弥漫性心肌纤维化诊治进展
Progress in Diagnosis and Treatment of Diffuse Myocardial Fibrosis
DOI: 10.12677/ACM.2023.131054, PDF,   
作者: 乔斌杰, 熊 珂, 梁林园:西安医学院,陕西 西安;陕西省人民医院心血管内二科,陕西 西安;寿锡凌*:陕西省人民医院心血管内二科,陕西 西安
关键词: 弥漫性心肌纤维化心力衰竭诊断治疗Diffuse Myocardial Fibrosis Heart Failure Diagnosis Treatment
摘要: 在许多慢性心脏病中,由于胶原纤维在整个心肌过度沉积而导致弥漫性心肌纤维化。这种损伤是由于成纤维细胞对原纤维胶原周转调节的改变,促进心肌间质和心肌内血管周围I型和III型胶原纤维的过度沉积。现有证据表明,除了纤维沉积的程度外,胶原成分和纤维的物理化学性质也与弥漫性心肌纤维化对心力衰竭患者心脏功能和临床结果的有害影响有关。研究结果表明,心力衰竭患者存在弥漫性心肌纤维化的各种临床病理表型。本篇综述中,主要总结了目前关于心力衰竭中弥漫性心肌纤维化的机制、目前可用的和潜在的未来治疗策略,旨在个性化地预防和逆转心力衰竭患者弥漫性心肌纤维化。
Abstract: In many chronic heart diseases, diffuse myocardial fibrosis is caused by excessive deposition of col-lagen fibers throughout the heart muscle. This injury is due to the altered regulation of collagen turnover by fibroblasts, which promotes excessive deposition of type I and III collagen fibers in the myocardial interstitium and perivascular myocardium. The available evidence suggests that in ad-dition to the extent of fiber deposition, collagen composition and the physicochemical properties of fibers are also associated with the detrimental effects of diffuse myocardial fibrosis on cardiac func-tion and clinical outcomes in patients with heart failure. The results show that patients with heart failure have various clinicopathological phenotypes of diffuse myocardial fibrosis. In many chronic heart diseases, diffuse myocardial fibrosis is caused by excessive deposition of collagen fibers throughout the heart muscle. In this review, we summarize the current mechanisms of diffuse my-ocardial fibrosis in heart failure, current available and potential future treatment strategies, and aim to personalize the prevention and reversal of diffuse myocardial fibrosis in patients with heart failure.
文章引用:乔斌杰, 熊珂, 梁林园, 寿锡凌. 弥漫性心肌纤维化诊治进展[J]. 临床医学进展, 2023, 13(1): 356-361. https://doi.org/10.12677/ACM.2023.131054

参考文献

[1] Travers, J.G., Kamal, F.A., Robbins, J., Yutzey, K.E. and Blaxall, B.C. (2016) Cardiac Fibrosis: The Fibroblast Awak-ens. Circulation Research, 118, 1021-1040. [Google Scholar] [CrossRef
[2] Frangogiannis, N.G. (2019) Cardiac Fibrosis: Cell Bio-logical Mechanisms, Molecular Pathways and Therapeutic Opportunities. Molecular Aspects of Medicine, 65, 70-99. [Google Scholar] [CrossRef] [PubMed]
[3] González, A., Schelbert, E.B., Díez, J. and Butler, J. (2018) Myo-cardial Interstitial Fibrosis in Heart Failure: Biological and Translational Perspectives. JACC: Journal of the American College of Cardiology, 71, 1696-1706. [Google Scholar] [CrossRef] [PubMed]
[4] Conrad, N., et al. (2018) Temporal Trends and Patterns in Heart Failure Incidence: A Population-Based Study of 4 Million Individuals. The Lancet, 391, 572-580. [Google Scholar] [CrossRef
[5] Murtha, L.A., et al. (2019) The Role of Pathologic Aging in Cardiac and Pulmonary Fibrosis. Aging and Disease, 10, 419-428. [Google Scholar] [CrossRef
[6] Pinto, A.R., et al. (2016) Revisiting Cardiac Cellular Composition. Circulation Research, 118, 400-409. [Google Scholar] [CrossRef
[7] T allquist, M.D. (2020) Cardiac Fibroblast Diversity. Annual Review of Physiology, 82, 63-78. [Google Scholar] [CrossRef] [PubMed]
