Thorac Cardiovasc Surg 2011; 59(8): 465-469
DOI: 10.1055/s-0031-1280370
Original Cardiovascular/Society Paper

© Georg Thieme Verlag KG Stuttgart · New York

Inflammatory Response in Transapical Transaortic Valve Replacement

A. Goetzenich1 , A. Roehl1 , J. Spillner2 , M. Haushofer2 , G. Dohmen2 , L. Tewarie2 , A. Moza3
  • 1Department of Anesthesiology, University Clinic RWTH Aachen, Aachen, Germany
  • 2Clinic for Cardiothoracic and Vascular Surgery, University Clinic RWTH Aachen, Aachen, Germany
  • 3Department of Cardiac Surgery and Transplantation, Royal Brompton and Harefield NHS Foundation Trust, Harefield, United Kingdom
Weitere Informationen

Publikationsverlauf

received April 26, 2011 resubmitted August 1, 2011

accepted Sept. 12, 2011

Publikationsdatum:
11. November 2011 (online)

Abstract

Objective: Transapical aortic valve implantation (TA-AVI) has become a fast growing alternative to conventional aortic valve replacement (cAVR) particularly for patients burdened with serious comorbidities. We investigated whether the inflammatory response triggered by TA-AVI reflects the less invasive nature of this procedure. Method: In this prospective observational study 25 patients undergoing aortic valve replacement (AVR; 15 cAVR and 10 TA-AVI) were included. Serial plasma cytokine concentrations (IL-6, IL-8, and IL-10) were measured by commercially available enzyme-linked immunosorbent assay kits at six different time points before, during, and after surgery. Results: Plasma levels of all three cytokines increased during and after both procedures and returned to baseline before the patient's discharge. Peak values of IL-6 were 258 ± 113 pg/mL in AVR patients versus 111 ± 101 pg/mL in TA-AVI patients and were reached 12 hours after surgery. For IL-8, peak values were 51 ± 29 pg/mL 1 hour after surgery in AVR patients versus 15 ± 20 pg/mL on wound closure in TA-AVI patients. Plasma levels of IL-6 and IL-8 were significantly reduced in the TA-AVI group as compared with cAVR. IL-10 is markedly activated in both groups yet its induction is more prominent in AVR patients with peak values of 51 ± 28 pg/mL for AVR versus 24 ± 18 pg/mL for TA-AVI on wound closure. Conclusion: TA-AVI compared with cAVR results in a significant reduction but not elimination of a systemic inflammatory response, which is attributable to cardiopulmonary bypass-dependent and bypass-independent factors.

