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Ann Thorac Surg 1998;65:1192-1193
© 1998 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Jichi Medical School, Yakushiji 3311-1, Minami-Kawachi, Tochigi 329-04, Japan
To the Editor
We read with much interest the article by Goldstein and associates [1]. They reported that patients in circulatory shock treated with the placement of a left ventricular assist device showed a significant decrease in levels of proinflammatory cytokines concomitant with hemodynamic improvement. We experienced a similar phenomenon in short-term cardiac support using extracorporeal membrane oxygenation (ECMO) with heparin-bonded circuits. We have characterized proinflammatory and antiinflammatory cytokines (interleukin [IL]-6 and -10) profiles in cardiogenic shock patients treated by ECMO.
Blood samples were obtained from 7 consecutive ECMO patients (2 men and 5 women, aged 59 ± 7 years) at the initiation of ECMO, on days 1 and 3 after initiation, and at the time of weaning. Six of them could not be weaned from cardiopulmonary bypass, and 1 suffered cardiogenic shock caused by acute myocarditis. The mean duration of ECMO was 205 ± 54 hours. Cytokine concentrations were measured with enzyme-linked immunoabsorbent assay kits. Data are reported as the mean ± the standard error of the mean and compared with the initial values by repeated-measures analysis of variance. Although both cytokines showed a high serum concentration at the time of ECMO placement (IL-6, 484 ± 123 ng/mL; IL-10, 48 ± 28 ng/mL), the concentrations decreased steadily after ECMO initiation. Both cytokine concentrations had decreased significantly by the time of weaning (IL-6, 69 ± 23 ng/mL; IL-10, 2 ± 1 ng/mL) (Fig 1).
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As to the IL-8 level, contrary to the results of Goldstein and associates, our IL-8 data indicated no difference between pre-ECMO and post-ECMO values (37 ± 14 versus 30 ± 7 ng/mL; not significant). Although the heart plays a major part in IL-8 release, the major source of IL-6 and IL-10 is the liver. Interleukin-8 seems to be more specific for myocardial injury, and IL-6 and -10 reflect the end-organ function. Left ventricular unloading by a left ventricular assist device strongly supports the heart as well as improves end-organ perfusion. However, although ECMO improves the end-organ circulation including coronary perfusion, it has no direct supporting effect on the diseased heart but increases the afterload. These factors may partially explain the persistent elevated IL-8 level during ECMO. Furthermore, prolonged exposure of blood to an artificial surface may keep activating circulating monocytes and T-lymphocytes, which play a major part in IL-8 release.
As Goldstein and associates suggested in their conclusion, these cytokines may be markers of tissue damage. Furthermore, prognostic evaluation may also be available by estimation of the reduction pattern [3]. From a prognostic viewpoint, we are currently investigating the recovery pattern of lymphocytopenia due to apoptosis for a simple parameter as well as cytokine kinetics. Our previous study demonstrated that the pattern of recovery from lymphocytopenia correlates well with patient prognosis after ECMO, and that delayed recovery indicates a poor prognosis [5].
References
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