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Prognostic impact of late gadolinium enhancement by cardiac magnetic resonance imaging in patients with non-ischaemic dilated cardiomyopathy
Letters to the Editor
4979
Prognostic impact of late gadolinium enhancement by cardiac magnetic resonance imaging in patients with non-ischaemic dilated cardiomyopathy Xiaoping Li a,1, Chin-Pang Chan b,1, Wei Hua a,⁎, Ligang Ding a, Jing Wang a, Shu Zhang a, Shiguo Li c, Yan Zhang c a Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, PR China b Division of Cardiology, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong c Department of Radiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, PR China
a r t i c l e
i n f o
Article history: Received 8 July 2013 Accepted 13 July 2013 Available online 2 August 2013 Keywords: Magnetic resonance imaging Late gadolinium enhancement Dilated cardiomyopathy Mortality
In the past decade, cardiovascular magnetic resonance (CMR) has emerged as a powerful tool for assessment of dilated cardiomyopathy (DCM) and provided additional data that were complementary to traditional clinical parameters. Late gadolinium enhancement (LGE)-CMR technique is suggested to be useful for evaluating various cardiac diseases such as hypertrophic cardiomyopathy [1–3]. Recent studies demonstrated the presence of LGE is also associated with a worse prognosis in DCM patients [4,5]. However, the sample sizes of these studies were relative small and without assessing the relationship between the location of LGE and mortality [4–7]. In this cohort study, the aims were to assess the association between different pattern of LGE and mortality in patients with DCM. Patients with DCM who was admitted in Fuwai Hospital from June 2005 to September 2011 were included in the cohort study. Dilated cardiomyopathy was defined as systolic dysfunction (left ventricular ejection fraction [LVEF] b50%) with LV dilation in the absence of an apparent secondary cause of cardiomyopathy [8]. Three hundred and sixty six patients underwent CMR-LGE examination upon admission and 73 patients were excluded from the study: 8 patients with missed CMR test results and 65 patients excluded from the study with patients who had various secondary cardiomyopathy. Finally 293 patients were included for analysis. Institutional review board approval was obtained, and patient consents for participation in retrospective data analysis were confirmed. CMR imaging was performed by using a 1.5-T scanner with electrocardiographic triggering. 15 to 20 minutes after injection of 0.2 mmol/kg of gadolinium diethylenetriamine pentaacetic acid (Magnevist, Schering, Berlin, Germany), the images of LGE were obtained in standard short axis covering the entire ventricle, and in long axis views to detect areas of LGE using a phase-sensitive inversion recovery spoiled gradient echo sequence.
⁎ Corresponding author at: Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100037, PR China. Tel.: + 86 10 88398290; fax: + 86 10 68313019. E-mail address: [email protected] (W. Hua). 1 These authors contribute equally to this work.
Continuous variables were expressed as mean ± SD or medians and interquartile ranges. Independent t-test was used for comparison of means between two groups. Kaplan–Meier survival curves were compared using the log-rank test. Cox proportional hazard modeling was used to examine associations between independent factors and survival with adjustment for potential confounders. Analyses were conducted with SPSS 16.0 (SPSS Inc.). All tests were 2-sided and a P value b0.05 was considered statistically significant. The study consisted of 293 patients with DCM, of those, 49.5% (n = 145) had LGE and 50.5% (n = 148) had no-LGE. Compared to the patients with no-LGE, patients with LGE was associated with male, longer duration of disease, larger left ventricle (LV) and left atrium (LA) diameter in CMR examination (Table 1). Among the 293 patients studied, 45 (15.4%) died and one patient (0.34%) underwent heart transplantation during a mean follow-up of 3.2 years and all-cause mortality rates were higher in patients with LGE than patients with no-LGE (21.4% vs. 9.5%, P b 0.001). Of the 145 LGE patients, 61 had LGE in ventricular septum (VS), 73 in other than VS and 11 in diffused location (both septum and non septum location). Among these three groups, patients with diffuseLGE had higher all-cause mortality rate compared to other subgroups (VS-LGE 19.7%, other than VS-LGE 20.5%, diffuse-LGE 36.4%, P b 0.001) (Fig. 1). In univariate analysis, LGE, QRS duration, LV and LA diameter, baseline blood pressure and history of hypertension were significantly associated with all-cause mortality in DCM patients. After adjustment for age, gender, history of diabetes mellitus, hypertension, disease duration, NYHA functional class, smoker status, baseline blood pressure, QT interval, LV diameter and LVEF, it was found that LGE, QRS duration and LA diameter were independently associated with all-cause mortality. DCM is a common primary heart muscle disorder and traditional risk factors did not adequately predict outcomes [9], the presence of myocardial fibrosis or scar detected by CMR as LGE has been proposed as a potential novel risk factor for adverse events [4–6]. The presence of myocardial LGE-CMR has been associated with lethal reentrant ventricular arrhythmias [4,5], increased LV stiffness and reduced LV compliance [2], this may be the reasons for the adverse outcome in DCM patients. The present study demonstrates that the presence of LGE by CMR is an independent predictor of increased all-cause mortality in patients with DCM and this association was independent of traditional risk factors for adverse outcome in DCM such as age, NYHA functional class, and the LVEF. Our study also demonstrates that patients with diffuse-LGE were associated with higher mortality than patients with LGE in ventricular septum or LGE in location other than ventricular septum. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. This study was supported in part by grants from the National Natural Science Foundation of China (no. 81000104) and 'Fivetwelfth' National Science and Technology Support Program (2011BA11B11).
