Suppr超能文献

[慢性肾脏病中的左心室肥厚、心脏纤维化与舒张功能障碍]

[Left ventricular hypertrophy, fibrosis heart, and diastolic dysfunction in chronic kidney disease].

作者信息

Orihuela-Rodríguez Oscar, Carmona-Ruíz Héctor A., Laredo-Sánchez Fernando, Paniagua-Sierra José Ramón

机构信息

Servicio de Cardiología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México Correo electrónico:

出版信息

Rev Med Inst Mex Seguro Soc. 2017;55(Suppl. 2):S195-200.

Abstract

Cardiovascular diseases occur 75 to 80% as causes of morbidity and mortality in patients with chronic kidney disease. In epidemiological studies the causes of cardiovascular deaths are sudden death, arrhythmias, heart failure, coronary arteries disease and myocardial infarction. Heart failure and cardiac arrhythmias are caused mainly by left ventricular hypertrophy and cardiac fibrosis. Pathophysiological factors involved in left ventricular hypertrophy ventricular hypertrophy have been divided into 3 categories: related to afterload, related to preload and not related to afterload or preload. Myocardial hypertrophy induces the activation of cellular apoptosis signals and activates metabolic pathways able to increase extracellular matrix production up to fibrosis. Fibrosis leads to progressive impairment in contractility with stiffening of myocardial wall, diastolic and systolic dysfunction and finally dilated cardiomyopathy with congestive heart failure. The main of this review is to understand the pathophysiology of left ventricular hypertrophy, cardiac fibrosis and diastolic dysfunction.

摘要

心血管疾病是慢性肾病患者发病和死亡的75%至80%的病因。在流行病学研究中,心血管死亡的原因是猝死、心律失常、心力衰竭、冠状动脉疾病和心肌梗死。心力衰竭和心律失常主要由左心室肥厚和心脏纤维化引起。参与左心室肥厚的病理生理因素已分为3类:与后负荷相关、与前负荷相关以及与后负荷或前负荷无关。心肌肥厚诱导细胞凋亡信号的激活,并激活能够增加细胞外基质产生直至纤维化的代谢途径。纤维化导致心肌壁僵硬,收缩性逐渐受损,舒张和收缩功能障碍,最终发展为扩张型心肌病并伴有充血性心力衰竭。本综述的主要目的是了解左心室肥厚、心脏纤维化和舒张功能障碍的病理生理学。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验