Fein F S, Sonnenblick E H
Albert Einstein College of Medicine, Bronx, NY 10461.
Cardiovasc Drugs Ther. 1994 Feb;8(1):65-73. doi: 10.1007/BF00877091.
Diabetic cardiomyopathy as a distinct entity was first recognized by Rubler et al. in diabetics with congestive heart failure (CHF), who had no evidence of coronary atherosclerosis. The Framingham study showed a 2.4-fold increased incidence of CHF in diabetic men and a 5.1-fold increase in diabetic women over 18 years. Pathological studies show left ventricular hypertrophy and fibrosis with varying degrees of small vessel disease, the functional significance of which is uncertain. Hypertension was recognized as an important cofactor in the development of fatal congestive heart failure in diabetics. On cardiac catheterization, in patients symptomatic of heart failure, either congestive or restrictive patterns have been observed. In contrast, asymptomatic diabetics had decreased left ventricular compliance but normal systolic function on hemodynamic study. Noninvasive studies show alterations in systolic and especially diastolic function, particularly in diabetics with microvascular complications and/or coexistent hypertension. Using load-independent measures of contractility, however, systolic function was generally found to be normal in asymptomatic normotensive diabetics. Experimental studies have focused on the mildly diabetic dog and the severely diabetic rat. Decreased left ventricular compliance and increased interstitial connective tissue were observed in chronically diabetic dogs. In contrast, ventricular myocardium from diabetic rats exhibits a reversible decrease in the speed of contraction, prolongation of contraction, and a delay in relaxation. These mechanical changes are associated with a decreased myosin ATPase, a shift in myosin isoenzyme distribution, alterations in a variety of Ca2+ fluxes, and changes in responses to alpha- and beta-adrenergic and cholinergic stimulation. These biochemical changes may be secondary to alterations in carbohydrate, lipid, and adenine nucleotide metabolism in the diabetic heart.(ABSTRACT TRUNCATED AT 250 WORDS)
糖尿病性心肌病作为一种独特的疾病实体，最早由鲁布勒等人在患有充血性心力衰竭（CHF）且无冠状动脉粥样硬化证据的糖尿病患者中识别出来。弗雷明汉研究表明，18岁以上的糖尿病男性CHF发病率增加2.4倍，糖尿病女性增加5.1倍。病理研究显示左心室肥厚和纤维化，并伴有不同程度的小血管疾病，但其功能意义尚不确定。高血压被认为是糖尿病患者发生致命性充血性心力衰竭的一个重要辅助因素。在心脏导管检查中，有心力衰竭症状的患者，观察到充血性或限制性模式。相比之下，无症状糖尿病患者在血流动力学研究中左心室顺应性降低但收缩功能正常。非侵入性研究显示收缩功能尤其是舒张功能发生改变，特别是在有微血管并发症和/或并存高血压的糖尿病患者中。然而，使用与负荷无关的收缩性测量方法，通常发现无症状血压正常的糖尿病患者收缩功能正常。实验研究主要集中在轻度糖尿病犬和重度糖尿病大鼠身上。长期糖尿病犬出现左心室顺应性降低和间质结缔组织增加。相比之下，糖尿病大鼠的心室心肌表现出收缩速度可逆性降低、收缩期延长和舒张延迟。这些机械变化与肌球蛋白ATP酶减少、肌球蛋白同工酶分布改变、多种Ca2+通量改变以及对α和β肾上腺素能及胆碱能刺激的反应变化有关。这些生化变化可能继发于糖尿病心脏中碳水化合物、脂质和腺嘌呤核苷酸代谢的改变。（摘要截选至250词）
