TITLE

The minimized extracorporeal circulation system causes less inflammation and organ damage

AUTHOR(S)
Kofidis, T.; Baraki, H.; Singh, H.; Kamiya, H.; Winterhalter, M.; Didilis, V.; Emmert, M.; Woitek, F.; Haverich, A.; Klima, U.
PUB. DATE
May 2008
SOURCE
Perfusion;May2008, Vol. 23 Issue 3, p147
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The minimized extracorporeal circulation system (MECC) is being used to reduce priming volume and blood/polymer contact during cardiac procedures. In this study, we evaluated the efficacy and potential advantages of the system in coronary artery bypass graft (CABG) patients. We included two groups of patients destined for CABG in a prospective, randomized study: Group A was operated on the usual pump (n = 30) while Group B was operated using the MECC (n = 50). Pre-operative demographics, intra-operative times and values as well as a series of post-operative outcome data (blood loss, transfusion requirements, ventilation time, ICU and hospital stay) were recorded. CK, CK-MB, troponin-T, IL-6 and IL-8 were measured. Pre-operative and post-operative lung function were assessed. In the MECC-operated group, patients developed less post-operative troponin-T (0.2 ± 0.3 vs. 0.5 ± 0.5 ng/mL, p=0.031) and less IL-8 (13.8 ± 5 vs. 22.5 ± 0.5 μg/L, p = 0.05). While blood loss was comparable in both groups, packed red blood cells and fresh frozen plasma were given less frequently in the MECC group (p = 0.015 resp. 0.022). The one-tailed Student's t-test revealed shorter bypass time in the MECC group (74 ± 17 vs. 82 ± 24 min). There was no difference in ventilation and ICU-time (patients were not treated in a fast-track fashion). The FEV1 was better in the MECC group (relative values: 70.1 ± 18.2% vs. 61.1 ± 12.3%, p = 0.02). Utilization of the MECC may cause less cytokine (IL-8) liberation, owing to less blood/tubing contact, as well as less red blood cell and fresh frozen plasma demand. It may also be the circuit in patients with chronic obstructive pulmonary disease (COPD).
ACCESSION #
35569722

 

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