Clinical Investigations

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1 Clinical Investigations Echocardiographic Serial Changes of Hypertensive Cardiomyopathy With Severely Reduced Ejection Fraction: Comparison With Idiopathic Dilated Cardiomyopathy Address for correspondence: Dae-Gyun Park, MD Cardiovascular Center Kangdong Sacred Heart Hospital Hallym University 445 Gil-dong, Kangdong-Gu Seoul , South Korea Dae-Gyun Park, MD; Sung-Eun Kim, MD; Jun-Hee Lee, MD; Kyoo-Rok Han, MD; Dong-Jin Oh, MD Department of Internal Medicine, Kangdong Sacred Heart Hospital, Hallym University, Seoul, South Korea Background: with reduced ejection fraction (HTCMREF) is known as an important cause of reversible cardiomyopathy, but its serial changes on echocardiography is yet to be elucidated. Hypothesis: HTCMREF on serial echocardiography has distinctive points as compared to idiopathic dilated cardiomyopathy (iddcm). Methods: We retrospectively studied 18 hypertensive patients (mean age, 63 ± 13 years, 56% women) admitted with severe left ventricular (LV) systolic dysfunction and heart failure. We compared clinical characteristics and echocardiographic parameters at admission and follow-up between the patients with HTCMREF and 18 age-matched patients with iddcm. Left ventricular mass (LVM) and left atrial volume (LAV) were calculated by a formula using echocardiographic measurement. Results: In HTCMREF, left ventricular ejection fraction improved to 52.3 ± 8.8% during a mean follow-up of 574 days. In HTCMREF, initial left atrial diameter was greater than in iddcm (43.6 ± 5.8mmvs38.9 ± 6.3, p = 0.027). At follow-up, LAV index decreased in HTCMREF (from 31.9 ± 8.3mL/m 2 to 21.0 ± 8.9, P < 0.001), as opposed to a significant increase in iddcm (from 28.5 ± 10.9mL/m 2 to 31.9 ± 8.3, P < 0.001). There was no significant difference in initial LVM index between the 2 groups, but only in HTCMREF did LVM index decrease significantly (151.4 ± 42.1g/m 2 from ± 43.7, P < 0.01) at follow-up. In HTCMREF, LV wall on M-mode was thicker than in iddcm. Conclusions: with severe LV systolic dysfunction might be characterized by eccentric left ventricular hypertrophy and enlarged left atrium in comparison with iddcm. Introduction Hypertension is a potent risk factor for heart failure. 1,2 The main mechanism of heart failure in patients with hypertension is left ventricular (LV) diastolic dysfunction. 3 LV diastolic dysfunction associated with hypertension is morphologically characterized by LV wall thickening and increased left atrium (LA) volume. In particular, LA volume is a chronic surrogate of LV filling pressure or LA pressure, and a prognostic marker of various cardiac diseases. 4,5 with reduced ejection fraction is known as an important cause of reversible cardiomyopathy, but its morphologic characteristics and prevalence remain unclear. At an advanced stage, hypertension induces eccentric LV hypertrophy and LV systolic The authors have no funding, financial relationships, or conflicts of interest to disclose. 554 dysfunction (LVSD). In the general population, a prevalence of asymptomatic LVSD ranges from 0.9% to 14% in patients with hypertension. 6 8 According to the Framingham Heart Study, severe LVSD developed in 3% to 6% among hypertensive patients. 9 Eccentric pattern of hypertrophy is a particularly strong risk factor for LVSD from the Cardiovascular Health Study. 10 Although dilated cardiomyopathy is diagnosed with findings of depressed ejection fraction and dilated LV based on echocardiography, it is very elusive to discern a specific cause of dilated cardiomyopathy, especially when heart failure is first diagnosed. We aimed to investigate whether initial echocardiographic parameters such as left atrial volume (LAV), left ventricular mass (LVM), LV sphericity, right ventricular systolic function, and changes of those parameters at follow-up could give clues to differentiate hypertensive cardiomyopathy with reduced ejection fraction (HTCMREF) from idiopathic dilated cardiomyopathy (iddcm). Received: April 19, 2011 Accepted with revision: April 18, 2012

