Thorac cardiovasc Surg 1999; 47(6): 347-351
DOI: 10.1055/s-2007-1013172
Original Cardiovascular

© Georg Thieme Verlag Stuttgart · New York

Post-Perfusion Syndrome and Disturbed Microcirculation After Cardiac Surgery: the Role of Angiotensin-Converting-Enzyme Inhibitors

U. Boeken, P. Feindt, E. Mohan, N. Zimmermann, M. Micek, G. Kalweit, E. Gams
  • Department of Thoracic and Cardiovascular Surgery, Heinrich Heine University Hospital, Düsseldorf, Germany
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Publication History


Publication Date:
19 March 2008 (online)


Background: The sympathoadrenal and the renin-angiotensin system (RAS) are involved in blood pressure regulation. They are known to be activated during cardiac surgery. We investigated the influence of preoperative RAS-blockade using angiotensin-converting-enzyme inhibitors (ACEI) on hemodynamic variables and on the perioperative need for exogenous catecholamines. Methods: 240 patients undergoing coronary artery bypass grafting (CABG) or valve surgery were divided into three matched groups (group A: pre- and postoperative ACEI; group B: ACEI only pre-, not postoperatively; group C: no ACEI). In these three groups we analyzed hemodynamic variables, the need for catecholamines and the incidence of a “post-perfusion syndrome" or systemic inflammatory response syndrome (SIRS) with impaired microcirculation. Results: There were significant differences in the intra- and postoperative need for catecholamines in groups A and B compared to C (intraop. A: 35 %, B: 35 %, C: 15 %; postop. A: 21.2 %, B: 16.2 %, C: 10 %) (p < 0.05). In the ACEI groups (A and B) there were 9 patients with a postoperative SIRS, only 2 cases in group C. Furthermore 4 patients of group B suffered from disturbances of the intestinal microcirculation postoperatively. Conclusions: Long-term ACEI treatment before cardiac surgery raises the perioperative need for catecholamines. Patients with preoperative long-term use of ACEI who do not receive ACEI postoperatively face an increased risk of impaired microcirculation. The inhibition of angiotensin-ll (AT II) generation causes the vasodilatatory effects of ACEI, and could be one reason for a post-perfusion syndrome or a SIRS.