http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-54390 A METABOLIC PROTECTIVE STRATEGY COULD IMPROVE LONG-TERM SURVIVAL IN PATIENTS WITH LV- DYSFUNCTION UNDERGOING CABG

A metabolic protective strategy could improve long-term survival in patients with LVdysfunction undergoing CAB

E-LIB Elektronische Bibliothek Bremen - Internet Publisher - Open Archives Initiative - OAI

Vortrag auf der 6. GBV-Verbundkonferenz an der deutschen Zentralbibliothek für Wirtschaftswissenschaften in Kiel - 04.09.200

A metabolic protective strategy could improve long-term survival in patients with LV-dysfunction undergoing CABG

Objective. Adverse outcome after CABG is closely related to postoperative heart failure precipitated by ischemia and myocardial infarction. Restrictive use of inotropes is therefore desirable. Patients with preoperative left ventricular dysfunction are a high-risk group in this respect. To reduce myocardial oxygen expenditure we evolved a metabolic strategy for perioperative care. Design. Observational study on 104 consecutive patients with severe left ventricular dysfunction undergoing CABG. The metabolic strategy implied physiological measures to minimize myocardial oxygen expenditure including restrictive use of inotropes and specific measures such as extended CPB and metabolic support to facilitate myocardial recovery. Hemodynamic state was primarily assessed by mixed venous oxygen saturation (SvO(2)). Follow-up averaged 9.7 +/- 1.4 years. Results. LVEF was 0.30 +/- 0.05 (range 0.20-0.37) and 3.5 +/- 1.3 vessels were bypassed. Inotropes were used in 6.7% for weaning from CPB. Increase of s-creatinine by andgt;= 50% compared to preoperative values was observed in 2.9%. Logistic EuroSCORE was 8.3% whereas observed 30-day mortality was 1.0%. Crude 5-year survival was 89.4%. Conclusions. The metabolic strategy allowed restrictive use of inotropes and was associated with encouraging long-term survival. Renal function was well preserved suggesting that SvO(2) served as an adequate marker of circulation. Randomized trials with metabolic support are warranted.Original Publication:Rolf Svedjeholm, Marten Vidlund, Ingemar Vanhanen and Erik Hakanson, A metabolic protective strategy could improve long-term survival in patients with LV-dysfunction undergoing CABG, 2010, SCANDINAVIAN CARDIOVASCULAR JOURNAL, (44), 1, 45-58.http://dx.doi.org/10.3109/14017430903531008Copyright: Informa Healthcarehttp://informahealthcare.com

Metabolic and hemodynamic effects of intravenous glutamate infusion early after coronary operations

AbstractAmino acids, particularly glutamate, have been proposed to play an important role in the recovery of cardiac oxidative metabolism after ischemia. In this investigation, the metabolic and hemodynamic effects of glutamate infusion after coronary operations were studied. From 220 to 240 ml 0.1 mol/L l-glutamic acid solution was infused in 10 patients during 1 hour starting 2 hours after operation. A control group of 10 patients received an infusion of 240 ml saline solution. During glutamate infusion, there were significant increases in the uptake of glutamate (from 0.7 ± 0.2 μmol/min in the basal state to a peak of 5.7 ± 1.2 μmol/min at 20 minutes) and lactate (from 4.9 ± 2.0 μmol/min in the basal state to 14.1 ± 4.4 μmol/min at 60 minutes; p < 0.01), whereas the uptake and release of other substrates remained essentially unaffected. Arterial glutamate levels (in whole blood) increased from 103 ± 10 μmol/L to 394 ± 20 μmol/L at 60 minutes. Thirty minutes after discontinuation of the glutamate infusion, arterial levels had decreased to 129 ± 17 μmol/L. The markedly improved utilization of lactate and the unchanged release of alanine together suggest that the oxidative metabolism of the heart was stimulated by glutamate. The metabolic changes were associated with improved myocardial performance. Left ventricular stroke work index increased from 26.8 ± 2.1 gm · beat-1 · m-2 body surface area to 31.3 ± 3.1 gm · beat-1 · m-2 body surface area during glutamate infusion. Metabolic support with amino acids may provide a means to improve recovery of metabolic and hemodynamic function of the heart early after cardiac operations. (J Thorac Cardiovasc Surg 1996;112:1468-77