Elevation of Plasma Copeptin in Acute Myocardial Infarction in Pigs is Related to Changes in Mean Arterial Blood Pressure but not to Myocardial Ischemia

Background: Copeptin increases early after myocardial infarction (MI). We used a porcine MI model with serial copeptin-testing and assessment of hemodynamic variables to evaluate the trigger for copetin-release and the liberation kinetics of copeptin in MI. Methods: AMI was induced by percutaneous transluminal coronary angioplasty (PTCA). Blood samples were taken in 30-minute intervals. Results: All animals (n=4) had a comparable infarction size (10.02 ± 2.11% of the left ventricle) and elevated troponin T levels. Highest copeptin levels were measured 30 minutes after the beginning of ischemia with a rapid decrease at 60 minutes, while coronary occlusion was still persisting. Animals with high copeptin values showed a significant drop of MAP (37.24% and 54.20% reduction from MAP-baseline). Conclusions: In experimental AMI in four pigs, the infarction-related decrease of MAP seemed to be the trigger for the copeptin increase. Remarkably, copeptin liberation was not correlated with infarction size and copeptin values already decreased while coronary artery occlusion was ongoing.