Cardioprotective effects of acute normovolemic hemodilution in patients with severe aortic stenosis undergoing valve replacement.
BACKGROUND
After acute normovolemic hemodilution (ANH), improvement of the rheologic conditions may contribute to optimize tissue oxygen delivery and attenuate ischemia-reperfusion injuries. It was hypothesized that ANH would confer additional cardioprotection in patients with ventricular hypertrophy undergoing open heart surgery.


METHODS
This study was a randomized controlled trial. Forty patients scheduled for elective aortic valve replacement were randomly assigned to a control group (standard care) or an ANH group (target hematocrit level of 28%). All patients were managed with standard myocardial preservation techniques (cold blood cardioplegia, anesthetic preconditioning). The outcome measures included the release of myocardial enzymes, perioperative hemodynamic changes, the need for pharmacologic cardiovascular support, and cardiac complications.


RESULTS
In the ANH group, the postoperative release of troponin I (mean peak plasma concentrations, 1.7 ng/mL; 95% confidence interval, 1.4-2.1 ng/mL) and myocardial fraction of creatine kinase (22 U/L; range, 18-24 U/L) was significantly lower than in the control group (3.6 [range, 3.0-4.2] ng/mL and 45 [range, 39-51] U/L, respectively). In addition, requirement for inotropic support was significantly lower and fewer hemodiluted patients presented adverse cardiac events. After ANH, there was a significant decrease in heart rate (-11 +/- 6%) and rate-pressure product (-16 +/- 8%) until the aortic cross-clamping time and, at the end of surgery, the circulating levels of erythropoietin (EPO) were higher than in control patients (13.6 +/- 4.2 mUI/mL vs. 7.3 +/- 2.4 mUI/mL; p < 0.05).


CONCLUSIONS
Besides conventional cardiac preservation techniques, preoperative ANH further attenuates myocardial injuries. Optimization of preischemic myocardial oxygen delivery and/or consumption and the postconditioning effects of endogenous EPO are potential mechanisms for ANH-induced cardioprotection.
Licker
Marc
M
Department of Anesthesiology, Pharmacology and Surgical Intensive Care, University Hospital of Geneva, Geneva, Switzerland. marc-joseph.licker@hcuge.ch
Sierra
Jorge
J
Kalangos
Afksendiyos
A
Panos
Aristote
A
Diaper
John
J
Ellenberger
Christoph
C
D000368:Aged; D001024:Aortic Valve Stenosis / Q000000981:diagnostic imaging / Q000601:surgery* / Q000628:therapy*; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D004452:Echocardiography; D004562:Electrocardiography; D004921:Erythropoietin / Q000097:blood; D005260:Female; D019918:Heart Valve Prosthesis Implantation; D006438:Hemodilution / Q000379:methods*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000601:surgery / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology; D011300:Preoperative Care; D012720:Severity of Illness Index; D016896:Treatment Outcome; D019210:Troponin I / Q000378:metabolism
D019210:Troponin I; D004921:Erythropoietin; D052279:Creatine Kinase, MB Form