Cerebral Oxygenation Impairment and S-100β Protein Release During Off-Pump Coronary Artery Revascularization

Abstract

To elucidate the magnitude of global cerebral oxygenation impairment, using cerebral oxygenation indices and S-100β protein as potential markers, during off-pump coronary artery bypass grafting (OPCAB). Prospective cohort study. Tertiary cardiac center. Thirty-five patients undergoing OPCAB. Jugular bulb and arterial blood samples for cerebral oxygenation indices (arterial oxygen and carbon dioxide partial pressures, jugular bulb oxygen saturation, arterial-jugular bulb oxygen content, arterial-jugular carbon dioxide partial pressure, brain oxygen extraction ratio, and estimated respiratory quotient) and S-100β protein determination were collected at anesthesia induction; anterior, inferior, and posterior wall anastomoses; after sternal closure; and 6 hours postoperatively. Concomitant hemodynamic data were obtained. The S-100β determination was extended to 12 and 24 hours postoperatively. Heart positioning for the target vessel exposure induced significant hemodynamic deterioration (p < 0.001). Although cerebral oxygenation indices were influenced adversely by a low-cardiac-output state mainly during vertical heart dislocation (p < 0.001), they remained within normal limits. Hemodynamic and cerebral oxygenation statuses reverted to baseline within 6 hours postoperatively. Similarly, S-100β jugular bulb and arterial protein levels presented a gradual increase, which peaked by the end of surgery (means, 0.54 and 0.62 μg/L, respectively; p < 0.001) and then decreased by the first postoperative day. Jugular bulb-arterial S-100β levels were maximized during posterior wall anastomosis (0.098 μg/L; p < 0.01). Although exposure of the 3 main coronary arteries during OPCAB promotes derangement of the cerebral oxygen indices and S-100β release, this seems to be transient, remains within the near-normal range, and is reversible almost completely 6 hours postoperatively.