2 Methods We retrospectively studied 18 hypertensive patients (mean age, 62.7 ± 13.2 years, 56% women) who were admitted with severe LVSD (ejection fraction <35%) and heart failure to Kangdong Sacred Heart hospital and recovered to normal ejection fraction (EF) on follow-up echocardiography, referred to as HTCMREF. We excluded patients with ischemic heart disease, valvular heart disease, chronic renal failure, acute myocarditis, tachycardia-induced cardiomyopathy, drug-induced cardiomyopathy, or other causes of reversible cardiomyopathy such as stress cardiomyopathy and alcoholic cardiomyopathy. We compared clinical, electrocardiographic and echocardiographic parameters between the patients with HTCM- REF and 18 age-matched patients with iddcm. iddcm was diagnosed when patients showed dilated LV and low left ventricular ejection fraction (EF <35%) without specific cause or abnormal loading condition (hypertension or valve disease), and no improvement on follow-up echocardiography at least 9 months later. We excluded ischemic cardiomyopathy performing coronary angiography. LVM and LAV were calculated by a formula using echocardiography, and were indexed to body surface area. To detect the involvement of right ventricular (RV) dysfunction, RV size and RV hypokinesia (RVHK) were evaluated. RV size was measured in diameter at end diastole in the parasternal long-axis view, and RVHK was defined as tricuspid annular plane systolic excursion <15 mm in the apical 4-chamber view. LV sphericity was measured as the ratio between the length (mitral annulus to apex) and diameter (midcavity) of the LV in the apical 4-chamber view. LVM, LAV, and relative wall thickness were calculated as follows 11 : LVM (g) = 0.8 (1.04[(diastolic LV dimension [LVDd]] + posterior wall thickness [PWT] + interventricular septal wall thickness [IVSWT]) 3 (LVDd) 3 ) g LAV = /6 (anteroposterior diameter of LA [LA1] inferomedial diameter of LA [LA2] superomedial diameter of LA [LA3]) by prolate ellipsoid formula Relative wall thickness = (PWT + IVSWT)/LVDd Laboratory data such as B-type natriuretic peptide, troponin, complete blood count, cholesterol were recorded. Left ventricular hypertrophy (LVH) on electrocardiogram was defined according to Sokolow-Lyon voltage criteria (SV1 + RV5 or RV6 35 mm). Statistics Continuous variables were expressed as the mean ± standard deviation. The dichotomous variables were expressed as percents. Statistical comparisons of continuous variables were performed by use of the Student t test. χ 2 analysis was conducted to compare categorical variables. A P value <0.05 was considered to be statistically significant. All statistical analyses were performed using of SPSS 12.0 for Windows (SPSS Inc., Chicago, IL). Results In the patients with HTCMREF, LV ejection fraction improved from 28.8 ± 4.9 to 52.3 ± 8.8%, and LV end-diastolic dimension decreased from 64.1 ± 7.7 to 52.3 ± 6.4 mm during a mean follow-up of 574 days with P < Follow-up P < 0.01 Initial P < P < Figure1. Serial change of left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), and left atrial volume index (LAVI) in patients with hypertensive cardiomyopathy with reduced EF and idiopathic dilated cardiomyopathy. A significant improvement in (A) LVEF, (B) LVMI, and (C) LAVI was observed in hypertensive cardiomyopathy with reduced EF. medications for systolic heart failure (Figure 1, part A). There were no significant differences in age, sex, and body mass index between the 2 groups (Table 1). Systolic blood pressure was higher in patients with HTCMREF than those with iddcm but not statistically significant between the 2 groups. Of the patients with HTCMREF, 8 patients (44%) had no history of hypertension, and 5 of those patients showed initially normal blood pressure but revealed high blood pressure along with the recovery of LVSD after medical treatment for systolic heart failure. On electrocardiogram, 14 (78%) of the HTCMREF patients and 12 (67%) of the iddcm patients showed LVH findings (Table 1). Echocardiographic Comparison Between Patients With HTCMREF and iddcm In HTCMREF, LV wall on M-mode was thicker (septum, 10.8 ± 1.7 vs 9.4 ± 1.9 mm; posterior wall, 10.9 ± 1.4 vs 9.7 ± 1.9 mm, P < 0.05) than in iddcm (Table 2). LA anteroposterior diameter was larger in HTCMREF, but LAV index (LAVI) showed no significant difference between the 2 groups. At follow-up, LAVI in HTCMREF decreased significantly from 31.9 ± 8.3 ml/m 2 to 21.0 ± 8.9 ml/m 2 (P < 0.001) (table 3), as opposed to a significant increase in iddcm (from 28.5 ± 10.9 ml/m 2 to 31.9 ± 8.3 ml/m 2, 555

