Department of Internal Medicine/Cardiology, Heart Center Leipzig at University of Leipzig, Leipzig, Germany.
Department of Internal Medicine II-Cardiology, Angiology, and Intensive Care Medicine, University Hospital Schleswig-Holstein, Kiel, Germany.
Shock. 2020 Jan;53(1):58-62. doi: 10.1097/SHK.0000000000001342.
Reperfusion strategies in acute myocardial infarction (AMI) may result in ischemia reperfusion injury characterized by increased oxidative stress, inflammation, and ultimately death of myocardial tissue which may be of particular importance in infarct-related cardiogenic shock (CS). Many anti-oxidative and immune regulatory processes depend on selenium which in large proportions is bound to circulating selenoprotein P (SelP). Individual SelP patterns may therefore be associated with inflammatory response and possibly mortality in patients with CS post AMI.
In the randomized Intra-Aortic Balloon Pump in cardiogenic Shock II (IABP-SHOCK II)-trial, 600 patients with CS complicating AMI were assigned to therapy with or without IABP. In a predefined biomarker substudy of 147 patients, we analyzed SelP levels 1 and 3 days following randomization. Samples were compared with healthy controls and associations with the unspecific inflammatory marker C-reactive protein (CRP) were analyzed.
Compared with controls SelP levels in patients with infarct-related CS were markedly higher (2.7-fold at day 1 and 5.7-fold at day 3 following AMI, all P < 0.001). Thirty-day mortality was significantly higher in patients with SelP levels above the 75th percentile at day 3 following AMI (26% vs. 46%, P = 0.045). SelP was significantly proportionally correlated with CRP 1 (R = 0.762, P < 0.0001) and 3 days (R = 0.777 P < 0.0001) following AMI.
SelP levels are significantly increased post AMI with CS. Higher SelP levels are associated with increased CRP levels indicative for inflammatory processes. Future studies should focus on the characterization of SelP profiles following AMI and the identification of pathomechanisms affected by SelP.
急性心肌梗死(AMI)的再灌注策略可能导致缺血再灌注损伤,其特征是氧化应激增加、炎症反应,最终导致心肌组织死亡,这在梗死相关心源性休克(CS)中可能尤为重要。许多抗氧化和免疫调节过程依赖于硒,而硒在很大程度上与循环中的硒蛋白 P(SelP)结合。因此,个体 SelP 模式可能与 AMI 后 CS 患者的炎症反应和可能的死亡率有关。
在随机的急性心肌梗死并发心源性休克的主动脉内球囊泵治疗 II 期临床试验(IABP-SHOCK II)中,600 例 AMI 并发 CS 的患者被分为接受 IABP 治疗或不接受 IABP 治疗的两组。在一项针对 147 例患者的预先设定的生物标志物亚研究中,我们分析了随机分组后第 1 天和第 3 天的 SelP 水平。将这些样本与健康对照组进行比较,并分析了 SelP 与非特异性炎症标志物 C 反应蛋白(CRP)之间的相关性。
与对照组相比,发生梗死相关 CS 的患者 SelP 水平明显升高(AMI 后第 1 天升高 2.7 倍,第 3 天升高 5.7 倍,均 P<0.001)。AMI 后第 3 天 SelP 水平高于第 75 百分位的患者 30 天死亡率显著升高(26%比 46%,P=0.045)。SelP 与 CRP 水平呈显著的比例相关(第 1 天:R=0.762,P<0.0001;第 3 天:R=0.777,P<0.0001)。
AMI 并发 CS 后 SelP 水平显著升高。较高的 SelP 水平与 CRP 水平升高相关,提示存在炎症反应。未来的研究应集中在 AMI 后 SelP 谱的特征描述以及确定受 SelP 影响的病理机制。