Seferović P M, Milinković I, Ristić A D, Seferović Mitrović J P, Lalić K, Jotić A, Kanjuh V, Lalić N, Maisch B
Department of Cardiology, Belgrade University School of Medicine and Clinical Centre of Serbia, Koste Todorovića 8, 11000, Belgrade, Serbia.
Herz. 2012 Dec;37(8):880-6. doi: 10.1007/s00059-012-3720-z.
Diabetic cardiomyopathy is a controversial clinical entity that in its initial state is usually characterized by left ventricular diastolic dysfunction in patients with diabetes mellitus that cannot be explained by coronary artery disease, hypertension, or any other known cardiac disease. It was reported in up to 52-60% of well-controlled type-II diabetic subjects, but more recent studies, using standardized tissue Doppler criteria and more strict patient selection, revealed a much lower prevalence. The pathological substrate is myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the small coronary vessels, metabolic disturbance, and autonomic cardiac neuropathy. Hyperglycemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function, and induce myocardial inflammation. Insulin resistance with hyperinsulinemia and decreased insulin sensitivity may also contribute to the left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy may include dyspnea, arrhythmias, atypical chest pain, and dizziness. Currently, there is no specific treatment of diabetic cardiomyopathy that targets its pathophysiological substrate, but various therapeutic options are discussed that include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), the use of ACE inhibitors, beta blockers, and calcium channel blockers. Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles.
糖尿病性心肌病是一种存在争议的临床病症，在其初始状态下，通常表现为糖尿病患者出现左心室舒张功能障碍，且无法用冠状动脉疾病、高血压或任何其他已知的心脏疾病来解释。据报道，在血糖控制良好的2型糖尿病患者中，这一比例高达52% - 60%，但最近的研究采用标准化的组织多普勒标准和更严格的患者选择标准后，发现患病率要低得多。其病理基础是心肌损伤、左心室肥厚、间质纤维化、小冠状动脉血管的结构和功能改变、代谢紊乱以及自主神经性心脏病。高血糖会导致心肌坏死和纤维化，以及心肌自由基和氧化剂增加，从而降低一氧化氮水平，使内皮功能恶化，并引发心肌炎症。伴有高胰岛素血症的胰岛素抵抗和胰岛素敏感性降低也可能导致左心室肥厚。糖尿病性心肌病的临床表现可能包括呼吸困难、心律失常、非典型胸痛和头晕。目前，尚无针对糖尿病性心肌病病理生理基础的特异性治疗方法，但讨论了各种治疗选择，包括通过饮食和药物（二甲双胍和噻唑烷二酮类药物）改善糖尿病控制情况、使用血管紧张素转换酶抑制剂、β受体阻滞剂和钙通道阻滞剂。日常体育活动和降低体重指数可能通过降低葡萄糖/胰岛素比值以及增加骨骼肌和心肌的胰岛素敏感性和葡萄糖氧化来改善葡萄糖稳态。
