We assessed the effect of surgical aortic valve replacement (SAVR) on cardiovascular and cerebrovascular controls via spontaneous variability analyses of heart period, approximated as the temporal distance between two consecutive R-wave peaks on the electrocardiogram (RR), systolic, diastolic and mean arterial pressure (SAP, DAP and MAP) and mean cerebral blood flow (MCBF). Powers in specific frequency bands, complexity, presence of nonlinear dynamics and markers of cardiac baroreflex and cerebral autoregulation were calculated. Variability series were acquired before (PRE) and after (POST) SAVR in 11 patients (age: 76±5 yrs, 7 males) at supine resting and during active standing. Parametric spectral analysis was performed based on the autoregressive model. Complexity was assessed via a local nonlinear prediction approach exploiting the k-nearest-neighbor strategy. The presence of nonlinear dynamics was checked by comparing the complexity marker computed over the original series with the distribution of the same index assessed over a set of surrogates preserving distribution and power spectral density of the original series. Cardiac baroreflex and cerebral autoregulation were estimated by assessing the transfer function from SAP to RR and from MAP to MCBF and squared coherence function via the bivariate autoregressive approach. We found that: i) orthostatic challenge had no effect on cardiovascular and cerebrovascular control markers in PRE; ii) RR variance was significantly reduced in POST; iii) complexity of SAP, DAP and MAP variabilities increased in POST with a greater likelihood of observing nonlinear dynamics over SAP compared to PRE at supine resting; iv) the amplitude of MCBF variations and MCBF complexity in POST remained similar to PRE; v) cardiac baroreflex sensitivity decreased in POST, while cerebrovascular autoregulation was preserved. SAVR induces important changes of cardiac and vascular autonomic controls and baroreflex regulation in patients exhibiting poor reactivity of cardiovascular regulatory mechanisms, while cerebrovascular autoregulation seems to be less affected.

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.

No abstract

A preoperative disturbance of the microcirculation is associated with a greater postoperative platelet dysfunction. Endothelial damage, chemical and mechanical stimuli are the possible link between the two patterns.

Coronary artery bypass graft (CABG) surgery may lead to postoperative complications such as the acute kidney dysfunction (AKD), identified as any post-intervention increase of serum creatinine level. Cardiovascular control reflexes like the baroreflex can play a role in the AKD development. The aim of this study is to test whether baroreflex sensitivity (BRS) estimates derived from non-causal and causal approaches applied to spontaneous systolic arterial pressure (SAP) and heart period (HP) fluctuations can help in identifying subjects at risk of developing AKD after CABG and which BRS estimates provide the best performance. Electrocardiogram and invasive arterial pressure were acquired from 129 subjects (67 ± 10 years, 112 males) before (PRE) and after (POST) general anesthesia induction with propofol and remifentanil. Subjects were divided into AKDs (n = 29) or no AKDs (noAKDs, n = 100) according to the AKD development after CABG. The non-causal approach assesses the transfer function from the HP-SAP cross-spectrum in the low frequency (LF, 0.04–0.15 Hz) band. BRS was estimated according to three strategies: (i) sampling of the transfer function gain at the maximum of the HP-SAP squared coherence in the LF band; (ii) averaging of the transfer function gain in the LF band; (iii) sampling of the transfer function gain at the weighted central frequency of the spectral components of the SAP series dropping in the LF band. The causal approach separated the two arms of cardiovascular control (i.e., from SAP to HP and vice versa) and accounted for the confounding influences of respiration via system identification and modeling techniques. The causal approach provided a direct estimate of the gain from SAP to HP by observing the HP response to a simulated SAP rise from the identified model structure. Results show that BRS was significantly lower in AKDs than noAKDs during POST regardless of the strategy adopted for its computation. Moreover, all the BRS estimates during POST remained associated with AKD even after correction for demographic and clinical factors. Non-causal and causal BRS estimates exhibited similar performances. Baroreflex impairment is associated with post-CABG AKD and both non-causal and causal methods can be exploited to improve risk stratification of AKD after CABG.