[8] Ivey, M.J. and Tallquist, M.D. (2016) Defining the Cardiac Fibroblast. Circulation Journal, 80, 2269-2276. [Google Scholar] [CrossRef
[9] Skelly, D.A., et al. (2018) Single-Cell Transcriptional Profiling Re-veals Cellular Diversity and Intercommunication in the Mouse Heart. Cell Reports, 22, 600-610. [Google Scholar] [CrossRef] [PubMed]
[10] Farbehi, N., et al. (2019) Single-Cell Expression Profiling Re-veals Dynamic Flux of Cardiac Stromal, Vascular and Immune Cells in Health and Injury. eLife, 8, e43882. [Google Scholar] [CrossRef
[11] Kong, P., Christia, P. and Frangogiannis, N.G. (2014) The Patho-genesis of Cardiac Fibrosis. Cellular and Molecular Life Sciences, 71, 549-574. [Google Scholar] [CrossRef] [PubMed]
[12] Neumann, S., et al. (2020) Aldosterone and D-Glucose Stimulate the Proliferation of Human Cardiac Myofibroblasts in Vitro. Hypertension, 39, 756-760. [Google Scholar] [CrossRef] [PubMed]
[13] Hanna, A. and Frangogiannis, N.G. (2019) The Role of the TGF-β Superfamily in Myocardial Infarction. Frontiers in Cardiovascular Medicine, 6, 140. [Google Scholar] [CrossRef] [PubMed]
[14] Nagaraju, C.K., et al. (2019) Myofibroblast Phenotype and Reversi-bility of Fibrosis in Patients with End-Stage Heart Failure. JACC: Journal of the American College of Cardiology, 73, 2267-2282. [Google Scholar] [CrossRef] [PubMed]
[15] Liu, C., et al. (2019) Collaborative Regulation of LRG1 by TGF-β1 and PPAR-β/δ Modulates Chronic Pressure Overload-Induced Cardiac Fibrosis. Circulation: Heart Failure, 12, e005962. [Google Scholar] [CrossRef
[16] López, B., et al. (2013) Osteopontin-Mediated Myocardial Fibrosis in Heart Failure: A Role for Lysyl Oxidase? Cardiovascular Research, 99, 111-120. [Google Scholar] [CrossRef] [PubMed]
[17] de Boer, R.A., et al. (2019) Towards Better Definition, Quantification and Treatment of Fibrosis in Heart Failure. A Scientific Roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology. European Journal of Heart Failure, 21, 272-285. [Google Scholar] [CrossRef] [PubMed]
[18] Aoki, T., et al. (2011) Prognostic Impact of Myocardial Interstitial Fibrosis in Non-Ischemic Heart Failure. Comparison between Preserved and Reduced Ejection Fraction Heart Failure. Circulation Journal, 75, 2605-2613. [Google Scholar] [CrossRef
[19] Echegaray, K., et al. (2017) Role of Myocardial Collagen in Severe Aortic Stenosis with Preserved Ejection Fraction and Symptoms of Heart Failure. Revista Española de Cardiología, 70, 832-840. [Google Scholar] [CrossRef] [PubMed]
[20] Polyakova, V., Hein, S., Kostin, S., Ziegelhoeffer, T. and Schaper, J. (2004) Matrix Metalloproteinases and Their Tissue Inhibitors in Pressure-Overloaded Human Myocardium during Heart Failure Progression. JACC: Journal of the American College of Cardiology, 44, 1609-1618. [Google Scholar] [CrossRef] [PubMed]
[21] Park, S.-J., et al. (2019) Assessment of Myocardial Fibrosis Using Multimodality Imaging in severe Aortic Stenosis Comparison with Histologic Fibrosis. JACC: Cardiovascular Imaging, 12, 109-119. [Google Scholar] [CrossRef] [PubMed]
[22] Arteaga, E., et al. (2009) Prognostic Value of the Collagen Volume Fraction in Hypertrophic Cardiomyopathy. Arquivos Brasileiros de Cardiologia, 92, 216-220.
