4.6 Article

Baroreflex sensitivity and outcomes following coronary surgery

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PLOS ONE
卷 12, 期 4, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0175008

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  1. IRCCS Policlinico San Donato, a Clinical Research Hospital
  2. Italian Ministry of Health

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Postoperative atrial fibrillation, acute kidney dysfunction and low cardiac output following coronary surgery are associated with morbidity and mortality. The purpose of this study is to determine if the preoperative autonomic control is a determinant of these postoperative complications. This is a prospective cohort study on 150 adult patients undergoing surgical coronary revascularization with cardiopulmonary bypass. The patients received an autonomic control assessment after the induction of anesthesia. Baroreflex sensitivity was computed by spectral analysis and expressed as BRSaHF and BRSaLF for measure respectively in the high and low frequency domains. Atrial fibrillation was adjudicated at any postoperative time during the hospital stay. Acute kidney dysfunction was defined as any increase of serum creatinine levels from preoperative values within the first 48 hours after surgery, and acute kidney injury was adjudicated at a 50% increase. Low cardiac ouput syndrome was defined as the need for inotropic support > 48 hours. Thirty-eight (26.4%) patients experienced postoperative atrial fibrillation; 32 (22.2%) had acute kidney dysfunction and 5 (3.5%) acute kidney injury; 14(10%) had a low cardiac output state. No indices of baroreflex sensitivity were associated with atrial fibrillation or acute kidney injury. A low value of BRS alpha LF was associated with acute kidney dysfunction and low cardiac output state. A BRS alpha LF < 3 msec/mmHg was an independent risk factor for acute kidney dysfunction (odds ratio 3.0, 95% confidence interval 1.02-8.8, P = 0.045) and of low cardiac output state (odds ratio 17.0, 95% confidence interval 2.9-99, P = 0.002). Preoperative baroreflex sensitivity is linked to postoperative complications through a number of possible mechanisms, including an autonomic nervous system-mediated vasoconstriction, a poor response to hypotension, and an increased inflammatory reaction.

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