Download PDF
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
Further Information

Publication History

received April 26, 2011 resubmitted August 1, 2011

accepted Sept. 12, 2011

Publication Date:
11 November 2011 (online)

    Permissions and Reprints All articles of this category

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.

Key words

aortic valve and root - inflammation - systemic (includes cells - mediators) - heart valve - transapical - percutaneous

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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 7 Butler J, Rocker G M, Westaby S. Inflammatory response to cardiopulmonary bypass.  Ann Thorac Surg. 1993;  55 (2) 552-559
    Google Scholar
  • 8 Levy J H, Tanaka K A. Inflammatory response to cardiopulmonary bypass.  Ann Thorac Surg. 2003;  75 (2) S715-S720
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar
  • 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
    Google Scholar

Dr. Andreas Goetzenich, MD

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

Pauwellstr. 30

52074 Aachen

Germany

Phone: +49 24 18 00

Fax: +49 24 13 33 55 56

Email: agoetzenich@ukaachen.de