inflow was assessed with pulsed-wave Doppler echocardiography from the apical 4-chamber view. The Doppler beam was aligned parallel to the direction of flow, and a 1–2-mm sample volume was placed between the tips of mitral leaflets during diastole. From the mitral inflow profile, the E- and A-wave velocity, E–deceleration time, and E/A velocity ratio were measured. The tissue Doppler imaging (TDI) of the mitral annulus was also obtained, and e' and a' velocities were noted.
The diastolic function was categorized as normal (grade 0), impaired relaxation (grade 1), pseudonormalization (grade 2), or restrictive filling (grade 3) by the combination of transmitral and pulmonary flow patterns. The E–deceleration time of >140 and <240 ms was regarded as normal, ≥240 ms as abnormally prolonged, and ≤140 ms as abnormally abbreviated.
The LAV was assessed by the biplane area-length method from apical 4-chamber and 2-chamber views. The measurements were obtained as per the ACC/AHA Recommendations of Chamber Quantification 2009/2015., The mitral regurgitation was quantified by the color Doppler imaging.
Each patient underwent coronary angiography either by radial or femoral route as per the discretion of the treating cardiologist. The lesion on angiography was quantified after viewing in two orthogonal views of the eight proximal segments as needed for the modified Gensini score (MGS). Each lesion is quantified based on the diameter of the vessel, if <50% - 1, 50%–75% - 2, 76%–99% - 3, and 100% occlusion as 4. The minimum score is 4 and the maximum score is 32. After the score, the lesion severity is graded as mild with MGS of 1–6, moderate as 7–13, and severe as >13 [Supplementary Data].,
The statistical analysis was done with SPSS statistics for Windows Version 17.0 (SPSS Inc; Chicago, Illinois, USA). Continuous variables were expressed as Mean ± SD standard deviation unless otherwise specified and the categorical variables as percentages. The Student's t-test was used for comparison of two means and Chi-square test was used for the categorical variables. A P< 0.05 was considered statistically significant. The correlation coefficient (Karl Pearson r) was done for the correlation of the LAVI with the comorbidities and the diastolic function parameters. The receiver operating characteristic (ROC) curve analysis has been done for assessing the specificity and sensitivity of the LAVI in ACS patients. Univariate and multivariate regression analysis was done for assessing the independent predictors of coronary artery disease (CAD). The Kaplan–Meier survival curve analysis and Cox regression survival analysis were done for both groups.
| Results|| |
Demographic data of study population
The total number of cases in the study was 160 (Both groups). The median age at presentation in the whole cohort was 55 years. Most common age group was 51–60 years (37%). The age range was from 31 to 80 years. On comparison of two groups, there was no significant difference in the mean age (55 vs. 54.5; P = 0.5). Males were predominant in both groups. The mean LAVI in patients with age ≤40 years in Group A was 36.27 ± 8.73 ml/m2 (n = 10) whereas that of patients with age ≥65 years was 36.89 ± 6.55 (n = 13). The difference was statistically insignificant (P = 0.38). The Chi-square test analysis of sex distribution in both Groups A and B with LAVI was statistically insignificant (χ2 = 0.0072, P = 0.321).
Baseline characteristics of both groups with regard to the risk factors, type of ACS at presentation, and whether they have been thrombolysed or not have been assessed [Table 1], [Figure 1]. There were more hypertensives (61 vs. 45) and diabetics (47 vs. 40) in Group A compared to Group B. They were frequent smokers, were alcoholics, and had more frequently a family history of CAD in Group A. The severity of lesions on coronary angiography as assessed by MGS did not show the significant difference between both the groups (12 vs. 11.5; P = 0.57).
The most common ACS was anterior wall STEMI seen in 43 patients of Group A and in 29 patients of Group B. Overall, 40 patients in Group A and 29 patients in Group B underwent thrombolysis. The most common thrombolytic agent used was streptokinase followed by tenecteplase in both the groups. Patients enrolled in the study were thrombolysed and underwent coronary angiography and stenting if required (pharmacoinvasive strategy). None of the patients underwent primary percutaneous coronary intervention (PCI).
