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Ann Thorac Surg 1997;63:971-974
© 1997 The Society of Thoracic Surgeons

Original Article: Cardiovascular

Circulatory Resuscitation With Left Ventricular Assist Device Support Reduces Interleukins 6 and 8 Levels

Daniel J. Goldstein, MD, Nader Moazami, MD, J. Alex Seldomridge, BS, Hui Laio, MD, Robert C. Ashton, Jr, MD, Yoshifumi Naka, MD, David J. Pinsky, MD, Mehmet C. Oz, MD

Departments of Surgery and Medicine, College of Physicians & Surgeons, Columbia University, New York, New York

Accepted for publication October 19, 1996.

Background. Elevated tumor necrosis factor serum levels have been reported in patients with severe congestive heart failure. This study was designed to characterize the cytokine profile in patients with acute circulatory collapse.

Methods. Blood drawn from 14 consecutive patients within 24 hours before undergoing left ventricular assist device placement and after at least 30 days of mechanical assistance or before transplantation was assayed for levels of interleukin 6, interleukin 8, and tumor necrosis factor-{alpha}.

Results. Interleukin 6 level was elevated in 11 (79%), interleukin 8 in 10 (71%), and tumor necrosis factor in 2 (14%) of the 14 patients. After hemodynamic recovery, interleukin 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 vary significantly; they were associated with infection in 2 left ventricular assist device recipients and normalized after left ventricular assist device support. All patients had resolution of circulatory shock after mechanical support and had improvement in parameters of end-organ function.

Conclusions. Circulatory shock treated with left ventricular assist device placement is associated with a proinflammatory response similar to that seen in septic shock. The decrease in cytokine serum levels that follows hemodynamic recovery suggests that these cytokines may be markers of tissue damage and may modulate cardiac dysfunction.




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