• Paul Mohacsi, Giovanni Pedrazzinia, Hildegard Tanner, Hans-Ueli Tschanz, Roger Hullin, and Thierry Carrel.
• Cardiology, Swiss Cardiovascular Center Bern, University Hospital (Inselspital), CH-3010, Bern, Switzerland. paul.mohacsi@insel.ch
• Eur. J. Heart Fail. 2002 Mar 1;4(2):175-9.

BackgroundLactic acidosis (LAc) is a common form of metabolic acidosis early after heart transplantation (HTX). The mechanism remains unclear. This study analyzed 13 patients who developed severe LAc after HTX.MethodsFrom a series of 60 consecutive heart transplant patients, we identified 13 patients with LAc in the first hours following HTX. Nine patients with normal or mildly elevated lactate levels (<5.0 mmol/l) were investigated as controls.ResultsThirteen patients developed a moderate or severe LAc (up to 14.6 mmol/l) after HTX. Serum lactate levels increased immediately following surgery with a peak after 6.3+/-1.4 h, spontaneously returning to normal values within 24 h. In contrast to the control group, a significant correlation was found between the maximal serum lactate level and the maximal dosage of inotropic drugs (r=0.93, P<0.02), administered during the reperfusion phase and continued for 12-24 h postoperatively. No correlation was found between LAc and blood gas analysis during extracorporeal perfusion period.ConclusionLAc can occur after HTX and seems to be related to the inotropic support of the graft. In contrast to other forms, LAc after HTX has an excellent prognosis and resolves rapidly and spontaneously without treatment. The fact that inotropic support during and immediately after cardiac transplantation can enhance preexisting severe peripheral metabolic cellular dysfunction remains hypothetical.

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