CIRCULATORY RESUSCITATION WITH LEFT-VENTRICULAR ASSIST DEVICE SUPPORTREDUCES INTERLEUKIN-6 AND INTERLEUKIN-8 LEVELS

Citation
Dj. Goldstein et al., CIRCULATORY RESUSCITATION WITH LEFT-VENTRICULAR ASSIST DEVICE SUPPORTREDUCES INTERLEUKIN-6 AND INTERLEUKIN-8 LEVELS, The Annals of thoracic surgery, 63(4), 1997, pp. 971-974
Citations number
28
Categorie Soggetti
Surgery,"Cardiac & Cardiovascular System
ISSN journal
00034975
Volume
63
Issue
4
Year of publication
1997
Pages
971 - 974
Database
ISI
SICI code
0003-4975(1997)63:4<971:CRWLAD>2.0.ZU;2-S
Abstract
Background. Elevated tumor necrosis factor serum levels have been repo rted in patients with severe congestive heart failure. This study was designed to characterize the cytokine profile in patients with acute c irculatory collapse. Methods. Blood drawn from 14 consecutive patients within 24 hours before undergoing left ventricular assist device plac ement and after at least 30 days of mechanical assistance or before tr ansplantation was assayed for levels of interleukin 6, interleukin 8, and tumor necrosis factor-alpha. Results. Interleukin 6 level was elev ated in 11 (79%), interleukin 8 in 10 (71%), and tumor necrosis factor in 2 (14%) of the 14 patients. After hemodynamic recovery, interleuki n 6 levels decreased from 33.6 +/- 9 pg/mL to 11.3 +/- 4 pg/mL (p = 0. 05) and interleukin 8 levels decreased from 122 +/- 34 pg/mL to 19.7 /- 8 pg/mL (p = 0.005). Tumor necrosis factor-alpha levels did not var y significantly; they were associated with infection in 2 left ventric ular assist device recipients and normalized after left ventricular as sist device support. All patients had resolution of circulatory shock after mechanical support and had improvement in parameters of end-orga n function. Conclusions. Circulatory shock treated with left ventricul ar assist device placement is associated with a proinflammatory respon se similar to that seen in septic shock. The decrease in cytokine seru m levels that follows hemodynamic recovery suggests that these cytokin es may be markers of tissue damage and may modulate cardiac dysfunctio n. (C) 1997 by The Society of Thoracic Surgeons.