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Background: Acute respiratory distress syndrome (ARDS) is a serious complication after cardiac surgery with a variety of clinical risk factors. It was hypothesized that genome variants predispose these patients to it. Material and methods: A cohort of 509 adult Caucasians undergoing on-pump cardiac surgery were observed for postoperative ARDS defined by the Berlin definition. Clinical variables and 10 single-nucleotide variants of genes involved in inflammatory pathways were analyzed for associations with four groups, defined by paO2/fiO2 (PF) ratio: 1) no ARDS (PF > 300 mmHg), 2) mild ARDS (200 < PF ≤ 300 mm Hg), 3) moderate ARDS (100 < PF ≤ 200 mm Hg), and 4) severe ARDS (PF ≤ 100 mmHg). Variables remaining in trends at p < 0.05 were considered significant. Results: The prevalence of ARDS was 7.9%. Only LBP1 rs2232582 remained in a genotypic trend with ARDS aggravation (p = 0.08). Clinical variables associated with ARDS aggravation: impaired left ventricular ejection fraction (p = 0.04), pulmonary hypertension (p = 0.01), intraoperative hypotension (p = 0.009), and postoperative day 1 white blood cell count (p = 0.015). More aggravated ARDS was associated with longer mechanical ventilation (p=0.01) and length of stay in ICU (p = 0.002). Conclusions: The borderline association with LBP1 rs2232582 and the identified risk factors suggest possible involvement of the LPS-LBP1 pathway in ARDS of the INFLACOR cohort.
EN
Background Acute respiratory distress syndrome (ARDS) is a serious complication after cardiac surgery with a variety of clinical risk factors. It was hypothesized that genome variants predispose these patients to it. Material and methods A cohort of 509 adult Caucasians undergoing on-pump cardiac surgery were observed for postoperative ARDS defined by the Berlin definition. Clinical variables and 10 single-nucleotide variants of genes involved in inflammatory pathways were analyzed for associations with four groups, defined by paO2/fiO2 (PF) ratio: 1) no ARDS (PF > 300 mmHg), 2) mild ARDS (200 < PF ≤ 300 mm Hg), 3) moderate ARDS (100 < PF ≤ 200 mm Hg), and 4) severe ARDS (PF ≤ 100 mmHg). Variables remaining in trends at p < 0.05 were considered significant. Results The prevalence of ARDS was 7.9%. Only LBP1 rs2232582 remained in a genotypic trend with ARDS aggravation (p = 0.08). Clinical variables associated with ARDS aggravation: impaired left ventricular ejection fraction (p = 0.04), pulmonary hypertension (p = 0.01), intraoperative hypotension (p = 0.009), and postoperative day 1 white blood cell count (p = 0.015). More aggravated ARDS was associated with longer mechanical ventilation (p=0.01) and length of stay in ICU (p = 0.002). Conclusions The borderline association with LBP1 rs2232582 and the identified risk factors suggest possible involvement of the LPS-LBP1 pathway in ARDS of the INFLACOR cohort.
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