Brugaletta Salvatore, Scalone Giancarla, Dantas Ana Paula, Ortega-Paz Luis, Garabito Manel, Roqué Mercè, Martin Victoria, Masotti Monica, Freixa Xavier, Sabaté Manel
Institut Clinic Cardiovascular, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS, University of Barcelona, Spain.
Institut Clinic Cardiovascular, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS, University of Barcelona, Spain.
Int J Cardiol. 2017 Apr 1;232:70-75. doi: 10.1016/j.ijcard.2017.01.050. Epub 2017 Jan 6.
Therapeutic hypothermia (HT) in out-of-hospital cardiac arrest STEMI patients aims to improve their neurological prognosis, but it has been associated with slow coronary flow and cardiac thrombotic events. We sought to serially assess endothelial function during the first 48h after admission in out-of-hospital cardiac arrest STEMI patients, under therapeutic hypothermia (HT).
From January 2015 to August 2015, eighteen consecutive out-of-hospital cardiac arrest STEMI patients eligible for primary PCI received HT at admission and were included in the study (HT group). During the same time period, eight consecutive patients with large anterior STEMI who received primary PCI but not HT were included as control group. Serial endothelial function by measuring flow-mediated dilatation (FMD) in the brachial artery, biomarkers of endothelial function and oxidative stress were assessed during the first 48h after admission in both groups.
HT group showed worse FMD as compared to the control group (p<0.001). Glutathione peroxidase-3 (GPx-3) values were higher in control as compared to HT group (p=0.019), without any interaction between time of observation and HT (p=0.864). A significant interaction between time and HT was found in the levels of sVCAM-1, which reached an earlier peak in control than in HT group (p=0.019). ET-1 values generally increase overtime (p=0.005), but without any main effect of HT (p=0.175).
HT is associated with endothelial dysfunction in out-of-hospital cardiac arrest STEMI patients during the first 48h after admission. This vascular dysfunction may be related to increased oxidative stress due to deficiency of GPx-3 in HT patients.
院外心脏骤停ST段抬高型心肌梗死（STEMI）患者进行治疗性低温（HT）旨在改善其神经学预后，但它与冠状动脉血流缓慢和心脏血栓形成事件有关。我们试图在治疗性低温（HT）下，对院外心脏骤停STEMI患者入院后的最初48小时内连续评估其内皮功能。
从2015年1月至2015年8月，18例符合直接经皮冠状动脉介入治疗（PCI）条件的院外心脏骤停STEMI患者在入院时接受了HT，并纳入研究（HT组）。在同一时期，8例接受直接PCI但未接受HT的大面积前壁STEMI连续患者被纳入对照组。在两组患者入院后的最初48小时内，通过测量肱动脉血流介导的扩张（FMD）、内皮功能生物标志物和氧化应激来连续评估内皮功能。
与对照组相比，HT组的FMD更差（p<0.001）。与HT组相比，对照组的谷胱甘肽过氧化物酶-3（GPx-3）值更高（p=0.019），观察时间与HT之间无任何相互作用（p=0.864）。在可溶性血管细胞黏附分子-1（sVCAM-1）水平上发现时间与HT之间存在显著相互作用，其在对照组中达到峰值的时间早于HT组（p=0.019）。内皮素-1（ET-1）值通常随时间增加（p=0.005），但HT无任何主要影响（p=0.175）。
HT与院外心脏骤停STEMI患者入院后最初48小时内的内皮功能障碍有关。这种血管功能障碍可能与HT患者中GPx-3缺乏导致的氧化应激增加有关。
