Myocardial fibrosis detected by late gadolinium enhancement in dilated cardiomyopathy and the relationship between left ventricular function and plasma NT-proBNP levels
ZHANG Ying-xue1, ZHAO Xin-xiang2
1. Department of Radiology, Nanyang Central Hospital, Nanyang Henan 473000, China;
2. Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China
Abstract Objective: To investigate the relationship between myocardial fibrosis detected by late gadolinium enhancement(LGE) and the left ventricular function as well as plasma NT-proBNP levels in dilated cardiomyopathy(DCM). Methods: Twenty-two cases of DCM were enrolled. All patients were examined by CMR and had NT-proBNP detection. According to the results of LGE, all cases were divided into group A(without LGE) and group B(with LGE). Group B were further divided into two subgroups, including group Ba(the number of LGE segments＜5) and group Bb(the number of LGE segments≥5). The LVEDV, LVESV, LVEF, SV, CO, CI, LVMM, FS, LVEDD SI and plasma NT-proBNP levels were analyzed and compared among groups. Result: There were sixteen(73%) cases with myocardial fibrosis detected by LGE. The most frequent locations were basal anteroseptal(13 cases) and basal inferoseptal segments (13 cases). The second most frequent locations were mid-anteroseptal(7 cases) and mid-inferoseptal segments(7 cases). Eight cases showed mutiple segments of myocardial fibrosis. The significant differences of LVEDV, LVESV, LVEF, LVMM, FS, LVEDD SI and plasma NT-proBNP levels were seen between group A and group B(P＜0.05), and the group B had poorer cardiac function and ventricular remodeling. Compared group Ba and group Bb, the significant differences of LVEDV, LVESV, LVEF, LVMM, FS, LVEDD SI and plasma NT-proBNP levels were seen(P＜0.05), and the group Bb showed worse ventricular remodeling and higher NT-proBNP levels. Conclusion: The presence and extent of myocardial fibrosis detected by LGE can reflect the severity of cardiac structure and function after ventricular remodeling in patients with DCM. The more numbers of myocardial fibrosis segments in patient with DCM are found, the poorer cardiac function, the worse ventricular remodeling and the higher the plasma NT-proBNP level will happen.
ZHANG Ying-xue1,ZHAO Xin-xiang2. Myocardial fibrosis detected by late gadolinium enhancement in dilated cardiomyopathy and the relationship between left ventricular function and plasma NT-proBNP levels[J]. JOURNAL OF CHINA MEDICAL IMAGING, 2019, 30(10): 703-707.
[1]Garcia-Pavia P, Cobo-Marcos M, Guzzo-Merello G, et al. Genetics in dilated cardiomyopathy[J]. Biomark Med, 2013, 7(4): 517-533.
[2]Lakdawala NK, Winterfield JR, Funke BH. Dilated cardiomyopathy[J]. Circ Arrhythm Electrophysiol, 2013, 6(1): 228-237.
[3]Assomull RG, Prasad SK, Lyne J, et al. Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy[J]. J Am Coll Cardiol, 2006, 48(10): 1977-1985.
[4]McCrohon JA, Moon JC, Prasad SK, et al. Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance[J]. Circulation, 2003, 108(1): 54-59.
[5]中华医学会心血管病学分会，中华心血管病杂志编辑委员会，中国心肌病诊断与治疗建议工作组. 心肌病诊断与治疗建议[J]. 中华心血管病杂志，2007，35（1）：5-16.
[6]Nishii T, Kono AK, Shigeru M, et al. Cardiovascular magnetic resonance T2 mapping can detect myocardial edema in idiopathic dilated cardiomyopathy[J]. Int J Cardiovasc Imaging, 2014, 30 Suppl(1): 65-72.
[7]Heling A, Zimmermann R, Kostin S, et al. Increased expression of cytoskeletal, linkage, and extracellular proteins in failing human myocardium[J]. Circ Res, 2000, 86(8): 846-853.
[8]Masci PG, Schuurman R, Andrea B, et al. Myocardial fibrosis as a key determinant of left ventricular remodeling in idiopathic dilated cardiomyopathy: a contrast-enhanced cardiovascular magnetic study[J]. Circ Cardiovasc Imaging, 2013, 6(5): 790-799.
[9]Leyva F, Taylor RJ, Foley PW, et al. Left ventricular midwall fibrosis as a predictor of mortality and morbidity after cardiac resynchronization therapy in patients with nonischemic cardiomyopathy[J]. J Am Coll Cardiol, 2012, 60(17): 1659-1667.
[10]Masci PG, Barison A, Aquaro GD, et al. Myocardial delayed enhancement in paucisymptomatic nonischemic dilated cardiomyopathy[J]. Int J Cardiol, 2012, 157(1): 43-47.
[11]Duan X, Li J, Zhang Q, et al. Prognostic value of late gadolinium enhancement in dilated cardiomyopathy patients: a meta-analysis[J]. Clin Radiol, 2015, 70(9): 999-1008.
[12]Machii M, Satoh H, Shiraki K, et al. Distribution of late gadolinium enhancement in end-stage hypertrophic cardiomyopathy and dilated cardiomyopathy: differential diagnosis and prediction of cardiac outcome[J]. Magn Reson Imaging, 2014, 32(2): 118-124.
