• Nikolaos Papoutsidakis, Nikolaos Arkadopoulos, Vassilios Smyrniotis, Helen Tzanatos, Konstantinos Kalimeris, Konstantinos Nastos, George Defterevos, Agathi Pafiti, and Georgia Kostopanagiotou.
• Second Department of Surgery, Athens University School of Medicine, Aretaieion Hospital, Athens, Greece.
• Arch Med Sci. 2011 Apr 1; 7 (2): 217223217-23.

IntroductionThere is accumulating clinical evidence that acute liver failure may be regularly associated with myocardial injury. To test this hypothesis in a standardized experimental setting, we used two porcine models of ALF.Material And MethodsIn 14 domestic pigs ALF was induced by either a) surgical devascularization of the liver (DV group, n = 7), or b) partial (70-75%) hepatectomy and ischaemia/reperfusion of the liver remnant for 150 min (I/R group, n = 7). Four additional animals constituted the sham operation group. All animals were monitored for a 12-h period, at the end of which their hearts were harvested. Plasma troponin I (cTnI) and malondialdehyde (MDA) were measured before the operation (baseline) and at 6 h and 12 h postoperatively. The harvested hearts were histologically analysed, appointing a score from 0 (no injury) to 3 (maximum injury) to selected injury indicators.ResultsIn the sham group, all cTnI measurements and total myocardial injury score were zero in all animals. In both ALF groups, plasma cTnI levels increased by the 6(th) and remained elevated up to the 12(th) postoperative hour (p < 0.01 vs. sham animals). Total myocardial injury score and total histological score revealed some extent of myocardial injury. The rise of MDA levels suggests an underlying oxidative mechanism.ConclusionsOur study provides direct evidence of early myocardial injury in the setting of acute liver failure in pigs. The mechanism of injury remains to be elucidated.

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