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The effect of Ventricular Assist Devices on cerebral autoregulation: A preliminary study Bellapart, Judith; Chan, Gregory S; Tzeng, Yu-Chieh; Ainslie, Philip; Barnett, Adrian G; Dunster, Kimble R; Boots, Rob; Fraser, John F Feb 22, 2011

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RESEARCH ARTICLE Open AccessThe effect of Ventricular Assist Devices oncerebral autoregulation: A preliminary studyJudith Bellapart1,2*, Gregory S Chan3, Yu-Chieh Tzeng4, Philip Ainslie5, Adrian G Barnett6, Kimble R Dunster7,Rob Boots1, John F Fraser2AbstractBackground: The insertion of Ventricular Assist Devices is a common strategy for cardiovascular support inpatients with refractory cardiogenic shock. This study sought to determine the impact of ventricular assist deviceson the dynamic relationship between arterial blood pressure and cerebral blood flow velocity.Methods: A sample of 5 patients supported with a pulsatile ventricular assist device was compared with 5 controlpatients. Controls were matched for age, co-morbidities, current diagnosis and cardiac output state, to cases. Beat-to-beat recordings of mean arterial pressure and cerebral blood flow velocity, using transcranial Doppler wereobtained. Transfer function analysis was performed on the lowpass filtered pressure and flow signals, to assess gain,phase and coherence of the relationship between mean arterial blood pressure and cerebral blood flow velocity.These parameters were derived from the very low frequency (0.02-0.07 Hz), low frequency (0.07-0.2 Hz) and highfrequency (0.2-0.35 Hz).Results: No significant difference was found in gain and phase values between the two groups, but the lowfrequency coherence was significantly higher in cases compared with controls (mean ± SD: 0.65 ± 0.16 vs 0.38 ±0.19, P = 0.04). The two cases with highest coherence (~0.8) also had much higher spectral power in mean arterialblood pressure.Conclusions: Pulsatile ventricular assist devices affect the coherence but not the gain or phase of the cerebralpressure-flow relationship in the low frequency range; thus whether there was any significant disruption of cerebralautoregulation mechanism was not exactly clear. The augmentation of input pressure fluctuations might contributein part to the higher coherence observed.BackgroundVentricular assist devices (VAD) are mechanical pumpsthat replace or augment left and/or right ventricularfunction in cases of refractory cardiogenic shock.A number of approaches are currently taken related tothe indications of these devices: VAD can be used as abridge to heart transplantation, as a bridge to myocar-dial recovery leading in some cases to their prolongeduse with meaningful survival and improved quality oflife [1]. Recently VAD have also begun to be used as a“bridge to destination” that is, they are the final plan forthe patient, being used for many years, until the patientsuccumbs.Fundamental differences regarding cardiac output andsystemic circulation distinguish two main types of VAD:pulsatile and continuous-flow VAD. The main advan-tages of continuous-flow VAD being the self-containednature, not requiring a pneumatic driver, longevity, lackof bearing contacting with blood and absence of artifi-cial valves with theoretically smaller thrombogenic sur-face [2]. However, the effects of non-pulsatile perfusionon end-organ function remain controversial [3-5]. Pulsa-tile circulation and its effects on systemic vascular resis-tances have been related to the improvement ofmicrocirculation and endothelial integrity [6,7]; reduc-tion in splanchnic perfusion and reduction of intestinaledema [8]; improvement of the cerebral haemodynamicsand cerebrospinal fluid drainage [2] and the mainte-nance of neuro-endocrine cascades, specifically within* Correspondence: 30489jbr@comb.es1Department of Intensive Care, Royal Brisbane and Women’s Hospital.Butterfield Street, Herston (4029), QLD, AustraliaFull list of author information is available at the end of the articleBellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4© 2011 Bellapart et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andreproduction in any medium, provided the original work is properly cited.the renin-angiotensine system and catecholamine release[5].Despite the use