4980
Letters to the Editor
Table 1 Patient characteristics categorized by LGE.
Age (years) Female sex, n (%) History Disease duration (years) Essential hypertension, n (%) Diabetes mellitus, n (%) Atrial fibrillation, n (%) Ventricular premature beat, n (%) Sustained ventricular tachycardia, n (%) Smoker, n (%) Drinker, n (%) NYHA class III or IV, n (%) Admission vital signs SBP (mm Hg) DBP (mm Hg) Heart rate, beat/min Laboratory values at admission Glucose (mmol/L) Creatinine (umol/L) BUN (umol/L) CK-MB (IU/L) Myoglobin (ng/mL) Troponin-I (ng/mL) Pro-NT BNP (fmol/mL) Electrograph data QRS duration (ms) QT (ms) P (ms) PR (ms) Echocardiography data LV (mm) LVEF (%) RV (mm) LA (mm) CMR LA (mm) LV (mm) LVEF (%) Medicine at admission Diuretics, n (%) ACEI/ARB, n (%) Beta-blockers, n (%)
With LGE (n = 145)
No LGE (n = 148)
P value
49.2 ± 14.9 21 (14.5)
48.5 ± 15.1 46 (31.1)
0.690 0.001
2 (0.35–6.5) 35 (24.1) 15 (10.3) 31 (21.4) 49 (33.8) 25 (17.2)
1 (0.16–5) 57 (38.5) 29 (19.6) 40 (27.0) 36 (24.3) 27 (18.2)
0.041 0.008 0.027 0.259 0.074 0.822
77 (53.1) 57 (39.3) 98 (67.6)
62 (41.9) 49 (33.1) 100 (67.6)
0.055 0.269 0.997
114.5 ± 19.2 73.5 ± 13.2 79.7 ± 15.9
116.7 ± 16.9 75.2 ± 13.0 84.8 ± 17.5
0.305 0.247 0.009
5.48 ± 1.93 93.0 ± 38.0 8.08 ± 5.18 12 (9–16) 54.5 ± 31.1 0.05 (0.022-0.05) 1918.6 ± 1480.9
5.47 ± 1.49 87.7 ± 24.5 7.23 ± 2.33 11 (8–15.75) 61.6 ± 31.6 0.05 (0.05-0.05) 1670.9 ± 1374.1
0.963 0.162 0.071 0.691 0.309 0.512 0.185
113.9 ± 28.1 394.9 ± 48.7 105.1 ± 20.1 180.0 ± 29.0
111.7 ± 26.5 397.5 ± 53.6 108.4 ± 18.9 178.1 ± 23.3
0.497 0.676 0.214 0.594
66.3 ± 8.2 33.3 ± 8.1 24.0 ± 5.7 43.7 ± 6.5
64.8 ± 8.6 33.7 ± 9.2 23.1 ± 4.3 42.1 ± 7.9
0.120 0.665 0.127 0.065
39.8 ± 8.3 69.3 ± 9.3 22.6 ± 8.3
37.6 ± 8.2 67.0 ± 9.2 24.1 ± 9.4
0.029 0.033 0.195
137 (94.5) 133 (91.7) 136 (93.8)
142 (95.9) 135 (91.2) 143 (96.6)
0.557 0.876 0.256
Data are expressed as mean ± SD or median (interquartile range) or as percentages. Abbreviations: NYHA, New York Heart Association; SBP, systolic blood pressure, DBP, diastolic blood pressure, BUN, blood urea nitrogen, CK-MB, heart type creatine kinase isoenzyme, NT-pro-BNP, N-terminal fragment pro-brain natriuretic peptide, LV, left ventricle, LA, left atrium, LVEF, left ventricular ejection fraction. ACEI, angiotensionconverting enzyme inhibitor; ARB, angiotension receptor blocker.