3 Table 1. Comparison of Baseline Characteristics Between Hypertensive Cardiomyopathy With Reduced Ejection Fraction and Idiopathic Dilated Cardiomyopathy HTCMREF [N = 18] iddcm [N = 18] P Value Age, y 62.7 ± ± 16.8 NS Female, n (%) 10 (55.6) 10 (55.6) NS BMI, kg/m ± ± DM, n (%) 3 (16.7) 5 (27.8) NS Smoking, n (%) 9 (50) 6 (33.3) NS SBP, mm Hg ± ± DBP, mm Hg 86.1 ± ± 15.7 NS Heart rate, bpm 91.8 ± ± 27.3 NS Cholesterol, mg/dl ± ± 56.7 NS Creatinine, mg/dl 1.05 ± ± 0.29 NS Hemoglobin, g/dl 12.6 ± ± 1.77 NS Follow-up duration, d 574 ± ± 702 NS Use of medications at discharge, n (%) ACE-I or ARB 9 (50) 13 (72) NS β-blocker 10 (55) 5 (27.7) NS Spironolactone 13 (72) 10 (55) NS Statin 9 (50) 8 (44.4) NS Electrocardiographic variables, n (%) LVH 7 (38.8) 7 (38.8) NS LVH with ST change 7 (38.8) 5 (27.7) NS Abbreviations: ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; DBP, diastolic blood pressure; DM, diabetes mellitus; HTCMREF, hypertensive cardiomyopathy with reduced ejection fraction, iddcm, idiopathic dilated cardiomyopathy, LVH, left ventricular hypertrophy; NS, not significant; SBP, systolic blood pressure. P < 0.001) (Figure 1, part C). Mitral regurgitation (MR) is known as an important contributor to LA enlargement. On initial echocardiography, MR of more than moderate severity was found in 5 HTCMREF patients and 4 iddcm patients. On follow-up test, all HTCMREF patients with significant MR showed improvement in severity, but MR severity in iddcm patients changed variably. There was no significant difference in initial LVM index between HTCMREF and iddcm patients (192.2 ± 43.8 vs ± 47.6 g/m 2 ), but only in HTCMREF did LVM index decrease significantly (151.5 ± 42.1g/m 2, P < 0.01) at follow-up (Figure 1, part B;, Table 3). The incidence of RV hypokinesia was higher in iddcm than in HTCMREF patients at initial examination (44% vs 11%, P = 0.026) (Table 2). RV hypokinesia in HTCMREF patients recovered completely on follow-up echocardiography. Table 2. Comparison of Initial Echocardiographic Data Between Hypertensive Cardiomyopathy With Reduced Ejection Fraction and Idiopathic Dilated Cardiomyopathy HTCMREF [N = 18] iddcm [N = 18] P Value LVDd, mm 64.1 ± ± 10.0 NS LVDs, mm 54.2 ± ± 8.6 NS LVEF, % 28.8 ± ± IVSWT, mm 10.8 ± ± PWT, mm 10.9 ± ± LVMI, g/m ± ± LA, mm 43.6 ± ± LAVI (ml/m2) 31.9 ± ± 10.9 NS RVHK, n (%) 2 (11) 8 (44) MR ( moderate), n (%) 5 (27.7) 4 (22.2) NS LV sphericity index 1.46± ± Abbreviations: HTCMREF, hypertensive cardiomyopathy with reduced ejection fraction; iddcm, idiopathic dilated cardiomyopathy; IVSWT, interventricular septal wall thickness; LA, left atrium; LAVI, left atrium volume index; LVDd, left ventricular diastolic dimension; LVDs, left ventricular systolic dimension; LVEF, left ventricular ejection fraction; LVMI, left ventricular mass index; MR, mitral regurgitation; NS, not significant; PWT, posterior wall thickness; RVHK, right ventricular hypokinesia. Table 3. Follow-up Echocardiographic Findings in Hypertensive Cardiomyopathy With Reduced Ejection Fraction HTCMREF [N = 18] P Value LVDd, mm 52.2 ± ± 7.7 <0.001 LVEF, % 52.3 ± ± 4.9 <0.001 IVSWT, mm 12.0 ± ± PWT, mm 11.9 ± ± LVMI, g/m ± ± LAVI, ml/m ± ± 8.3 <0.001 LV sphericity 1.60 ± ± RVHK (%) 0 (0) 2 (11) Abbreviations: HTCMREF, hypertensive cardiomyopathy with reduced ejection fraction; IVSWT, interventricular septal wall thickness; LAVI, left atrial volume index; LV, left ventricular; LVDd, left ventricular diastolic dimension; LVEF, left ventricular ejection fraction; LVMI, left ventricualr mass index; PWT, posterior wall thickness; RVHK, right ventricular hypokinesia. Electrocardiography Changes After Medications in Patients With HTCMREF On initial Electrocardiography (ECG) in patients with HTCMREF, 14 patients (78%, 14/18) revealed LVH in voltage or LVH with secondary ST segment change. On the follow-up examination, we observed a significant regression of LVH on ECG in 8 patients (57%, 8/14), of whom the 556

