当前位置: X-MOL 学术Endocr. Rev. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications.
Endocrine Reviews ( IF 22.0 ) Pub Date : 2004-08-06 , DOI: 10.1210/er.2003-0012
Zhi You Fang 1 , Johannes B Prins , Thomas H Marwick
Affiliation  

The presence of a diabetic cardiomyopathy, independent of hypertension and coronary artery disease, is still controversial. This systematic review seeks to evaluate the evidence for the existence of this condition, to clarify the possible mechanisms responsible, and to consider possible therapeutic implications. The existence of a diabetic cardiomyopathy is supported by epidemiological findings showing the association of diabetes with heart failure; clinical studies confirming the association of diabetes with left ventricular dysfunction independent of hypertension, coronary artery disease, and other heart disease; and experimental evidence of myocardial structural and functional changes. The most important mechanisms of diabetic cardiomyopathy are metabolic disturbances (depletion of glucose transporter 4, increased free fatty acids, carnitine deficiency, changes in calcium homeostasis), myocardial fibrosis (association with increases in angiotensin II, IGF-I, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, and endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels), and insulin resistance (hyperinsulinemia and reduced insulin sensitivity). This review presents evidence that diabetes is associated with a cardiomyopathy, independent of comorbid conditions, and that metabolic disturbances, myocardial fibrosis, small vessel disease, cardiac autonomic neuropathy, and insulin resistance may all contribute to the development of diabetic heart disease.

中文翻译:

糖尿病性心肌病:证据,机制和治疗意义。

与高血压和冠状动脉疾病无关的糖尿病性心肌病的存在仍存在争议。该系统评价旨在评估存在该病的证据,阐明可能的原因机制,并考虑可能的治疗意义。糖尿病性心肌病的存在得到流行病学研究结果的支持,这些发现表明糖尿病与心力衰竭的相关性。临床研究证实了糖尿病与左心室功能障碍的相关性,而与高血压,冠状动脉疾病和其他心脏病无关;和心肌结构和功能变化的实验证据。糖尿病性心肌病的最重要机制是新陈代谢紊乱(葡萄糖转运蛋白4耗竭,游离脂肪酸增加,肉碱缺乏,钙稳态改变,心肌纤维化(与血管紧张素II,IGF-I和炎性细胞因子增加相关),小血管疾病(微血管病,冠状动脉血流储备受损和内皮功能障碍),心脏自主神经病变(神经支配和去神经支配)心肌儿茶酚胺水平的改变)和胰岛素抵抗(高胰岛素血症和胰岛素敏感性降低)。这篇综述提供了证据,表明糖尿病与心肌病相关,独立于合并症,并且代谢紊乱,心肌纤维化,小血管疾病,心脏自主神经病变和胰岛素抵抗都可能导致糖尿病性心脏病的发展。和炎性细胞因子),小血管疾病(微血管病,冠状动脉血流储备受损和内皮功能障碍),心脏自主神经病变(心肌儿茶酚胺水平的去神经和改变)和胰岛素抵抗(高胰岛素血症和胰岛素敏感性降低)。这篇综述提供了证据,表明糖尿病与心肌病相关,独立于合并症,并且代谢紊乱,心肌纤维化,小血管疾病,心脏自主神经病变和胰岛素抵抗都可能导致糖尿病性心脏病的发展。和炎性细胞因子),小血管疾病(微血管病,冠状动脉血流储备受损和内皮功能障碍),心脏自主神经病变(心肌儿茶酚胺水平的去神经和改变)和胰岛素抵抗(高胰岛素血症和胰岛素敏感性降低)。这篇综述提供了证据,表明糖尿病与心肌病相关,独立于合并症,并且代谢紊乱,心肌纤维化,小血管疾病,心脏自主神经病变和胰岛素抵抗都可能导致糖尿病性心脏病的发展。和胰岛素抵抗(高胰岛素血症和胰岛素敏感性降低)。这篇综述提供了证据,表明糖尿病与心肌病相关,独立于合并症,并且代谢紊乱,心肌纤维化,小血管疾病,心脏自主神经病变和胰岛素抵抗都可能导致糖尿病性心脏病的发展。和胰岛素抵抗(高胰岛素血症和胰岛素敏感性降低)。这篇综述提供了证据,表明糖尿病与心肌病相关,独立于合并症,并且代谢紊乱,心肌纤维化,小血管疾病,心脏自主神经病变和胰岛素抵抗都可能导致糖尿病性心脏病的发展。
更新日期:2019-11-01
down
wechat
bug