Aronson D, Rayfield E J, Chesebro J H
Joslin Diabetes Center, Boston, Massachusetts, USA.
Ann Intern Med. 1997 Feb 15;126(4):296-306. doi: 10.7326/0003-4819-126-4-199702150-00006.
To review the pathogenic mechanism that lead to the poor prognosis of diabetic patients after myocardial infarction and to determine the efficacy of current interventions for myocardial infarction in these patients.
Search of the MEDLINE database from 1985 to 1995, using the keywords diabetes, myocardial infarction, and cardiomyopathy, and a search of the reference citations of relevant articles.
Experimental and clinical studies on myocardial infarction in diabetic patients and basic research studies relevant to this topic.
The excess in-hospital mortality of diabetic patients results primarily from an increased incidence of congestive heart failure. Several combined mechanisms reduce the compensatory ability of the noninfarcted myocardium; such mechanisms include preexisting congestive heart failure caused by diabetic cardiomyopathy, severe coronary artery disease, decreased vasodilatory reserve of epicardial and resistance arteries, and possibly abnormal metabolism of myocardial substrate. Late mortality results from increased reinfarction rates caused by the diffuse nature of the atherosclerotic disease and hypercoagulable state. Platelet hyperactivity, reduced fibrinolytic capacity, increased concentrations of hemostatic proteins, and endothelial dysfunction promote thrombosis at the site of plaque rupture. Autonomic neuropathy predisposes patients to ventricular arrhythmias. Thrombolytic agents, aspirin, beta-blockers, and angiotensin-converting enzyme inhibitors are effective in patients with diabetes.
In the thrombolytic era, mortality rates of diabetic patients who have had acute myocardial infarction remain 1.5 to 2 times higher than those in nondiabetic patients. This increased mortality rate is caused by diverse mechanisms that affect myocardial function and blood supply and by the tendency toward thrombosis in diabetic patients. Current therapies for myocardial infarction are effective in these patients. Improved metabolic control may also decrease mortality rates.
回顾导致糖尿病患者心肌梗死后预后不良的致病机制,并确定当前针对这些患者心肌梗死的干预措施的疗效。
检索1985年至1995年的MEDLINE数据库,使用关键词糖尿病、心肌梗死和心肌病,并检索相关文章的参考文献。
关于糖尿病患者心肌梗死的实验和临床研究以及与此主题相关的基础研究。
糖尿病患者住院死亡率过高主要是由于充血性心力衰竭发病率增加。多种联合机制降低了未梗死心肌的代偿能力;这些机制包括由糖尿病性心肌病引起的既往充血性心力衰竭、严重冠状动脉疾病、心外膜和阻力动脉血管舒张储备降低以及心肌底物代谢可能异常。晚期死亡率是由动脉粥样硬化疾病的弥漫性和高凝状态导致的再梗死率增加所致。血小板活性过高、纤溶能力降低、止血蛋白浓度增加以及内皮功能障碍促进斑块破裂部位的血栓形成。自主神经病变使患者易患室性心律失常。溶栓剂、阿司匹林、β受体阻滞剂和血管紧张素转换酶抑制剂对糖尿病患者有效。
在溶栓时代,急性心肌梗死的糖尿病患者死亡率仍比非糖尿病患者高1.5至2倍。这种死亡率增加是由影响心肌功能和血液供应的多种机制以及糖尿病患者的血栓形成倾向所致。目前针对心肌梗死的治疗方法对这些患者有效。改善代谢控制也可能降低死亡率。