Lo S S, Medici F, Rowe R, Hawa M, St John Sutton M, Leslie R D
Royal Brompton National Heart Hospital, London, UK.
Int J Cardiol. 2000 Jul 31;74(2-3):139-44. doi: 10.1016/s0167-5273(00)00255-2.
A major cause of morbidity in type I diabetes is congestive heart failure due predominantly to left ventricular diastolic dysfunction. The mechanism of diastolic dysfunction remains unknown and does not relate to blood pressure, microvascular complications and glycated haemoglobin. Hyperglycaemia is the hallmark of diabetes and is a potential determinant of left ventricular diastolic dysfunction.
To determine whether acute hyperglycaemia can induce changes in left ventricular diastolic function in normal subjects similar to those observed in insulin-dependent diabetes mellitus (IDDM).
Cross-sectional study.
London teaching hospital.
Sixteen twins from eight identical twin pairs discordant for IDDM (age 18-38 years, five male) were studied; none had a history or evidence of myocardial ischaemia, valvular or primary heart muscle disease, systemic hypertension or nephropathy.
Non-diabetic twins underwent a hyperglycaemic clamp at 10 mmol/l.
Doppler echocardiography was performed in basal condition in identical twin pairs discordant for IDDM and repeated in the non-diabetic twins during hyperglycaemia. Blood glucose, insulin and catecholamines were measured at baseline and during hyperglycaemia.
Transmitral Doppler E/A velocity ratio was significantly lower in diabetic than non-diabetic twins at baseline (1.44 (0.38) vs. 1.51 (0.19), P<0.05). Glucose infusion in the non-diabetic twins resulted in an increase in their E/A ratio (1.51 (0.19) vs. 1.82 (0. 47), P<0.05) due to an increase in E velocity (68 (12) to 64.7 (10. 7), P<0.05) and a decrease in the peak A velocity (42.7 (3.85) to 38. 0 (4.1), P<0.05). No significant changes were observed in peak E velocity or isovolumic relaxation time in the non-diabetic twins between baseline and hyperglycaemia.
The alterations in left ventricular diastolic function induced by acute hyperglycaemia and consequent increase in plasma catecholamines do not mimic those demonstrated in IDDM patients.
I型糖尿病发病的一个主要原因是充血性心力衰竭，主要是由于左心室舒张功能障碍。舒张功能障碍的机制尚不清楚，且与血压、微血管并发症及糖化血红蛋白无关。高血糖是糖尿病的标志，是左心室舒张功能障碍的一个潜在决定因素。
确定急性高血糖是否能在正常受试者中诱发左心室舒张功能的改变，类似于在胰岛素依赖型糖尿病（IDDM）患者中观察到的改变。
横断面研究。
伦敦教学医院。
选取来自8对同卵双胞胎中16名双胞胎，这些双胞胎中一方患有IDDM（年龄18 - 38岁，5名男性）；均无心肌缺血、瓣膜或原发性心肌疾病、系统性高血压或肾病的病史或证据。
非糖尿病双胞胎接受10 mmol/l的高血糖钳夹试验。
对患IDDM的同卵双胞胎在基础状态下进行多普勒超声心动图检查，并在非糖尿病双胞胎高血糖期间重复检查。在基线和高血糖期间测量血糖、胰岛素和儿茶酚胺。
在基线时，糖尿病双胞胎的二尖瓣多普勒E/A速度比值显著低于非糖尿病双胞胎（1.44（0.38）对1.51（0.19），P<0.05）。非糖尿病双胞胎进行葡萄糖输注后，其E/A比值升高（1.51（0.19）对1.82（0.47），P<0.05），这是由于E速度增加（68（12）至64.7（10.7），P<0.05）以及A峰速度降低（42.7（3.85）至38.0（4.1），P<0.05）。在非糖尿病双胞胎中，基线和高血糖期间的E峰速度或等容舒张时间无显著变化。
急性高血糖诱导的左心室舒张功能改变以及随之而来的血浆儿茶酚胺增加，并不模拟IDDM患者中所表现出的情况。