4 Table 4. PossibleFactorsin Association With Regression ofleftventricular Hypertrophy on Electrocardiogram in Patients With Hypertensive Cardiomyopathy With Reduced Ejection Fraction Regression [N = 8] No Regression [N = 9] P Value Age, y 62.2 ± ± 15.8 NS Recovery time, d 638 ± ± 421 NS SBP, mm Hg ± ± 38.3 NS LVEF, % 27.1 ± ± 3.1 NS LVDd, mm 62.7 ± ± 9.6 NS LV sphericity index 1.47± ± 0.25 NS LAVI, ml/m ± ± 9.3 NS LVMI, g/m ± ± 51.2 NS D-LVEF 25.8 ± ± 11.5 NS D-LAVI 11.1 ± ± 7.37 NS D-LVMI 37.9 ± ± 57.6 NS Abbreviations: D-LAVI, difference of LAVI; D-LVEF, difference of LVEF between initial and follow-up; D-LVMI, difference of LVMI; LAVI, left atraila volume index; LV, left ventricular; LVDd, left ventricular diastolic dimension; LVEF, left ventricular ejection fraction; LVMI, LV mass index; NS, not significant; SBP, systolic blood pressure. initial LVH pattern improved from LVH in voltage or LVH with secondary ST segment changes to normal or LVH in voltage, respectively. We performed a subgroup analysis in which patients with HTCMREF were divided into 2 groups (ECG regression vs nonregression) to clarify whether the regression of LVH on ECG is a sensitive marker for short recovery time, reduction of LV mass, or reduction of LA size. The regression of LVH on ECG was not associated with age, recovery days, initial echocardiographic parameters such as left ventricular ejection fraction (LVEF), LAVI, and LVM index, or the amount of change of 3 echocardiographic parameters (Table 4). Predicting Factors for Determining Recovery Time of LVSD in Patients With HTCMREF In patients with HTCMREF, echocardiographic parameters such as LVEF, LV dimension, LAVI, LVM index, and LV sphericity were not associated with recovery time of LVSD. Age, laboratory data, and regression of LVH on ECG were also not associated with recovery time of LVSD. Discussion In our study, we found that the HTCMREF group showed eccentric LVH and higher LA diameter and lower incidence of RV hypokinesia compared to iddcm, but there were no differences in clinical characteristics, incidence of LVH on ECG, and LV sphericity between the 2 groups. Severe LVSD by hypertension has been reported to be uncommon. Severe LVSD (EF <30%) occurred 6% in the Framingham Heart Study. 9 The prevalence of asymptomatic LVSD ranges from 0.9% to 14%, depending on the clinical characteristics and LVEF. 6 8 was difficult to detect in real practice because other comorbidities including ischemic heart disease, uremia, and anemia might contribute in part to aggravation of LVEF. Asymptomatic LVSD correlated with male, smoking and LV mass, and heart rate in 1 study. 6 In our study, we could not find predictors for developing LVSD in hypertensive patients because we had no prospective data to compare between hypertensive patients with LVSD and without LVSD; nonetheless, we found eccentric LVH and increased LA dimension in HTCMREF patients when compared with iddcm patients. According to the Cardiovascular Health Study by Drazner et al, 18% of the patients developed reduced EF on an average follow-up period of 4 years in 159 hypertensive patients with LVH. 10 However, there has been no robust evidence that LVH is a risk factor for LVSD. In this context, we tried to evaluate whether regression of LVH on ECG is associated with the recovery time of LVSD or initial echocardiographic parameters, but no differences were found between the 2 groups. We found that the group of HTCMREF patients had a lower incidence of RVD than iddcm. One explanation is that increased