ABSTRACT
Myocardial revascularization has been known to not affect the prognosis in some patients. Coronary artery bypass graft (CABG) failure may develop one year after CABG surgery. This is accompanied by a high risk of developing myocardial infarction after complete myocardial revascularization in obstructive coronary artery disease (CAD) due to microvascular dysfunction. The study of microvascular dysfunction using intraoperative stress tests with adenosine triphosphate (ATP) allows for the assessment of the coronary bypass flow reserve (CBFR) and the risk of graft failure one year after surgery. The study included 79 CAD patients (238 grafts) who underwent dynamic single-photon emission computed tomography (SPECT) before CABG and dynamic transit time flow measurement (TTFM) during CABG at rest and at stress. The CBFR was calculated by the ratio of the mean graft flow (MGF) at stress to the MGF at rest. A multivariate regression model showed that the MGF at rest (p = 0.043), the MGF at stress (p = 0.026) and the CBFR (p = 0.0001) were significant independent predictors of graft failure. As a result of ROC analysis, the threshold CBFR < 1.67 units correlated with graft failure more closely (sensitivity 82%, specificity 90%) The CBFR is a significant independent predictor of graft failure for up to 16 months.
ABSTRACT
Performing cardiac surgery under cardiopulmonary bypass (CPB) and circulatory arrest (CA) provokes the development of complications caused by tissue metabolism, microcirculatory disorders, and endogenous nitric oxide (NO) deficiency. This study aimed to investigate the potential mechanisms for systemic organoprotective effects of exogenous NO during CPB and CA based on the assessment of dynamic changes in glycocalyx degradation markers, deformation properties of erythrocytes, and tissue metabolism in the experiment. A single-center prospective randomized controlled study was conducted on sheep, n = 24, comprising four groups of six in each. In two groups, NO was delivered at a dose of 80 ppm during CPB ("CPB + NO" group) or CPB and CA ("CPB + CA + NO"). In the "CPB" and "CPB + CA" groups, NO supply was not carried out. NO therapy prevented the deterioration of erythrocyte deformability. It was associated with improved tissue metabolism, lower lactate levels, and higher ATP levels in myocardial and lung tissues. The degree of glycocalyx degradation and endothelial dysfunction, assessed by the concentration of heparan sulfate proteoglycan and asymmetric dimethylarginine, did not change when exogenous NO was supplied. Intraoperative delivery of NO provides systemic organoprotection, which results in reducing the damaging effects of CPB on erythrocyte deformability and maintaining normal functioning of tissue metabolism.