of pulsatile VADs, non-homogeneousoutput is often generated as pulsatile VADs eject oncethe pre-established filling volume (stroke volume) hasbeen reached. Therefore, the VAD ejection rate variesdepending on preload and systemic resistance. Fre-quently there is a variable degree of persistent nativecardiac contractibility, leading to asynchrony, and irre-gularities in arterial blood pressure waveform (Figure 1).In such situations of circulatory irregularity, end-organperfusion such as cerebral blood flow may require anintact autoregulation to ensure stable microcirculation.Cerebral autoregulation is the mechanism by whichcerebral blood flow (CBF) is maintained despite changesin cerebral perfusion pressure (CPP). Cerebral autoregu-lation mediates states of hyperemia and ischemia toavoid vasogenic edema or infarction respectively [9].Impaired autoregulation has been regarded as a risk fac-tor associated with adverse neurological outcome aftercardiac surgery [10,11]. As a dynamic phenomenon,cerebral autoregulation may respond to spontaneousand induced changes in arterial blood pressure (BP)such as those occurring with pulsatile VADs [12,13].Cerebral autoregulation has been extensively studiedusing transcranial Doppler (TCD) which measures cere-bral blood flow velocities (CBFV) as a surrogate of CBF[14,15] using a variety of methods [16]. From alldescribed methods, transfer function analysis (TFA)enables the analysis of phase shift, gain and coherencebetween two signals (arterial BP as input and CBFV asoutput) at a range of frequencies, and has the advantageof being applicable for continuous and non-invasivetesting of cerebral autoregulation at the bedside.Rider and coworkers assessed cerebral autoregulationin patients supported with non-pulsatile VADs, byexposing them to dynamic maneuvers such as head-uptilting and measuring the change in CBFV. They foundthat cerebral autoregulation was impaired, suggestingthat circulatory pulsatility is crucial for the maintenanceof cerebral autoregulation [17]. However, their studyoccurred during the acute phase of the disease, after theFigure 1 Real time, beat-to-beat traces of arterial blood pressure (BP) and cerebral blood flow velocity (CBFV) with a ventricular assistdevice (VAD). Upper channel: arterial BP waveform in a patient supported with a VAD, showing irregular fluctuations; middle channel: CBFV(insonated at the level of middle cerebral artery) with fluctuations transmitted from arterial BP; lower channel: electrocardiogram (ECG).Bellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 2 of 8insertion of a non-pulsatile VAD and prior to any myo-cardial “modeling” [18] could have occurred. Someauthors have demonstrated that even with the use ofnon-pulsatile VAD, if a recovery time is allowed, CBFshows recovery of its pulsatility [2], attributing this find-ing to overall myocardial recovery and specifically rightventricular recovery. Whilst previous study examinedthe effects of non-pulsatile VAD on the regulation ofsteady state CBF, this study is the first to investigate theeffects of pulsatile VAD, which generates irregular pres-sure waveform patterns, on the dynamic cerebral pres-sure-flow relationship by applying the cross-spectralTFA technique.MethodsInstitutional Ethics Committee approval for the perfor-mance of the study was granted. All patients or theirnext of kin gave informed consent prior to enrolment inthe study.A convenience sample of five patients supported witha pulsatile Thoratec VAD (Thoratec corporation, Plea-senton, CA, US) was compared with five controlpatients, matched for age, comorbidities, current diagno-sis and cardiac output state (Table 1). All cases weresupported with a left ventricular pulsatile VAD and ino-tropic drugs for an average of 7 days. All patients werein their acute phase of their disease. Control subjectswere in a low output state requiring inotropic or vaso-pressor support but without the support of VAD.Although their mean arterial blood pressure (MAP) wassimilar to the VAD cases, their native left ventricularejection fraction (LV EF) was better. All patients in thecontrol group survived, whereas 2 of the VAD casesdied (Table 2).We recorded at least 5 minutes of data under restingconditions in all subjects. Simultaneous beat-to-beatrecordings of BP and cerebral