Anemia as a Risk Factor for Organ Dysfunctions in Patients Operated on Heart Valves.

Aim      To study the effects of pre- and postoperative anemia on the risk and the structure of internal organ dysfunction in patients undergoing surgery for acquired heart diseases (AHD).Material and methods  This was a retrospective cohort study including 610 primarily operated patients with AHD. A comparative analysis of the incidence and the structure of internal organ dysfunction was performed, and the likelihood of intraoperative hemotransfusion was determined for patients with preoperative anemia (Hb <130 g/l) and without it. The incidence and the nature of internal organ damage were compared in patients with postoperative Hb < 90 g/l and 90-130 g/l.Results The presence of postoperative anemia detected in 45 % of patients at two days after the surgery 6-fold increased the risk of acute heart failure (odds ratio [OR], 5.75; 95 % confidence interval [CI], 1.23-26.84; р=0.016), 4-fold increased the risk of multiorgan failure (MOF) (OR, 4.2; 95 % CI, 1.16-15.64; р=0.03), and 5-fold increased the likelihood of hemotransfusion (OR, 4.74; 95 % CI, 3.12-7.19; р<0.0001). Severe and moderate anemia (Hb <90 g/l) was observed in 11.2 % of patients, which presence 6-fold increased the risk of brain dysfunction (OR, 5.72; 95 % CI, 2.17-15.06; р=0.001) and MOF (OR, 5.97; 95 % CI, 1.94-18.35; р=0.004) compared to patients with Hb 90-130 g/l.Conclusion      In patients with AHD, postoperative anemia increases the risk of circulatory decompensation at two days after the surgery and of MOF and also increases the likelihood of intraoperative hemotransfusion; postoperative anemia with Hb <90 g/l increases the risk of brain damage and MOF.

Perinatal hypoxic-ischemic brain injury affects the glutamatergic signal transduction coupled with neuronal ADP-ribosyl cyclase activity.

Agonists of glutamate ionotropic (NMDA) and metabotropic receptors (mGluRI and mGluRIII) had the regulatory effect on ADP-ribosyl cyclase/CD38 activity in cerebellar granular cells of newborn rats. Perinatal hypoxic-ischemic brain injury was followed by dysregulation of this mechanism.