References [1] Harris KM, Spirito P, Maron MS, et al. Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy. Circulation 2006;114:216–25. [2] Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC, Pennell DJ. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol 2003;41:1561–7. [3] O'Hanlon R, Grasso A, Roughton M, et al. Prognostic significance of myocardial fibrosis in hypertrophic cardiomyopathy. J Am Coll Cardiol 2010;56:867–74. [4] Assomull RG, Prasad SK, Lyne J, et al. Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy. J Am Coll Cardiol 2006;48:1977–85. [5] Wu KC, Weiss RG, Thiemann DR, et al. Late gadolinium enhancement by cardiovascular magnetic resonance heralds an adverse prognosis in nonischemic cardiomyopathy. J Am Coll Cardiol 2008;51:2414–21.
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.134
Fig. 1. Kaplan–Meier survival curves for patients with dilated cardiomyopathy: The upper: patients with LGE and no-LGE (log-rank P b 0.001). The lower: patients with no-LGE, VS-LGE, Other than VS-LGE and diffuse- LGE (log-rank P b 0.001).LGE: late gadolinium enhancement; VS: ventricular septum; LV: left ventricle. [6] Hombach V, Merkle N, Torzewski J, et al. Electrocardiographic and cardiac magnetic resonance imaging parameters as predictors of a worse outcome in p a t i e n t s w i t h i d i o p a t h i c d i l a t e d c a r d i o m y o p a t h y. E u r H e a r t J 2009;30(16):2011–8. [7] Lehrke S, Lossnitzer D, Schob M, et al. Use of cardiovascular magnetic resonance for risk stratification in chronic heart failure: prognostic value of late gadolinium enhancement in patients with non-ischaemic dilated cardiomyopathy. Heart 2011;97:727–32. [8] Maron BJ, Towbin JA, Thiene G, et al. Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 2006;11(113):1807–16. [9] Keeling PJ, Goldman JH, Slade AK, et al. Prognosis of idiopathic dilated cardiomyopathy. J Card Fail 1995;1:337–45.
4979
Prognostic impact of late gadolinium enhancement by cardiac magnetic resonance imaging in patients with non-ischaemic dilated cardiomyopathy Xiaoping Li a,1, Chin-Pang Chan b,1, Wei Hua a,⁎, Ligang Ding a, Jing Wang a, Shu Zhang a, Shiguo Li c, Yan Zhang c a Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, PR China b Division of Cardiology, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong c Department of Radiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, PR China
a r t i c l e
i n f o
Article history: Received 8 July 2013 Accepted 13 July 2013 Available online 2 August 2013 Keywords: Magnetic resonance imaging Late gadolinium enhancement Dilated cardiomyopathy Mortality
In the past decade, cardiovascular magnetic resonance (CMR) has emerged as a powerful tool for assessment of dilated cardiomyopathy (DCM) and provided additional data that were complementary to traditional clinical parameters. Late gadolinium enhancement (LGE)-CMR technique is suggested to be useful for evaluating various cardiac diseases such as hypertrophic cardiomyopathy [1–3]. Recent studies demonstrated the presence of LGE is also associated with a worse prognosis in DCM patients [4,5]. However, the sample sizes of these studies were relative small and without assessing the relationship between the location of LGE and mortality [4–7]. In this cohort study, the aims were to assess the association between different pattern of LGE and mortality in patients with DCM. Patients with DCM who was admitted in Fuwai Hospital from June 2005 to September 2011 were included in the cohort study. Dilated cardiomyopathy was defined as systolic dysfunction (left ventricular ejection fraction [LVEF] b50%) with LV dilation in the absence of an apparent secondary cause of cardiomyopathy [8]. Three hundred and sixty six patients underwent CMR-LGE examination upon admission and 73 patients were excluded from the study: 8 patients with missed CMR test results and 65 patients excluded from the study with patients who had various secondary cardiomyopathy. Finally 293 patients were included for analysis. Institutional review board approval was obtained, and patient consents for participation in retrospective data analysis were confirmed. CMR imaging was performed by using a 1.5-T scanner with electrocardiographic triggering. 15 to 20 minutes after injection of 0.2 mmol/kg of gadolinium diethylenetriamine pentaacetic acid (Magnevist, Schering, Berlin, Germany), the images of LGE were obtained in standard short axis covering the entire ventricle, and in long axis views to detect areas of LGE using a phase-sensitive inversion recovery spoiled gradient echo sequence.