blood flow velocity (CBFV)waveforms were sampled using a data acquisition unit(ADInstruments, Australia). The BP waveform wasacquired from an intra-arterial catheter; CBFV of middlecerebral artery (MCA) was measured using a transcranialDoppler device with a 2 MHz probe and a power of 100mW/cm2 (DWL, Germany). CBFV of middle cerebralarteries (MCAs) were measured using TCD followingreferenced criteria at the temporal acoustic window [15].Both MCAs were insonated and the side with best acousticcharacteristics chosen for study. Intra-patient variabilitywas minimized by using only one investigator formallytrained in TCD [16]. Stability of the insonated vessel dia-meter was assumed by maintaining a stable partial pressureof arterial carbon dioxide (pCO2) during measurements.Therapeutic and clinical variables were recorded at themoment of data acquisition. This study was merelyobservational and did not interfere with the treatingphysician’s management plan.Spectral AnalysisFor the assessment of cerebral autoregulation, this studyused TFA based on frequency domain cross-spectralanalysis. TFA assesses the relationship between two sig-nals in the frequency domain and yields three interpre-table parameters (i.e. gain, phase, and coherence). Gainis the indicator of the magnitude with which the changeof output signal (i.e. CBFV) is caused by the change ofinput signal (i.e. BP). In the context of cerebral autore-gulation analysis, a small gain indicates that cerebralblood flow does not change significantly when bloodpressure changes, indicating that the cerebral autoregu-latory mechanisms are intact. Phase shift relates to thetemporal lag between BP and CBFV at each frequency.Zero phase lag signifies synchronous fluctuations, whilstpositive phase suggests CBFV leading BP, and negativephase suggests BP leading CBFV.The gain and phase metrics, however, need to beinterpreted in the context of the cross-spectral coher-ence, which is an estimation of the linear correlationbetween the input and output signals at particular fre-quencies. Coherence varies between 0 and 1; where 0indicates no linear relationship and 1 indicates perfectlinear relationship. It has been suggested that anincrease in coherence may be indicative of a bluntedcerebral autoregulation [21]. A low coherence, however,can be interpreted as presence of external noise/input,or nonlinear/lack of relationship between input andoutput.In this study, spectral analysis was performed on5 min artifact-free segments of continuous CBFV andBP signals. Signals were downsampled to 1 Hz afterappropriate anti-aliasing lowpass filtering, with any slowtrend removed by cubic spline detrending. The fre-quency spectra and transfer function were obtainedusing the Welch method [21]. This involved subdividingTable 1 Demographics and patients’ characteristicsVAD Age (years) Pathology comorbidities day of admissionVAD1 52 MI none day 2VAD2 43 MI hypertension day 29VAD3 25 OHCA + MI none day 25VAD4 35 OHCA hypertension day 7VAD5 63 OHCA hypertension day 25ControlC1 64 MI none day 5C2 65 MI hypertension day 4C3 69 OHCA + MI hypertension day 3C4 55 OHCA hypertension day 3C5 50 OHCA hypertension day 2MI: Myocardial infarct; OHCA: Out of hospital cardiac arrest.Bellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 3 of 8the signal into 120s segments with 75% overlap (result-ing in 7 segments), multiplying each segment with aHanning window, then performing a Fast Fourier Trans-form (FFT), and finally averaging to give the spectra.Defining the autospectra of BP and CBFV as Sxx(f) andSyy(f) (with f denoting frequency), the cross-spectrum ofBP and CBFV, Sxy(f), was computed as the product ofSxx*(f) and Syy(f) (asterisk denotes the complex conjugate).The transfer function from BP to CBFV was computedas H(f) = Sxy(f)/Sxx(f), and the gain magnitude and phaseangle of the transfer function was obtained accordingly.The magnitude-squared coherence function was com-puted as g2(f) = |Sxy(f)|2/Sxx(f)Syy(f), for detecting linearcorrelation between the spectral components in the twosignals. Coherence ranged from 0 (lack of linear correla-tion) to 1 (perfect linear relationship).The spectral powers of BP and CBFV and the meanvalues of the transfer function gain, phase and coher-ence were calculated in the very low frequency (VLF,0.02-0.07 