The mean mitral inflow early wave (E) divided by early wave assessed by TDI, i.e., E/e', was more in Group A compared to Group B (14.7 ± 3.1 vs. 13.0 ± 2.7) but did not reach statistical significance (P = 0.054). The mean E wave velocity divided by propagation velocity (E/PV) was more in Group A compared to Group B (2.9 ± 1.0 vs. 2.4 ± 1.0, P = 0.0114). There was a statistical difference in the LV ejection fraction (LVEF) in Group A compared to Group B as assessed by Simpson's method; it was lower in Group A compared to Group B (38.6 ± 10.1 vs. 45.9 ± 10.7, P = 0.0014). The LVEF was considerably lower in the patients with increased LAVI compared to the normal LAVI, indicating increased filling pressures and more burden on the failing LV. The overall LVEF was of moderate LV dysfunction in Group A compared to Group B where the LV dysfunction was mild.
The diastolic dysfunction was more in Group A patients compared to Group B patients across the spectrum from Grade I to Grade III but did not attain a statistical significance (P = 0.45 overall), thereby ruling out the confounding factor of increased diastolic dysfunction favoring increased LAVI. Mild mitral regurgitation as assessed by color flow Doppler was more in Group A patients compared to Group B patients (14 vs. 06, P = 0.07). Moderate mitral regurgitation was seen in TWO patients of Group A but none in Group B [Table 2].
The LAVI had no correlation with E/e' as assessed by Pearson correlation method (r = 0.163, P = 0.090), had positive correlation with E/PV (r = 0.321, P = 0.0036), and had negative correlation with LVEF (r = −0.29, P = 0.0005) and PV (r = −0.24, P = 0.0097), respectively.
Assessment of events during hospital stay
Atrial fibrillation was noticed during the initial hospital stay in six patients in Group A and one patient of Group B. Killip class ≥II was noted in 30 patients with LAVI >34 ml/m2 and seven patients with normal LAVI. No events were noticed in 44 patients in Group B compared to 24 patients in Group A. Atrial infarction was seen in eight patients; five in Group A and three in Group B [Table 3].
Follow up of the patients
The echocardiographic parameter LAVI at follow-up of 1 month and 6 months and 12 months between two groups are shown in [Table 4]. The number of patients who completed the 12 months of follow-up period and who died during the study was included in the analysis. The number of patients in Group A was 70 and in Group B was 56 patients. Sixteen patients died in Group A compared to five patients in Group B [Table 5]. All the MACE events were more in Group A compared to Group B but did not reach statistically significant value on individual Chi-square test analysis. The stroke was seen in two patients of Group A. Patients with normal LAVI were more asymptomatic compared to patients with increased LAVI at the end of 12 months of follow-up (26 [72.7%] vs. 23 [29.0%], χ2 = 22.138; P < 0.00001).
|Table 4: Comparison of left atrial volume index between two groups during follow.up at 1 month, 6 months, and 12 months|
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Overall MACEs when combined were statistically significant between two groups on Chi-square test analysis (5 × 5 contingency table) (32 patients of Group A vs. 7 patients of Group B, P < 0.00001). Repeat hospitalization was more in Group A compared to Group B (32 vs 7, P = 0.00073) [Table 5]. Repeat hospitalization for HF seen in 21 patients of Group A compared to 4 patients in Group B (P = 0.03).