⁎ Corresponding author at: Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100037, PR China. Tel.: + 86 10 88398290; fax: + 86 10 68313019. E-mail address: [email protected] (W. Hua). 1 These authors contribute equally to this work.
Continuous variables were expressed as mean ± SD or medians and interquartile ranges. Independent t-test was used for comparison of means between two groups. Kaplan–Meier survival curves were compared using the log-rank test. Cox proportional hazard modeling was used to examine associations between independent factors and survival with adjustment for potential confounders. Analyses were conducted with SPSS 16.0 (SPSS Inc.). All tests were 2-sided and a P value b0.05 was considered statistically significant. The study consisted of 293 patients with DCM, of those, 49.5% (n = 145) had LGE and 50.5% (n = 148) had no-LGE. Compared to the patients with no-LGE, patients with LGE was associated with male, longer duration of disease, larger left ventricle (LV) and left atrium (LA) diameter in CMR examination (Table 1). Among the 293 patients studied, 45 (15.4%) died and one patient (0.34%) underwent heart transplantation during a mean follow-up of 3.2 years and all-cause mortality rates were higher in patients with LGE than patients with no-LGE (21.4% vs. 9.5%, P b 0.001). Of the 145 LGE patients, 61 had LGE in ventricular septum (VS), 73 in other than VS and 11 in diffused location (both septum and non septum location). Among these three groups, patients with diffuseLGE had higher all-cause mortality rate compared to other subgroups (VS-LGE 19.7%, other than VS-LGE 20.5%, diffuse-LGE 36.4%, P b 0.001) (Fig. 1). In univariate analysis, LGE, QRS duration, LV and LA diameter, baseline blood pressure and history of hypertension were significantly associated with all-cause mortality in DCM patients. After adjustment for age, gender, history of diabetes mellitus, hypertension, disease duration, NYHA functional class, smoker status, baseline blood pressure, QT interval, LV diameter and LVEF, it was found that LGE, QRS duration and LA diameter were independently associated with all-cause mortality. DCM is a common primary heart muscle disorder and traditional risk factors did not adequately predict outcomes [9], the presence of myocardial fibrosis or scar detected by CMR as LGE has been proposed as a potential novel risk factor for adverse events [4–6]. The presence of myocardial LGE-CMR has been associated with lethal reentrant ventricular arrhythmias [4,5], increased LV stiffness and reduced LV compliance [2], this may be the reasons for the adverse outcome in DCM patients. The present study demonstrates that the presence of LGE by CMR is an independent predictor of increased all-cause mortality in patients with DCM and this association was independent of traditional risk factors for adverse outcome in DCM such as age, NYHA functional class, and the LVEF. Our study also demonstrates that patients with diffuse-LGE were associated with higher mortality than patients with LGE in ventricular septum or LGE in location other than ventricular septum. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. This study was supported in part by grants from the National Natural Science Foundation of China (no. 81000104) and 'Fivetwelfth' National Science and Technology Support Program (2011BA11B11).
4980
Letters to the Editor
Table 1 Patient characteristics categorized by LGE.
Age (years) Female sex, n (%) History Disease duration (years) Essential hypertension, n (%) Diabetes mellitus, n (%) Atrial fibrillation, n (%) Ventricular premature beat, n (%) Sustained ventricular tachycardia, n (%) Smoker, n (%) Drinker, n (%) NYHA class III or IV, n (%) Admission vital signs SBP (mm Hg) DBP (mm Hg) Heart rate, beat/min Laboratory values at admission Glucose (mmol/L) Creatinine (umol/L) BUN (umol/L) CK-MB (IU/L) Myoglobin (ng/mL) Troponin-I (ng/mL) Pro-NT BNP (fmol/mL) Electrograph data QRS duration (ms) QT (ms) P (ms) PR (ms) Echocardiography data LV (mm) LVEF (%) RV (mm) LA (mm) CMR LA (mm) LV (mm) LVEF (%) Medicine at admission Diuretics, n (%) ACEI/ARB, n (%) Beta-blockers, n (%)
