Iatrogenic Myocardial Edema: Increased Diastolic Compliance and Time Course of Resolution in Vivo

BackgroundPerfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals.MethodsEdema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion.ResultsIn the edema group, average left ventricular mass (132 ± 7 standard error of the mean versus 106 ± 4 g) and ventricular stiffness constant (0.15 ± 0.02 versus 0.05 ± 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 ± 6 versus 116 ± 4 g) and ventricular stiffness (0.06 ± 0.01 versus 0.05 ± 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups.ConclusionsCrystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction. Perfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals. Edema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion. In the edema group, average left ventricular mass (132 ± 7 standard error of the mean versus 106 ± 4 g) and ventricular stiffness constant (0.15 ± 0.02 versus 0.05 ± 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 ± 6 versus 116 ± 4 g) and ventricular stiffness (0.06 ± 0.01 versus 0.05 ± 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups. Crystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction.