Kluge Karsten E, Langseth Miriam S, Andersen Geir Ø, Halvorsen Sigrun, Opstad Trine B, Arnesen Harald, Tønnessen Theis, Seljeflot Ingebjørg, Helseth Ragnhild
Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullevål, Norway.
University of Oslo, Norway.
Am Heart J Plus. 2022 Nov 19;24:100228. doi: 10.1016/j.ahjo.2022.100228. eCollection 2022 Dec.
The complement system and neutrophil extracellular traps (NETs) might contribute to ischemia-reperfusion injury in ST-elevation myocardial infarction (STEMI). We aimed to estimate associations between complement activation and NETs in STEMI, and their prognostic value on clinical endpoints.
In this cohort study, 864 patients admitted for PCI during STEMI were included. Complement activation was analyzed by the terminal complement complex (TCC), while NETs were analyzed by myeloperoxidase-DNA, citrullinated histone 3 (CitH3) and dsDNA. The composite endpoint was reinfarction, unscheduled revascularization, stroke, hospitalization due to heart failure, or death, and the secondary endpoint was total mortality. The association between TCC and clinical endpoints was assessed by Cox regression and ROC curve analysis.
TCC was weakly correlated to dsDNA ( = 0.127, < 0.001) and CitH3 ( = 0.102, = 0.003). After a median follow-up time of 4.6 years, 184 (21.3 %) patients had reached a clinical endpoint. TCC was not associated with the composite endpoint, but with total mortality (HR: 1.673, 95 % CI: [1.014, 2.761], = 0.044). The significant association was lost when adjusting for CRP, NT-proBNP, LVEF and time from symptoms to PCI. In ROC curve analysis of total mortality, the AUC for TCC alone was 0.549 (95 % CI: [0.472, 0.625]), AUC for dsDNA alone was 0.653 (95 % CI: [0.579, 0.720]), while AUC for TCC and dsDNA combined was 0.660 (95 % CI: [0.590, 0.730]).
In this STEMI cohort, TCC was not associated with the composite endpoint, but somewhat with total mortality. Combining TCC and dsDNA did not increase the prognostic value compared to dsDNA alone.
补体系统和中性粒细胞胞外诱捕网（NETs）可能在ST段抬高型心肌梗死（STEMI）的缺血再灌注损伤中起作用。我们旨在评估STEMI中补体激活与NETs之间的关联，以及它们对临床终点的预后价值。
在这项队列研究中，纳入了864例在STEMI期间接受PCI治疗的患者。通过终末补体复合物（TCC）分析补体激活情况，通过髓过氧化物酶-DNA、瓜氨酸化组蛋白3（CitH3）和双链DNA（dsDNA）分析NETs。复合终点为再梗死、非计划血管重建、中风、因心力衰竭住院或死亡，次要终点为全因死亡率。通过Cox回归和ROC曲线分析评估TCC与临床终点之间的关联。
TCC与dsDNA（r = 0.127，P < 0.001）和CitH3（r = 0.102，P = 0.003）呈弱相关。中位随访时间4.6年后，184例（21.3%）患者达到临床终点。TCC与复合终点无关，但与全因死亡率相关（HR：1.673，95%CI：[1.014，2.761]，P = 0.044）。在调整CRP、NT-proBNP、左心室射血分数（LVEF）以及症状发作至PCI的时间后，这种显著关联消失。在全因死亡率的ROC曲线分析中，单独TCC的AUC为0.549（95%CI：[0.472，0.625]），单独dsDNA的AUC为0.653（95%CI：[0.579，0.720]），而TCC和dsDNA联合的AUC为0.660（95%CI：[0.590，0.730]）。
在这个STEMI队列中，TCC与复合终点无关，但与全因死亡率有一定关联。与单独的dsDNA相比，联合TCC和dsDNA并未增加预后价值。
