Methylprednisolone and Endothelial Dysfunction in Cardiac Surgery: A Pilot Randomized Trial
Abstract
Background
Cardiac surgery involving cardiopulmonary bypass (CPB) serves as a clinical model of ischemia–reperfusion injury and endothelial dysfunction. Endothelial injury is often manifested clinically by vasoplegia and microcirculatory disturbances. The administration of a single dose of corticosteroids at the time of anesthesia induction has been hypothesized to exert a protective effect.
Methods
In this parallel-group, randomized, controlled single-center trial, patients scheduled for elective cardiac surgery with CPB were assigned to receive intravenous methylprednisolone or placebo at anesthesia induction. The primary outcome was the occurrence of endothelial dysfunction, assessed using flow-mediated dilation (FMD) during a vascular occlusion test. Secondary outcomes included peripheral tissue reperfusion slope measured by near-infrared spectroscopy (NIRS StO2) and syndecan-1 levels, variations of FMD, NIRS StO2, and syndecan-1 over time, and the correlation between the three measurements.
Results
Thirty-nine patients were assigned to receive either methylprednisolone (n = 20) or placebo (n = 20). Maximal post-CPB median FMD was 5.7% (IQR: 3.4%–7.0%) in the methylprednisolone group and 4.7% (2.2%–6.6%) in the placebo group (difference: 0.60, 95% CI: −1.5 to 2.7; p = 0.57). On the first postoperative day, median FMD was 6.9% (3.6%–9.8%) in the methylprednisolone group and 8.1% (4.3%–11.6%) in the placebo group (difference: −1.0, 95% CI: −3.6 to 1.6; p = 0.46). No other significant differences between groups were observed for other measurements. A significant correlation was found between the severity of FMD alteration and syndecan-1 levels (r = 0.21, p = 0.03).
Conclusions
Methylprednisolone did not significantly affect CPB-associated endothelial dysfunction markers in elective cardiac surgery patients. Nevertheless, a correlation between syndecan-1 levels and the peak arterial dilation suggests a link between the severity of glycocalyx damage and vascular reactivity.