Sano Motoaki
Department of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Email:
J Clin Med Res. 2017 Jun;9(6):457-460. doi: 10.14740/jocmr3011w. Epub 2017 Apr 26.
It is widely accepted that obesity and type 2 diabetes mellitus (T2DM) increase the risk of heart failure (HF) independently of underlying coronary artery disease. The changes in myocardial structure or function associated with diabetes have been termed diabetic cardiomyopathy. Corresponding to changes in the risk factors for HF, an epidemiologic transition is underway from HF with a reduced ejection fraction to HF with a preserved ejection fraction. Hyperglycemia can damage the myocardium, even before diagnosis of diabetes, but intensive glycemic control has no impact on the risk of HF in patients with T2DM. Recent clinical studies have demonstrated that sodium-glucose cotransporter 2 (SGLT2) inhibitors, which inhibit renal reabsorption of glucose, decrease the risk of HF in T2DM patients. The cardioprotective mechanisms involved appear to be multifactorial and have been the subject of considerable debate. This review focuses on the hemodynamic effects of SGLT2 inhibitors in T2DM patients and the mechanisms by which these drugs decrease the risk of HF.
人们普遍认为,肥胖和2型糖尿病(T2DM)会独立于潜在冠状动脉疾病而增加心力衰竭(HF)的风险。与糖尿病相关的心肌结构或功能变化被称为糖尿病性心肌病。随着HF危险因素的变化,正在发生从射血分数降低的HF到射血分数保留的HF的流行病学转变。高血糖甚至在糖尿病诊断之前就可损害心肌,但强化血糖控制对T2DM患者的HF风险没有影响。最近的临床研究表明,抑制肾脏对葡萄糖重吸收的钠-葡萄糖协同转运蛋白2(SGLT2)抑制剂可降低T2DM患者的HF风险。所涉及的心脏保护机制似乎是多因素的,并且一直是大量争论的主题。本综述重点关注SGLT2抑制剂对T2DM患者的血流动力学影响以及这些药物降低HF风险的机制。