Of the 12 patients who died, when stratified across the quartiles of LAVI as shown in [Figure 2], it is seen that the mortality increased along with the quartiles specified with more number of deaths, i.e., 3 noted in >50 ml/m2.
|Figure 2: Mortality along the quartiles of increased left atrial volume index|
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On univariate analysis of the parameters [Table 6], LAVI by area length (AL) method and MGS were found to be the predictors of mortality in the CAD patients. A P< 0.20 was considered for inclusion in the multivariable Cox regression model to evaluate the parameters with the independent predictor of mortality. On multivariate analysis by Cox regression model, LAVI AL (P = 0.005) and MGS (P = 0.006) were found to be independent predictors of mortality compared to LVEF (P = 0.347) [Table 7].
|Table 6: Univariate analysis of mortality in acute coronary syndrome patients|
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| Discussion|| |
Physiologically, the mean LA pressure is equal to LV end-diastolic pressure (LVEDP) in a normal heart in the absence of mitral stenosis. The worsening of LV diastolic dysfunction after acute MI is due to the progressive increase in the LVEDP as a result of LV remodeling. The LA is influenced by the LVEDP when the mitral valve is open, and with a persistent rise in LVEDP, LA pressure increases and hence the LAVI. Progressive diastolic dysfunction and an increased LVEDP after acute MI were found to have a poorer prognosis.
Importance of left atrial volume index in acute coronary syndrome
The significance of LAV in acute MI patients was first described by Moller et al. in 2003. A LAVI of value <28 ml/m2 at rest predicts normal stress echocardiogram. A value of >32 ml/m2 was found to be the independent predictor of all-cause mortality in the study by Moller et al. at 15 months of follow-up period, even after adjustment for conventional indices of systolic and diastolic function.
Patients with LAVI >32 ml/m2 had worse prognosis regarding in-hospital outcomes; in addition, they had a higher number of major CV events in 365 days of follow-up, in which the stroke was important. Similar findings were found in the present study and a cohort of African Americans published recently. It is the first study in India to prospectively follow up patients with ACS (UA/NSTEMI/STEMI) for 1 year whereas the previous studies evaluated specific subset of patients and follow up period was less than a year.
Gunasekaran et al. reported that an increased LAVI (>28 ml/m2) is an independent predictor for MACES (except for mortality) 6 months after ACS. LAVI >50 ml/m2 predicts HF hospitalization and mortality with similar statistical power as LVEF <45% in ambulatory patients with CAD, because of the reasons: (i) LAV reflects the duration and severity of increased LA pressures and (ii) in patients with the pseudonormal pattern, the LAVI differentiates such patients from the normal diastolic function.,,
There is an independent association of increased LAVI with the duration of diabetes and the presence of comorbidities in the diabetic population. The duration of diabetes was not assessed in the following study. Smokers will have endothelial dysfunction, increased peripheral resistance, and peripheral artery disease (PAD) – which increase the diastolic burden of the LV and thus LA. The duration of smoking and the number of pack-years have not been considered in the present study; instead, the current status of smoking was taken. There was no significant difference in the CAD management between two groups (thrombolysis and PCI) though the complications were more in patients with increased LAVI.
The E/e' at admission was not predictive of mortality, similar to Sakaguchi et al.
 probably because of the exclusion of patients with prior MI (included in Hillis et al.) and less number of patients with severe diastolic dysfunction (n = 13). The E/e' accuracy is reduced in patients with segmental RWMAs. It can be increased in patients with increased flow as in moderate – to- severe mitral regurgitation (secondary to lateral wall RWMA or papillary muscle ischemia, rupture). Because of the aforementioned limitations it cannot be taken in isolation for assessing the severity of diastolic function as per the recommendation of LV diastolic function evaluation by echocardiography in 2009 by American Society of Echocardiography.
The positive correlation of E/PV with LAVI is indicative of increased diastolic dysfunction. The E/PV is relatively preload and afterload independent and correlates well with increased LA pressures. It is a semi-quantitative marker of diastolic dysfunction and in the presence of inconclusive parameters in patients with diastolic dysfunction, the E/PV >2.5 predicts pulmonary capillary wedge pressure (PCWP) >15 mm Hg with reasonable accuracy. The E/PV ratio of >2.5 is indicative of severe diastolic dysfunction.
