Adaptation and maladaptation of the heart in diabetes: Part I General concepts
Adaptation and maladaptation of the heart in diabetes: Part I General concepts
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DOI：
10.1161/01.cir.0000012466.50373.e8
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发表时间：
2002-04-09
期刊：
影响因子：
37.8
通讯作者：
Young, ME
中科院分区：
文献类型：
--
作者：
Taegtmeyer, H;McNulty, P;Young, ME
心室肥大和心脏质量增加，左心室收缩功能轻度降低。22在显微镜水平上，尸检和活检标本的组织学研究表明，糖尿病患者和糖尿病动物具有一系列心脏形态学异常，包括肌细胞肥大、血管周围纤维化和基质胶原、细胞甘油三酯和细胞膜脂质的增加。所有这些发现与血管和膜蛋白的非酶糖化、细胞脂肪酸摄取增加和高血糖诱导的氧化应激一致，这些都是糖尿病状态的特征。23，24这些形态学变化，特别是当与实验性糖尿病中观察到的心肌钙代谢和收缩蛋白组成的变化一起考虑时，预计会对舒张顺应性造成临床显着损害。多普勒超声心动图研究表明，在动物模型25和人类中，舒张功能障碍的定性相似模式是糖尿病的早期特征。26，27在糖尿病患者中，舒张期顺应性降低与心肌声学特性异常有关，与糖尿病的严重程度和持续时间呈正相关，与进行平板运动的能力呈负相关。[28]这种舒张功能障碍与糖尿病本身的相关性被高血压与糖尿病的频繁共存所掩盖;然而，在动物模型中，在单基因2型糖尿病的病程中，在高血压、血管病变或甚至空腹高血糖症发作之前，表明舒张功能障碍是糖尿病本身的影响。[25]糖尿病与心肌舒张功能障碍和运动能力差的关系是无可争议的。很少有证据表明，在没有冠状动脉疾病或高血压的情况下，糖尿病本身会导致左心室扩张和衰竭。然而，由于糖尿病、高血压和冠状动脉疾病的共存，这些因素可能协同作用，在左心室收缩功能障碍的基础上产生心力衰竭。由于这个原因，很难靶向糖尿病特异性代谢、功能或结构异常用于糖尿病心力衰竭的药物治疗。此外，代谢控制的程度是否会影响糖尿病患者的心脏功能仍有待观察。因此，重点再次转移到糖尿病合并症的识别和治疗。
ular hypertrophy and increased heart mass, with mildly reduced left ventricular systolic performance. 22 On the microscopic level, histological studies of autopsy and biopsy specimens demonstrate that diabetic humans and animals made diabetic share a constellation of cardiac morphological abnormalities, including myocyte hypertrophy, perivascular fibrosis, and increased quantities of matrix collagen, cellular triglyceride, and cell membrane lipid. All of these findings are consistent with the nonenzymatic glycation of vascular and membrane proteins, increased cellular fatty acid uptake, and hyperglycemia-induced oxidative stress, which are characteristic of the diabetes state. 23, 24 These morphological changes, especially when considered together with the changes in myocardial calcium metabolism and contractile protein composition observed in experimental diabetes, would be predicted to confer clinically significant impairment in diastolic compliance. Doppler echocardiographic studies have revealed that qualitatively similar patterns of diastolic dysfunction are an early feature of diabetes in both animal models25 and humans. 26, 27 In patients with diabetes, the reduction of diastolic compliance is associated with characteristically abnormal myocardial acoustic properties and correlates positively with the severity and duration of diabetes and negatively with the ability to perform treadmill exercise. 28 The relevance of this type of diastolic dysfunction to diabetes per se is clouded by the frequent coexistence of hypertension with diabetes; however, the recognition that impaired left ventricular diastolic filling can be demonstrated very early in the course of monogenetic type-2 diabetes in animal models, before the onset of hypertension, vasculopathy, or even fasting hyperglycemia, suggests diastolic dysfunction is an effect of diabetes itself. 25 An association of diabetes with myocardial diastolic dysfunction and poor exercise performance is undisputed. There is less evidence that diabetes itself can cause left ventricular dilatation and failure in the absence of coronary artery disease or hypertension. Nevertheless, because of the coexistence of diabetes, hypertension, and coronary artery disease, these factors may act synergistically to produce heart failure on the basis of left ventricular systolic dysfunction. For this reason, it is difficult to target a diabetes-specific metabolic, functional, or structural abnormality for pharmacological treatment of heart failure in diabetes. Furthermore, it still remains to be seen whether the degree of metabolic control affects the function of the heart in diabetes. The focus therefore shifts once more to the identification and treatment of comorbidities in diabetes.