With LGE (n = 145)
No LGE (n = 148)
P value
49.2 ± 14.9 21 (14.5)
48.5 ± 15.1 46 (31.1)
0.690 0.001
2 (0.35–6.5) 35 (24.1) 15 (10.3) 31 (21.4) 49 (33.8) 25 (17.2)
1 (0.16–5) 57 (38.5) 29 (19.6) 40 (27.0) 36 (24.3) 27 (18.2)
0.041 0.008 0.027 0.259 0.074 0.822
77 (53.1) 57 (39.3) 98 (67.6)
62 (41.9) 49 (33.1) 100 (67.6)
0.055 0.269 0.997
114.5 ± 19.2 73.5 ± 13.2 79.7 ± 15.9
116.7 ± 16.9 75.2 ± 13.0 84.8 ± 17.5
0.305 0.247 0.009
5.48 ± 1.93 93.0 ± 38.0 8.08 ± 5.18 12 (9–16) 54.5 ± 31.1 0.05 (0.022-0.05) 1918.6 ± 1480.9
5.47 ± 1.49 87.7 ± 24.5 7.23 ± 2.33 11 (8–15.75) 61.6 ± 31.6 0.05 (0.05-0.05) 1670.9 ± 1374.1
0.963 0.162 0.071 0.691 0.309 0.512 0.185
113.9 ± 28.1 394.9 ± 48.7 105.1 ± 20.1 180.0 ± 29.0
111.7 ± 26.5 397.5 ± 53.6 108.4 ± 18.9 178.1 ± 23.3
0.497 0.676 0.214 0.594
66.3 ± 8.2 33.3 ± 8.1 24.0 ± 5.7 43.7 ± 6.5
64.8 ± 8.6 33.7 ± 9.2 23.1 ± 4.3 42.1 ± 7.9
0.120 0.665 0.127 0.065
39.8 ± 8.3 69.3 ± 9.3 22.6 ± 8.3
37.6 ± 8.2 67.0 ± 9.2 24.1 ± 9.4
0.029 0.033 0.195
137 (94.5) 133 (91.7) 136 (93.8)
142 (95.9) 135 (91.2) 143 (96.6)
0.557 0.876 0.256
Data are expressed as mean ± SD or median (interquartile range) or as percentages. Abbreviations: NYHA, New York Heart Association; SBP, systolic blood pressure, DBP, diastolic blood pressure, BUN, blood urea nitrogen, CK-MB, heart type creatine kinase isoenzyme, NT-pro-BNP, N-terminal fragment pro-brain natriuretic peptide, LV, left ventricle, LA, left atrium, LVEF, left ventricular ejection fraction. ACEI, angiotensionconverting enzyme inhibitor; ARB, angiotension receptor blocker.
References [1] Harris KM, Spirito P, Maron MS, et al. Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy. Circulation 2006;114:216–25. [2] Moon JC, McKenna WJ, McCrohon JA, Elliott PM, Smith GC, Pennell DJ. Toward clinical risk assessment in hypertrophic cardiomyopathy with gadolinium cardiovascular magnetic resonance. J Am Coll Cardiol 2003;41:1561–7. [3] O'Hanlon R, Grasso A, Roughton M, et al. Prognostic significance of myocardial fibrosis in hypertrophic cardiomyopathy. J Am Coll Cardiol 2010;56:867–74. [4] Assomull RG, Prasad SK, Lyne J, et al. Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy. J Am Coll Cardiol 2006;48:1977–85. [5] Wu KC, Weiss RG, Thiemann DR, et al. Late gadolinium enhancement by cardiovascular magnetic resonance heralds an adverse prognosis in nonischemic cardiomyopathy. J Am Coll Cardiol 2008;51:2414–21.
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.134
Fig. 1. Kaplan–Meier survival curves for patients with dilated cardiomyopathy: The upper: patients with LGE and no-LGE (log-rank P b 0.001). The lower: patients with no-LGE, VS-LGE, Other than VS-LGE and diffuse- LGE (log-rank P b 0.001).LGE: late gadolinium enhancement; VS: ventricular septum; LV: left ventricle. [6] Hombach V, Merkle N, Torzewski J, et al. Electrocardiographic and cardiac magnetic resonance imaging parameters as predictors of a worse outcome in p a t i e n t s w i t h i d i o p a t h i c d i l a t e d c a r d i o m y o p a t h y. E u r H e a r t J 2009;30(16):2011–8. [7] Lehrke S, Lossnitzer D, Schob M, et al. Use of cardiovascular magnetic resonance for risk stratification in chronic heart failure: prognostic value of late gadolinium enhancement in patients with non-ischaemic dilated cardiomyopathy. Heart 2011;97:727–32. [8] Maron BJ, Towbin JA, Thiene G, et al. Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation 2006;11(113):1807–16. [9] Keeling PJ, Goldman JH, Slade AK, et al. Prognosis of idiopathic dilated cardiomyopathy. J Card Fail 1995;1:337–45.