Data set from the article Vaini E, Bari V, Fantinato A, Pistuddi V, Cairo B, De Maria B, Ranucci M, Porta A. Causality analysis reveals the link between cerebrovascular control and acute kidney dysfunction after coronary artery bypass grafting. Physiol Meas. 2019 Jul 1;40(6):064006. doi: 10.1088/1361-6579/ab21b1. PMID: 31091519.

Data set from the article Vaini E, Bari V, Fantinato A, et al. Causality analysis reveals the link between cerebrovascular control and acute kidney dysfunction after coronary artery bypass grafting. Physiol Meas. 2019;40(6):064006. Published 2019 Jul 1. doi:10.1088/1361-6579/ab21b1

This is the abstract:

Background: Patients undergoing coronary artery bypass graft (CABG) surgery might experience postoperative complications and some of them, such as acute kidney dysfunction (AKD), are the likely consequence of hypoperfusion. We hypothesized that an impaired cerebrovascular control is a hallmark of a vascular damage that might favor AKD after CABG.

Objective: Our aim is to characterize cerebrovascular control in CABG patients through the assessment of the relationship between mean arterial pressure (MAP) and mean cerebral blood flow velocity (MCBFV) and to check whether markers describing MCBFV-MAP dynamical interactions could identify subjects at risk to develop postoperative AKD.

Approach: MAP and MCBFV beat-to-beat series were extracted from invasive arterial pressure and transcranial Doppler recordings acquired simultaneously in 23 patients just before CABG after the induction of propofol general anesthesia. Subjects were divided into AKD group (n = 9, age: 68 ± 9, 8 males) and noAKD group (n = 14, age: 65 ± 8, 12 males) according to whether they developed postoperative AKD or not after CABG. We computed MAP and MCBFV time-domain and spectral markers as well as MCBFV-MAP cross-spectral indexes in very-low-frequency (VLF, 0.02-0.07 Hz), low-frequency (LF, 0.07-0.15 Hz) and high-frequency (HF, 0.15-0.30 Hz) bands. We also calculated model-based transfer entropy (TE) to quantify the degree of MCBFV dependence on MAP and vice versa. The null hypothesis of MCBFV-MAP uncoupling was tested via a surrogate approach associating MAP and MCBFV in different patients.

Main results: Time, spectral and cross-spectral markers had a limited power in separating AKD from noAKD individuals. Conversely, TE from MAP to MCBFV was significantly above the level set by surrogates only in AKD groups and significantly larger than that computed in noAKD.

Significance: The reduced cerebrovascular autoregulation in AKD patients suggest a vascular impairment likely making them more at risk of hypoperfusion during CABG and AKD after CABG.