Pericardial Mitochondrial DNA Levels Are Associated With Atrial Fibrillation After Cardiac Surgery.
Pericardial Mitochondrial DNA Levels Are Associated With Atrial Fibrillation After Cardiac Surgery.
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DOI:
10.1016/j.athoracsur.2020.07.011
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发表时间:
2021-05
期刊:
影响因子:
--
通讯作者:
Melby SJ
中科院分区:
文献类型:
--
作者:
Manghelli JL;Kelly MO;Carter DI;Gauthier JM;Scozzi D;Lancaster TS;MacGregor RM;Khiabani AJ;Schuessler RB;Gelman AE;Damiano RJ;Melby SJ
Postoperative atrial fibrillation (POAF) is the most common complication following cardiac surgery, and is associated with increased morbidity and mortality. Inflammation has been implicated as an etiology of POAF. Mitochondrial DNA (mtDNA) has been shown to initiate inflammation. This study analyzed inflammatory mechanisms of POAF by evaluating mtDNA, neutrophils, and cytokines/chemokines in the pericardial fluid (PCF) and blood following cardiac surgery. Blood and PCF from patients who underwent coronary bypass and/or heart valve surgery were collected intraoperatively and at 4, 12, 24, and 48 hours postoperatively. Real-Time PCR was used to quantify mtDNA in the PCF and blood. A luminex assay was used to study cytokine and chemokine levels. Flow cytometry was employed to analyze neutrophil infiltration and activation in the PCF. Samples from 100 patients were available for analysis. Postoperatively, mtDNA and multiple cytokine levels were higher in the PCF versus blood. Patients who developed POAF had significantly higher levels of mtDNA in the PCF compared to those who did not (p<0.0001, AUC =0.74). There was no difference in the mtDNA concentration in the blood between the POAF and non-POAF groups (p=0.897). Neutrophil concentration increased in the PCF over time from a baseline of 0.8% to 56% at 48 hours (p<0.01). The pericardial space has a high concentration of inflammatory mediators postoperatively. mtDNA in the PCF was strongly associated with the development of POAF. This finding provides insight into a possible mechanism of inflammation that may contribute to POAF, and may offer novel therapeutic targets.
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影响因子:
64.8
作者:
通讯作者:
--
影响因子:
64.8
作者:
Oka, Takafumi;Hikoso, Shungo;Yamaguchi, Osamu;Taneike, Manabu;Takeda, Toshihiro;Tamai, Takahito;Oyabu, Jota;Murakawa, Tomokazu;Nakayama, Hiroyuki;Nishida, Kazuhiko;Akira, Shizuo;Yamamoto, Akitsugu;Komuro, Issei;Otsu, Kinya
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6
作者:
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通讯作者:
Schuessler, Richard B.
影响因子:
4.4
作者:
Gelman, Andrew E.;Okazaki, Mikio;Kreisel, Daniel
通讯作者:
Kreisel, Daniel
DOI:
10.1111/j.1540-8167.1997.tb01831.x
发表时间:
1997-06-01
影响因子:
2.7
作者:
Hoffman, BF;Feinmark, SJ;Guo, SD
通讯作者:
Guo, SD