The LVEF decreases with increased diastolic dysfunction, because of impaired relaxation and decreased volume of blood at the end-diastole which determines the ejection fraction as per the Starling's law. The decreased LVEF can be secondary to the added burden of subendocardial ischemia or RWMA secondary to MI in patients with prior increased LAVI.
The increased atrial fibrillation is secondary to atrial myopathy and decreased contractility resulting from an increased LAV. Patients with LAVI > 34 ml/m2 were more clinically symptomatic due to the diastolic burden of the heart precipitated by the acute event in the form of ACS. These patients are symptomatic and having complications during the initial hospital stay due to the already compromised myocardium. When appropriate treatment strategies are not initiated in such patients, they are more prone to subsequent complications after hospital discharge. Similar to this study, Beinart et al.
 found that increased LAVI had a higher frequency of symptoms. When stratified according to the quartiles of LAVI in mortality patients, it is seen that the number of deaths was more when LAVI is increasing >34 ml/m2.
The independent predictor of mortality by LAVI in patients with ACS was assessed by Moller et al., Secundo Junior et al., and Sakaguchi et al., though there is variation in the cutoff values among these studies and the subset of ACS sample compared to the present study.
On univariate multivariate analysis, the LAVI AL, LVEF, and MGS were found to be significant. Further, on Cox regression analysis, the LAVI AL and MGS but not LVEF were significant. There was almost three times the risk of increased events in patients with increased LAVI (relative risk 2.74). The hazard ratio for adverse events was 2.83. On analyzing the ROC curve, LAVI >34 ml/m2 had area under the curve of 0.801 in predicting the presence or absence of CAD [Figure 3].
|Figure 3: Receiver operating characteristic curve for left atrial volume index in diagnosing presence or absence of coronary artery disease|
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This prospective study confirmed that LAVI is an independent predictor of mortality in ACS patients and is an important predictor of MACEs. Patients with increased LAVI >34 ml/m2 were more symptomatic and worse outcome compared to patients with normal LAVI.
This was a single-center study. The LAVI was not assessed by three-dimensional (3D) ECHO. The follow-up period was only for 12 months. Interobserver variability was not assessed.
Follow-up for a long time. Assessment of LAVI by 3D ECHO at admission and discharge. Assessing the change in LAVI at discharge compared to that of admission. Correlation with eGFR; serum creatinine, NT-proBNP. Correlation with novel parameters on biochemical analysis that is interleukin–6, ischemia modified albumin, and pregnancy-associated plasma protein a.
| Conclusions|| |
An LAVI of value >34 ml/m2 is associated with increased comorbidities at admission and an independent predictor of adverse events during the initial hospital stay. Increased LAVI is associated with increased adverse outcomes (MACE) at follow-up. It can be used as a prognostic marker of adverse events and independent predictor of mortality in a patient with ACS.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Zachariah G. Coronary artery disease: Risk factor stratification. In: CSI Cardiology Update. Ch. 24. Jaypee Publishers: New Delhi ; 2014. p. 131-5.
Anderson RN. U.S. Decennial Life Tables for 1989-91. In: United States Life Tables. Eliminating Certain Causes of Death. Vol. 1. Hyattsville, MD: National Center for Health Statistics; 1999.
Echocardiography and coronary artery disease. In: Feigen Baum's Echocardiography. 7th
ed., Ch. 16. Lippincott Williams Wilkins, USA ; 2010. p. 427.
Suryawanshi SN. Acute coronary syndrome management strategies: Recent advances 2014. In: CSI Cardiology Update. Ch. 22. Jaypee Publsihers: New Delhi ; 2014. p. 119-24.
Tsang TS, Barnes ME, Bailey KR, Leibson CL, Montgomery SC, Takemoto Y, et al
. Left atrial volume: Important risk marker of incident atrial fibrillation in 1655 older men and women. Mayo Clin Proc 2001;76:467-75.
de Onis M, Habicht JP. Anthropometric reference data for international use: Recommendations from a World Health Organization Expert Committee. Am J Clin Nutr 1996;64:650-8.