[23] López, B., et al. (2016) Myocardial Collagen Cross-Linking Is Associated with Heart Failure Hospitalization in Patients with Hyperten-sive Heart Failure. JACC: Journal of the American College of Cardiology, 67, 251-260. [Google Scholar] [CrossRef] [PubMed]
[24] Ravassa, S., et al. (2017) Phenotyping of Myocardial Fibrosis in Hypertensive Patients with Heart Failure. Influence on Clinical Outcome. Journal of Hypertension, 35, 853-861. [Google Scholar] [CrossRef
[25] Chimenti, C. and Frustaci, A. (2013) Contribution and Risks of Left Ventricular Endomyocardial Biopsy in Patients with Cardiomyopathies: A Retrospective Study over a 28-Year Period. Circulation, 128, 1531-1541. [Google Scholar] [CrossRef
[26] Scully, P.R., Bastarrika, G., Moon, J.C. and Treibel, T.A. (2018) Myocardial Extracellular Volume Quantification by Cardiovascular Magnetic Resonance and Computed Tomography. Current Cardiology Reports, 20, 15. [Google Scholar] [CrossRef] [PubMed]
[27] Bandula, S., et al. (2013) Measurement of Myocardial Extracellu-lar Volume Fraction by Using Equilibrium Contrast-Enhanced CT: Validation against Histologic Findings. Radiology, 269, 396-403. [Google Scholar] [CrossRef
[28] Treibel, T.A., et al. (2017) Automatic Quantification of the Myocardi-al Extracellular Volume by Cardiac Computed Tomography: Synthetic ECV by CCT. Journal of Cardiovascular Com-puted Tomography, 11, 221-226. [Google Scholar] [CrossRef] [PubMed]
[29] Lisi, M., et al. (2015) RV Longitudinal Deformation Correlates with Myocardial Fibrosis in Patients with End-Stage Heart Failure. JACC: Cardiovascular Imaging, 8, 514-522. [Google Scholar] [CrossRef] [PubMed]
[30] Fabiani, I., et al. (2016) Micro-RNA-21 (Biomarker) and Global Longitudinal Strain (Functional Marker) in Detection of Myocardial Fibrotic Burden in Severe Aortic Valve Stenosis: A Pilot Study. Journal of Translational Medicine, 14, 248. [Google Scholar] [CrossRef] [PubMed]
[31] Yang, E.Y., et al. (2019) Myocardial Extracellular Volume Fraction Adds Prognostic Information beyond Myocardial Replace-ment Fibrosis. Circulation: Cardiovascular Imaging, 12, e009535. [Google Scholar] [CrossRef
[32] Chalikias, G.K. and Tziakas, D.N. (2015) Biomarkers of the Extracellular Matrix and of Collagen Fragments. Clinica Chimica Acta, 443, 39-47. [Google Scholar] [CrossRef] [PubMed]
[33] Ferreira, J.P., et al. (2020) Plasma Protein Biomarkers and Their Association with Mutually Exclusive Cardiovascular Phenotypes: The FIBRO-TARGETS Case-Control Analyses. Clin-ical Research in Cardiology, 109, 22-33. [Google Scholar] [CrossRef] [PubMed]
[34] Brilla, C.G., Funck, R.C. and Rupp, H. (2000) Lis-inopril-Mediated Regression of Myocardial Fibrosis in Patients with Hypertensive Heart Disease. Circulation, 102, 1388-1393. [Google Scholar] [CrossRef
[35] Díez, J., et al. (2002) Losartan-Dependent Regres-sion of Myocardial Fibrosis Is Associated with Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients. Circulation, 105, 2512-2517. [Google Scholar] [CrossRef
[36] Izawa, H., et al. (2005) Mineralocorticoid Receptor Antagonism Ameliorates Left Ventricular Diastolic Dysfunction and Myocardial Fibrosis in Mildly Symptomatic Patients with Idiopathic Dilated Cardiomyopathy: A Pilot Study. Circulation, 112, 2940-2945. [Google Scholar] [CrossRef
[37] Pfau, D., et al. (2019) Angiotensin Receptor Neprilysin Inhibitor Attenuates Myocardial Remodeling and Improves Infarct Perfusion in Experimental Heart Failure. Scientific Reports, 9, 5791. [Google Scholar] [CrossRef] [PubMed]
[38] Franco, V., et al. (2006) Eplerenone Prevents Adverse Cardiac Remodelling Induced by Pressure Overload in Atrial Natriuretic Peptide-Null Mice. Clinical and Experimental Pharmacology and Physiology, 33, 773-779. [Google Scholar] [CrossRef] [PubMed]
[39] Morita, H., et al. (2002) Effects of Long-Term Monother-apy with Metoprolol CR/XL on the Progression of Left Ventricular Dysfunction and Remodeling in Dogs with Chronic Heart Failure. Cardiovascular Drugs and Therapy, 16, 443- 449.