afterload by untreated hypertension affect mainly LV in early status, whereas RVD might develop at an advanced stage, due to pulmonary vascular resistance along with secondary pulmonary hypertension. In contrast, iddcm might be caused by direct myocardial damage involving both ventricles. To our knowledge, there has been no study regarding the incidence of RVD in HTCMREF. Hypertension can lead to a variety of changes in the myocardial structure and coronary vasculature of the heart in 2 ways: directly, by increased hemodynamic load (afterload) on the heart, or indirectly, by associated neurohormonal activation and vascular changes In addition to contractile disturbances of cardiomyocyte function and interstitial and perivascular fibrosis, loss is now being considered as 1 of the determinants of the maladaptive processes implicated in the transition from compensated LVH to decompensated LVH. Several experimental studies have demonstrated that apoptosis may play an important role in the transition from compensated LVH to failure in pressureoverloaded hearts. 16 In our study, we found LVH on ECG in 14 HTCMREF patients (86%) and 12 (67%) iddcm patients. There is no difference in incidence between 2 the groups. LVH is an adaptive process to increase cardiac workload to preserve systolic ventricular dysfunction through reducing wall tension by increased wall thickening. Although left ventricular mass index could not reach a significant difference between the 2 groups (P = 0.09), the LV wall was thicker in HTCMREF patients at initial echocardiography. Paradoxically, the LV wall thickness of HTCMREF patients seemed to increase at a follow-up echocardiogram, but in fact, LVMI was decreased along with a decrease of LV size, reflecting the finding that regression on ECG was observed only in 47% of HTCMREF patients after recovery of LVEF in our study. Hypertension is a potent risk factor for heart failure, and also a primary cause of heart failure itself. In most cases, heart failure in hypertension is associated with diastolic dysfunction. In general, diastolic heart failure develops in older patients, women, or those with hypertension. 557

5 Mechanisms of diastolic heart failure in hypertension are attributed to concentric LVH and increased afterload of LV, which induce LA enlargement and pulmonary congestion. Gandhi et al reported that systolic dysfunction was found in 20/38 in hypertensive patients admitted with acute pulmonary edema, of whom follow-up echocardiography revealed no significant change, thus they concluded that diastolic dysfunction may be a main contributing factor to acute pulmonary edema. 3 In our study, LA diameter and LA volume index were increased compared to the normal value (24 28 ml/m 2 according to the various studies) LA size could be a marker of chronic LA pressure or LV filling pressure, and enlarged LA volume was associated with increased incidence of heart failure. 20,21 In contrast to Doppler diastolic variables of LV, which are affected by acute hemodynamic changes, LA volume is a more stable parameter, integrating the effects of elevated LV filling pressures from preexisting cardiovascular conditions as well as acute other diseases. In iddcm, LA volume is associated with LV remodeling, diastolic dysfunction, and the degree of MR. LA volume has an independent and incremental prognostic value. We treated all patients according to Heart Failure Guidelines of European Society of Cardiology. In 5 patients with HTCMREF, blood pressure increased along with improvement of LVEF, despite the fact that initial blood pressure was normal or below normal before medications for systolic heart failure started. Hypertension is frequently under-recognized as an underlying cause of systolic ventricular dysfunction, partly because the failing heart is unable to generate sufficient blood pressure by the time cardiac pumping function deteriorate seriously, thus obscuring the hypertensive nature of the disease. Limitations Our study was a retrospective and observational study that could not