Protective effect of dexmedetomidine on perioperative myocardial injury in patients with Stanford type-A aortic dissection

• Autor(a) principal: Wang,Dalong
• Data de Publicação: 2020
• Outros Autores: Lin,Quan, Du,Meiqing, Zheng,Guanrong, Xu,Weimin, Zhang,Haishan, Liu,Ke
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Revista da Associação Médica Brasileira (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0104-42302020001201638
• topic: Dexmedetomidine; Aneurysm, dissecting; Myocardium; Oxidative stress; Inflammation/metabolism; Inflammation mediators/metabolism

SUMMARY OBJECTIVE: To investigate the protective effect and mechanism of dexmedetomidine (Dex) on perioperative myocardial injury in patients with Stanford type-A aortic dissection (AD). METHODS: Eighty-six patients with Stanford type-A AD were randomly divided into Dex and control groups, with 43 cases in each group. During the surgery, the control group received the routine anesthesia, and the Dex group received Dex treatment based on routine anesthesia. The heart rate (HR) and mean arterial pressure (MAP) were recorded before Dex loading (t0), 10 min after Dex loading (t1), at the skin incision (t2), sternum sawing (t3), before cardiopulmonary bypass (t4), at the extubation (t5), and at end of surgery (t6). The blood indexes were determined before anesthesia induction (T0) and postoperatively after 12h (T1), 24h (T2), 48h (T3), and 72h (T4). RESULTS: At t2 and t3, the HR and MAP in the Dex group were lower than in the control group (P < 0.05). Compared with the control group, in the Dex group at T1, T2, and T3, the serum creatine kinase-MB, cardiac troponin-I, C-reactive protein, and tumor necrosis factor-α levels were decreased, and the interleukin-10 level, the serum total superoxide dismutase, and total anti-oxidant capability increased, while the myeloperoxidase and malondialdehyde levels decreased (all P < 0.05). CONCLUSIONS: Dex treatment may alleviate perioperative myocardial injury in patients with Stanford type-A AD by resisting inflammatory response and oxidative stress.