Key result
Continuation of ACE inhibitors until coronary artery bypass surgery resulted in significantly higher arterial bradykinin concentrations compared with discontinuation 48 hours prior (P=0.017).
Why the study?
Does continuing ACE inhibitors until surgery affect bradykinin concentrations during cardiopulmonary bypass in patients undergoing CABG?
RCT (n=31)
randomized
Does continuing ACE inhibitors until surgery affect bradykinin concentrations during cardiopulmonary bypass in patients undergoing CABG?
Continuing ACE inhibitors until CABG surgery potentiates the kinin response during cardiopulmonary bypass, which may contribute to hemodynamic and fibrinolytic responses.
Suggests perioperative hemodynamic implications with ACE inhibitor continuation in CABG; extends mechanistic evidence on kinin responses during bypass.
BACKGROUND: This study tested the hypothesis that angiotensin-converting enzyme (ACE) inhibitors potentiate activation of the kallikrein-kinin system during cardiopulmonary bypass (CPB). METHODS: The effects of CPB on concentrations of bradykinin and its metabolite bradykinin 1-5 (BK1-5) were determined in 31 patients taking an ACE inhibitor who were randomized to continue ACE inhibitors until coronary artery bypass surgery (ACE inhibitor group, N = 19) or to discontinue them 48 hours before surgery (no ACE inhibitor group, N = 12). Arterial and venous blood was sampled before CPB, at 30 minutes of CPB, at 60 minutes of CPB, after separation from CPB, and on postoperative day 1. RESULTS: Arterial bradykinin ( P < .001 [from 22.4 +/- 24.1 fmol/mL to 86.2 +/- 98.7 fmol/mL in the no ACE inhibitor group]) and arterial ( P < .001) and venous ( P = .016) BK1-5 concentrations increased significantly during CPB. Arterial bradykinin concentrations were significantly higher ( P = .017), whereas BK1-5 concentrations ( P = .024) and the molar ratio of BK1-5/bradykinin ( P = .008) were significantly lower in the ACE inhibitor group compared with the no ACE inhibitor group. In addition, arterial bradykinin concentrations were significantly increased in smokers compared with nonsmokers ( P = .015), when we controlled for the ACE inhibitor group. There was no effect of smoking on ACE activity ( P = .597 overall). There was a significant inverse correlation between arterial bradykinin and mean arterial pressure ( r 2 = 0.2137, P = .010) and a significant correlation between arterial bradykinin and tissue-type plasminogen activator antigen concentrations ( r 2 = 0.174, P = .022) during CPB. Tissue-type plasminogen activator antigen was significantly higher in the ACE inhibitor group than in the no ACE inhibitor group (18.0 +/- 7.8 ng/mL versus 12.4 +/- 4.5 ng/mL, P = .016) but not in smokers compared with nonsmokers ( P = .451). CONCLUSION: Preoperative ACE inhibitors and smoking potentiate the kinin response to CPB and may contribute to the hemodynamic and fibrinolytic response observed during CPB.
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Pretorius et al. (2004) conducted an RCT in Coronary artery bypass surgery (n=31). Continuation of ACE inhibitors vs. Discontinuation of ACE inhibitors 48 hours before surgery was evaluated on Arterial bradykinin concentrations during cardiopulmonary bypass (p=0.017). Continuation of ACE inhibitors until coronary artery bypass surgery resulted in significantly higher arterial bradykinin concentrations compared with discontinuation 48 hours prior (P=0.017).
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