escape selection bias, and with such a small number statistical power is lacking. We could not evaluate initial diastolic Doppler parameters because many patients had a fusion of E and A flow with sinus tachycardia during the acute decompensated stage. Conclusion HTCMREF might be characterized by eccentric LVH and enlarged LA, and less frequently combined with RV dysfunction in comparison to iddcm. Therefore, patients with dilated LV, low EF, and a thick LV wall should be targeted for aggressive medical therapy, even though initial blood pressure is not high, because some patients with HTCMREF showed normal blood pressure in real practice at the initial manifestation of heart failure. References 1. Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA. 1996;275: Kannel WB, Castelli WP, McNamara PM, et al. Role of blood pressure in the development of congestive heart failure. The Framingham study. N Engl J Med. 1972;287: Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. NEngl JMed.2001:344: Kizer JR, Bella JN, Palmieri V, et al. Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS). Am Heart J. 2006;151: Rossi A, Temporelli PL, Quintana M, et al. Independent relationship of left atrial size and mortality in patients with heart failure: an individual patient meta-analysis of longitudinal data (MeRGE Heart Failure). Eur J Heart Fail. 2009;11: Verdecchia P, Angeli F, Gattobigio R, et al. Asymptomatic left ventricular systolic dysfunction in essential hypertension prevalence, determinants, and prognostic value. Hypertension. 2005;45: McDonagh TA, Morrison CE, Lawrence A, et al. Symptomatic and asymptomatic left-ventricular systolic dysfunction in an urban population. Lancet. 1997;350: Devereux RB, Bella JN, Palmieri V, et al. Hypertension genetic epidemiology network study group. left ventricular systolic dysfunction in a biracial sample of hypertensive adults: The Hypertension Genetic Epidemiology Network (HyperGEN) Study. Hypertension. 2001;38: Wang TJ, Evans JC, Benjamin EJ, et al. Natural history of asymptomatic left ventricular systolic dysfunction in the community. Circulation. 2003;108: Drazner MH, Rame JE, Marino EK, et al. Increased left ventricular mass is a risk factor for the development of a depressed left ventricular ejection fraction within five years: the Cardiovascular Health Study. J Am Coll Cardiol. 2004;43: Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986;57: Briest W, Holzl A, Rassler B, et al. Cardiac remodeling after long term norepinephrine treatment in rats. Cardiovasc Res. 2001;52: Rosendorff C. The renin-angiotensin system and vascular hypertrophy. J Am Coll Cardiol. 1996;28: Hamasaki S, Al Suwaidi J, Higano ST, et al. Attenuated coronary flow reserve in patients with hypertension and left ventricular hypertrophy. J Am Coll Cardiol. 2000;35: Gradman AH, Alfayoumi F. From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease. Prog Cardiovasc Dis. 2006;48: Gonzalez A, Fortuno MA, Querejeta R, et al. Cardiomyocyte apoptosis in hypertensive cardiomyopathy. Cardiovasc Res. 2003;59: Lim TK, Ashrafian H, Dwivedi G, et al. Increased left atrial volume index is an independent predictor of raised serum natriuretic peptide in patients with suspected heart failure but normal left ventricular ejection fraction: implication for diagnosis of diastolic heart failure. Eur J Heart Fail. 2006;8: Gottdiener JS, Kitzman DW, Aurigemma GP, et al. Left atrial volume, geometry, and function in systolic and diastolic heart failure of persons> or = 65 years of age (the cardiovascular health study). Am J Cardiol. 2006;97: Meris A, Amigoni M, Uno H, et al. Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo study. Eur Heart J. 2009;30: Abhayaratna WP, Seward JB, Appleton CP, et al. Left atrial size: physiologic determinants and clinical applications. JAm Coll Cardiol. 2006;47: Pritchett AM, Jacobsen SJ, Mahoney DW, et al. Left atrial volume as an index of left atrial size: a population-based study. JAmColl Cardiol. 2003;41:

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