Department of Experimental Cardiac Surgery, Anesthesiology, and Cardiology, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland.
Krakow Center for Medical Research and Technologies, John Paul II Hospital, Kraków, Poland.
Kardiol Pol. 2021;79(10):1060-1067. doi: 10.33963/KP.a2021.0137. Epub 2021 Oct 13.
Aortic stenosis (AS) is a progressive disease, with no pharmacological treatment. The prevalence of diabetes mellitus (DM) among AS patients is higher than in the general population. DM significantly increases the risk of AS development and the rate of its progression from mild to severe. However, the mechanism of the interaction between AS and DM is not fully understood. Limited data regarding the influence of hyperglycemia on valvular calcification are available while understanding the cross-talk between them is pivotal in designing an effective therapeutic approach to prevent or at least retard AS development and/or progression in DM patients. Analysis of aortic stenotic valves revealed that increased accumulation of advanced glycoxidation end products (AGEs) was associated with enhanced valvular oxidative stress, inflammation, expression of coagulation factors and markers of calcification. Moreover, AGEs valvular expression correlated with AS severity. Interestingly, in diabetic AS patients, valvular inflammation correlated only with long-term glycemic control parameters, i.e. glycated hemoglobin and fructosamine but not with serum glucose levels. It has been demonstrated that transcatheter aortic valve replacement (TAVI) is beneficial for AS patients also with concomitant DM and safer as compared to surgical aortic valve replacement (SAVR). Moreover, new antidiabetic drugs, such as glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors, targeting inhibition of AGEs-mediated oxidative stress, have been proposed to reduce the risk of AS development in DM patients. This review aimed to comprehensively discuss the impact of DM on AS and its potential therapeutic implications.
主动脉瓣狭窄（AS）是一种进行性疾病，目前尚无药物治疗方法。AS 患者中糖尿病（DM）的患病率高于一般人群。DM 显著增加了 AS 发展的风险，以及从轻度到重度进展的速度。然而，AS 和 DM 之间相互作用的机制尚不完全清楚。目前有关高血糖对瓣膜钙化影响的相关数据有限，而了解它们之间的相互作用对于设计有效的治疗方法来预防或至少延缓 DM 患者的 AS 发展和/或进展至关重要。对主动脉瓣狭窄瓣膜的分析表明，晚期糖基化终产物（AGEs）的积累增加与增强的瓣膜氧化应激、炎症、凝血因子表达和钙化标志物有关。此外，AGEs 在瓣膜中的表达与 AS 的严重程度相关。有趣的是，在糖尿病性 AS 患者中，瓣膜炎症仅与长期血糖控制参数相关，即糖化血红蛋白和果糖胺，而与血清葡萄糖水平无关。已经证明，经导管主动脉瓣置换术（TAVI）对同时患有 DM 的 AS 患者有益，并且比外科主动脉瓣置换术（SAVR）更安全。此外，新的抗糖尿病药物，如胰高血糖素样肽-1 受体激动剂和钠-葡萄糖共转运蛋白-2 抑制剂，通过靶向抑制 AGEs 介导的氧化应激，已被提议用于降低 DM 患者 AS 发展的风险。这篇综述旨在全面讨论 DM 对 AS 的影响及其潜在的治疗意义。
