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首页> 外文期刊>Journal of Clinical Medicine Research >Possibility of a New Therapeutic Strategy for Left Ventricular Dysfunction in Type 2 Diabetes
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Possibility of a New Therapeutic Strategy for Left Ventricular Dysfunction in Type 2 Diabetes

机译：2型糖尿病左心室功能不全的新治疗策略的可能性

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Type 2 diabetes mellitus (T2DM) substantially increases the risk of cardiovascular events, including heart failure (HF), due to complications such as hypertension, obesity and dyslipidemia based on metabolic syndrome, which plays the central pathological role in HF. A reason is that T2DM causes left ventricular (LV) diastolic dysfunction beginning in the early phase of the disease, which in turn increases the risk of development of HF independently of the control of blood glucose levels, blood pressure or the presence of coronary artery diseases. Intracellular metabolic disorders and increased oxidative stress due to hyperglycemia, increased insulin resistance and chronic inflammation are pathogenic mechanisms involved in the LV diastolic dysfunction caused by T2DM. These mechanisms lead to structural changes in the heart such as LV hypertrophy and interstitial fibrosis, resulting in HF. The prevalence of HF with preserved ejection fraction (HFpEF), the major pathology of LV diastolic dysfunction, has been increasing recently, and a high incidence of HFpEF in patients with T2DM was reported. An effective therapy has not been established for HFpEF because multiple comorbidities such as advanced age, hypertension, obesity, dyslipidemia, chronic kidney disease and atrial fibrillation as well as diabetes are involved in its pathology. In the present review, we review the involvement of associated conditions such as hypertension, obesity and advanced age from the aspect of the T2DM and LV diastolic dysfunction and discuss the possibility of the development of a new therapeutic strategy for LV diastolic dysfunction and HFpEF.
机译：2型糖尿病（T2DM）由于诸如代谢综合征等高血压，肥胖和血脂异常等并发症而大大增加了包括心力衰竭（HF）在内的心血管事件的风险，而代谢综合征在HF中起着重要的病理作用。原因是T2DM从疾病的早期开始就引起左心室（LV）舒张功能障碍，这反过来又增加了发生HF的风险，而与控制血糖水平，血压或冠状动脉疾病无关。细胞内代谢紊乱和由于高血糖引起的氧化应激增加，胰岛素抵抗增强和慢性炎症是由T2DM引起的LV舒张功能障碍的致病机制。这些机制导致心脏的结构变化，例如左心室肥大和间质纤维化，从而导致心衰。最近，心室射血分数（HFpEF）保留，HF舒张功能障碍的主要病理变化的HF患病率不断上升，据报道，T2DM患者中HFpEF的发生率很高。 HFpEF尚无有效的治疗方法，因为它的病理学涉及多种合并症，如高龄，高血压，肥胖，血脂异常，慢性肾脏疾病和心房纤颤以及糖尿病。在本综述中，我们从T2DM和LV舒张功能障碍的角度回顾了高血压，肥胖和高龄等相关疾病的参与，并讨论了开发新的LV舒张功能障碍和HFpEF治疗策略的可能性。

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