Jneid H, Anderson JL, Wright RS, Adams CD, Bridges CR, Casey DE Jr., et al
. 2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol 2012;60:645-81.
O'Gara PT, Kushner FG, Ascheim DD, Casey DE Jr., Chung MK, de Lemos JA, et al
. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2013;127:e362-425.
Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, et al
. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581-98.
Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA, et al
. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr 2009;22:107-33.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al
. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1-39.
Gensini GG, Chapter x. The pathological anatomy of the coronary arteries of man. In: Gensini GGMD, ed Coronary arteriography 1975 Mount Kisco, New YorkFutura Publishing Co:271-274.
Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol. 1983;51:606.
Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright RS, et al
. Left atrial volume: A powerful predictor of survival after acute myocardial infarction. Circulation 2003;107:2207-12.
Alsaileek AA, Osranek M, Fatema K, McCully RB, Tsang TS, Seward JB, et al
. Predictive value of normal left atrial volume in stress echocardiography. J Am Coll Cardiol 2006;47:1024-8.
Secundo Junior JA, Santos MA, Faro GB, Soares CB, Silva AM, Secundo PF, et al
. Left atrial volume index and prediction of events in acute coronary syndrome: Solar registry. Arq Bras Cardiol 2014;103:282-91.
Nagarajarao HS, Penman AD, Taylor HA, Mosley TH, Butler K, Skelton TN, et al
. The predictive value of left atrial size for incident ischemic stroke and all-cause mortality in African Americans: The Atherosclerosis Risk In Communities (ARIC) study. Stroke 2008;39:2701-6.
Gunasekaran R, Maskon O, Hassan HH, Safian N, Sakthiswary R. Left atrial volume index is an independent predictor of major adverse cardiovascular events in acute coronary syndrome. Can J Cardiol 2012;28:561-6.
Ristow B, Ali S, Whooley MA, Schiller NB. Usefulness of left atrial volume index to predict heart failure hospitalization and mortality in ambulatory patients with coronary heart disease and comparison to left ventricular ejection fraction (from the heart and soul study). Am J Cardiol 2008;102:70-6.
Simek CL, Feldman MD, Haber HL, Wu CC, Jayaweera AR, Kaul S, et al
. 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.
Møller JE, Søndergaard E, Poulsen SH, Egstrup K. Pseudonormal and restrictive filling patterns predict left ventricular dilation and cardiac death after a first myocardial infarction: A serial color M-mode Doppler echocardiographic study. J Am Coll Cardiol 2000;36:1841-6.
Kou S, Caballero L, Dulgheru R, Voilliot D, De Sousa C, Kacharava G, et al.
Echocardiographic reference ranges for normal cardiac chamber size: Results from the NORRE study. Eur Heart J Cardiovasc Imaging 2014;15:680-90.
Poulsen MK, Dahl JS, Henriksen JE, Hey TM, Høilund-Carlsen PF, Beck-Nielsen H, et al
. Left atrial volume index: Relation to long-term clinical outcome in type 2 diabetes. J Am Coll Cardiol 2013;62:2416-21.
Sakaguchi E, Yamada A, Sugimoto K, Ito Y, Shiino K, Takada K, et al
. Prognostic value of left atrial volume index in patents with first acute myocardial infarction. Eur J Echocardiogr 2011;12:440-4.
Hillis GS, Møller JE, Pellikka PA, Gersh BJ, Wright RS, Ommen SR, et al
. Noninvasive estimation of left ventricular filling pressure by E/e' is a powerful predictor of survival after acute myocardial infarction. J Am Coll Cardiol 2004;43:360-7.
Beinart R, Boyko V, Schwammenthal E, Kuperstein R, Sagie A, Hod H, et al
. Long-term prognostic significance of left atrial volume in acute myocardial infarction. J Am Coll Cardiol 2004;44:327-34.
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]