References

  • 1 Iung B, Baron G, Butchart E G et al. A prospective survey of patients with valvular heart disease in Europe: the Euro Heart Survey on Valvular Heart Disease.  Eur Heart J. 2003;  24 (13) 1231-1243
  • 2 Bonow R O, Carabello B A, Chatterjee K et al. 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.  Circulation. 2008;  118 (15) e523-e661
  • 3 Wendt D, Osswald B R, Kayser K et al. Society of Thoracic Surgeons score is superior to the EuroSCORE determining mortality in high risk patients undergoing isolated aortic valve replacement.  Ann Thorac Surg. 2009;  88 (2) 468-475
  • 4 Iung B, Cachier A, Baron G et al. Decision-making in elderly patients with severe aortic stenosis: why are so many denied surgery?.  Eur Heart J. 2005;  26 (24) 2714-2720
  • 5 Paparella D, Yau T M, Young E. Cardiopulmonary bypass induced inflammation: pathophysiology and treatment. An update.  Eur J Cardiothorac Surg. 2002;  21 (2) 232-244
  • 6 Laffey J G, Boylan J F, Cheng D C. The systemic inflammatory response to cardiac surgery: implications for the anesthesiologist.  Anesthesiology. 2002;  97 (1) 215-252
  • 7 Butler J, Rocker G M, Westaby S. Inflammatory response to cardiopulmonary bypass.  Ann Thorac Surg. 1993;  55 (2) 552-559
  • 8 Levy J H, Tanaka K A. Inflammatory response to cardiopulmonary bypass.  Ann Thorac Surg. 2003;  75 (2) S715-S720
  • 9 Kukielka G L, Smith C W, Manning A M, Youker K A, Michael L H, Entman M L. Induction of interleukin-6 synthesis in the myocardium. Potential role in postreperfusion inflammatory injury.  Circulation. 1995;  92 (7) 1866-1875
  • 10 Frering B, Philip I, Dehoux M, Rolland C, Langlois J M, Desmonts J M. Circulating cytokines in patients undergoing normothermic cardiopulmonary bypass.  J Thorac Cardiovasc Surg. 1994;  108 (4) 636-641
  • 11 Walther T, Dewey T, Borger M A et al. Transapical aortic valve implantation: step by step.  Ann Thorac Surg. 2009;  87 (1) 276-283
  • 12 Franke A, Lante W, Fackeldey V et al. Pro-inflammatory cytokines after different kinds of cardio-thoracic surgical procedures: is what we see what we know?.  Eur J Cardiothorac Surg. 2005;  28 (4) 569-575
  • 13 Wan S, Izzat M B, Lee T W, Wan I Y, Tang N L, Yim A P. Avoiding cardiopulmonary bypass in multivessel CABG reduces cytokine response and myocardial injury.  Ann Thorac Surg. 1999;  68 (1) 52-57
  • 14 Wan I Y, Arifi A A, Wan S et al. Beating heart revascularization with or without cardiopulmonary bypass: evaluation of inflammatory response in a prospective randomized study.  J Thorac Cardiovasc Surg. 2004;  127 (6) 1624-1631
  • 15 Wan S, DeSmet J M, Barvais L, Goldstein M, Vincent J L, LeClerc J L. Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass.  J Thorac Cardiovasc Surg. 1996;  112 (3) 806-811
  • 16 Biancari F, Lahtinen J, Lepojärvi S et al. Preoperative C-reactive protein and outcome after coronary artery bypass surgery.  Ann Thorac Surg. 2003;  76 (6) 2007-2012
  • 17 Eppinger M J, Ward P A, Bolling S F, Deeb G M. Regulatory effects of interleukin-10 on lung ischemia-reperfusion injury.  J Thorac Cardiovasc Surg. 1996;  112 (5) 1301-1306
  • 18 Frangogiannis N G, Mendoza L H, Lindsey M L et al. IL-10 is induced in the reperfused myocardium and may modulate the reaction to injury.  J Immunol. 2000;  165 (5) 2798-2808
  • 19 Allan C K, Newburger J W, McGrath E et al. The relationship between inflammatory activation and clinical outcome after infant cardiopulmonary bypass.  Anesth Analg. 2010;  111 (5) 1244-1251
  • 20 Gormley S M, Armstrong M A, McMurray T J, McBride W T. The effect of methylprednisolone on cytokine concentration and leukocyte adhesion molecule expression in an isolated cardiopulmonary bypass system.  Cytokine. 2003;  22 (5) 149-155
  • 21 Bedi A, McBride W T, Armstrong M A, Murray J M, Fee J P. Xenon has no effect on cytokine balance and adhesion molecule expression within an isolated cardiopulmonary bypass system.  Br J Anaesth. 2002;  89 (4) 546-550
  • 22 Wan S, LeClerc J L, Vincent J L. Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies.  Chest. 1997;  112 (3) 676-692
  • 23 Gormley S M, McBride W T, Armstrong M A et al. Plasma and urinary cytokine homeostasis and renal function during cardiac surgery without cardiopulmonary bypass.  Cytokine. 2002;  17 (2) 61-65
  • 24 McBride W T, Armstrong M A, Crockard A D, McMurray T J, Rea J M. Cytokine balance and immunosuppressive changes at cardiac surgery: contrasting response between patients and isolated CPB circuits.  Br J Anaesth. 1995;  75 (6) 724-733

Dr. Andreas Goetzenich, MD

Department of Anesthesiology
Research Fellow & Specialist in Anesthesiology
University Clinic RWTH Aachen

Pauwellstr. 30

52074 Aachen

Germany

Telefon: +49 24 18 00

Fax: +49 24 13 33 55 56

eMail: [email protected]