Thorac Cardiovasc Surg 2020; 68(S 01): S1-S72
DOI: 10.1055/s-0040-1705421
Oral Presentations
Tuesday, March 3rd, 2020
Arrhythmias and Cardiac Implantable Electronic Devices
Georg Thieme Verlag KG Stuttgart · New York

New-Onset Atrial Fibrillation—Metabolic Markers, Cytokines, and Remodeling Anticipating Paroxysmal Atrial Fibrillation

M. Salzmann-Djufri
1   Giessen, Germany
,
T. Giessler
1   Giessen, Germany
,
S. Rohrbach
1   Giessen, Germany
,
F. Knapp
1   Giessen, Germany
,
L. Ling
1   Giessen, Germany
,
S. Vogt
1   Giessen, Germany
,
N. Mirow
1   Giessen, Germany
,
A. Böning
1   Giessen, Germany
,
B. Niemann
1   Giessen, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
13 February 2020 (online)

 

    Objectives: New-onset atrial fibrillation (NOAF) is frequent during postoperative course. Confounders comprise a changing variety. We hypothesize metabolic and clinical characteristics, cytokine patterns and markers of structural remodeling to impact for perioperative morbidity and therapeutic targets for prevention of NOAF. We analyze predisposition to initiate steady forms of atrial fibrillation.

    Methods: We prospectively investigated 200 sinus rhythm patients, during CABG, aortic valve surgery or a combination of both. NOAF incidence and morbidity, stroke, and mortality and parameters of cardiac morbidity and (peri-)operative course were recorded. Serum samples and Right atrial appendage samples drawn before, during, and after operation, at incidence (NOAF) or discharge (SR). We analyzed for serum and tissue cytokine patterns, metabolic parameters, and expression of markers of remodeling.

    Results: At day 2.5 ± 0.27, twenty-six percent of patients developed NOAF. NOAF incidence was independent from sex (p = 0.377), type of operative procedure (p = 0.106), extracorporal circulation time (p = 0.673), clamp time (p = 0.925), BMI (p = 0.499), diabetes mellitus (p = 0.130), left ventricular function (p = 0.225), postoperative delirium (p = 0.064), and wound healing disorders (p = 0.726), all reported to predispose for structural remodeling in AF before. ICU stay (p = 0.023), hemodynamic support (p = 0.001), and mechanical ventilation time (p = 0.531) were longer in NOAF. Age (70,608 ± 1,326 vs. 65,397 ± 1,038 years; p = 0,026), reoperation (p = 0,001), preoperative STEMI/NSTEMI (p < 0,001), increased left atrial area (19,903 ± 1,007 vs. 16,995 ± 0.792, cm2, p = 0.041), use of diuretics (p = 0.01), reduced glomerular filtration rate (76,474 ± 3,986 vs. 92,740 ± 4,200; p = 0.028), increased white blood cell count (16,940 ± 1,111 vs. 14,538 ± 0.488; p = 0.023), and transfusion of red blood cells (1,114 ± 0.309 vs. 0.527 ± 0.107; p = 0.024) increased NOAF incidence. Dysbalance serum lipids and obesity increased incidence and perpetuation of AF. Postoperative increase of adipocytokines and load-induced natriuretic peptides facilitated NOAF. NOAF patients expressed higher levels of structural proteins, comparable to paroxysmal AF.

    Conclusion: NOAF is frequent and may complicate postoperative course. Predisposing metabolic and inflammatory risk factors may offer additional therapeutic or preventive targets to lessen NOAF and perioperative morbidity. However, maintenance of NOAF is rare. Nonetheless expression patterns are related to paroxysmal AF and may justify intensified follow-up.


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    No conflict of interest has been declared by the author(s).