Hz), low frequency (LF, 0.07-0.20 Hz) andhigh frequency (HF, 0.20-0.35 Hz) ranges as previouslydefined [22]. Unpaired Student’s t-test was performed tocompare the variables between the VAD and the controlgroups. P < 0.05 was considered statistically significant.ResultsThe patient characteristics are presented in table 1 and 2.No significant difference in MAP, pCO2 and LVEF wasfound between the VAD and the control groups. Thelevels of pCO2 were maintained within normal rangesand stable throughout the study, thus the effect of CO2on cerebral vessel was minimised. LVEF was generallylower for the VAD cases, whichwas expected as thesewere patients with baseline refractory cardiogenic shockwho required a VAD for life support. However the differ-ence did not reached statistical significance.The results from spectral and cross-spectral transferfunction analysis of MAP and CBFV were presented intable 3 and 4. Display of gain, phase and coherence fora representative case and control are shown in figures 2and 3 respectively. No significant difference was foundbetween the VAD and the control groups, apart from asignificantly higher LF coherence between MAP andCBFV in the VAD cases (P = 0.04).DiscussionIn this study, the cross-spectral transfer function analy-sis technique was applied to study the dynamic relation-ship between systemic BP and CBFV in patients usingpulsatile VAD. The rationale was to describe any poten-tial alteration of cerebral autoregulation function asso-ciated with the use of VAD, as the long term use ofVAD may lead to impaired cerebral autoregulation andworse neurological outcomes.The key finding of the study was the higher coherencebetween MAP and CBFV in the VAD patients comparedwith the controls, at the LF range. A low coherencebetween MAP and CBFV (<0.5)indicates a lack of linearrelationship between pressure and flow at the particularfrequency range, and can be attributed to the presenceof an intact cerebral autoregulation that introduces non-linearity relationship [21,22]. It has been suggested thatthe complex nonlinear behavior of the cerebral vascula-ture might be responsible for the low coherences at theVLF and LF ranges [24-26]. The augmented LF coher-ence in the VAD patients, on the other hand, mightsuggest a lower degree of cerebral autoregulation, possi-bly due to disruption of autoregulatory mechanisms byTable 2 Therapy and clinical variablesVAD Support therapy MAP (mmHg) CBFV (cm/s) PCO2 (mmHg) LV EF (%) OutcomeVAD1 VAD 82 38 36 35 SurvivedVAD2 VAD 96 47 40 30 SurvivedVAD3 VAD + DPM + NA 60 101 42 20 Intrahospital deathVAD4 VAD 74 45 40 20 SurvivedVAD5 VAD + DPM 70 39 32 15 Intrahospital deathMean ± SD 76 ± 14 54 ± 26 38 ± 4 24 ± 8ControlC1 DPM 79 36 42 40 SurvivedC2 DPM 90 43 35 25 SurvivedC3 DPM + DBT 70 53 48 30 SurvivedC4 DPM + NA 75 39 41 30 SurvivedC5 DPM 80 42 37 40 SurvivedMean ± SD 79 ± 7 43 ± 6 41 ± 5 33 ± 7P 0.74 0.36 0.39 0.09VAD: Ventricular Assist Device; MAP: Mean Arterial Pressure; CBFV: cerebral blood flow velocity (mean values are given); LV EF: Left Ventricular Ejection Fraction;NA: Noradrenaline; DPM: Dopamine; DBT: Dobutamine.Bellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 4 of 8the use of VAD. However, one potential limitation tothis interpretation was that, although no significant dif-ference in the MAP power was observed between thetwo groups, the two VAD patients with the highestcoherence (~0.8) also had much higher spectral powerin MAP than the rest of the group. It has been sug-gested that an increased input pressure change mightlead to an increase in coherence, via an improved“signal-to-noise” ratio [27]. This effect might contributein part to the higher coherence in the VAD group.The lack of differences in TFA gain and phase betweenthe VAD and the control group also raised questionswhether there was significant disruption of cerebral auto-regulation by the use of pulsatile VAD. Alterations inTable 3 Power spectrum analysis of mean arterial pressure (MAP) and mean cerebral blood flow velocity (CBFV) inventricular assist device (VAD) cases and controlsVAD VLF LF HFpMAP pCBFV pMAP pCBFV pMAP pCBFVVAD1 0.80 2.77 0.28 0.48 0.94 0.47VAD2 2.34 7.94 2.41 3.77 0.32 1.46VAD3 1.06 3.22 0.20 0.94 8.88 3.72VAD4 3.26 6.55 4.42 3.67 2.15 1.79VAD5 2.97 2.61 0.49 1.14 5.44 2.24Mean ± SD 2.09 ± 1.11 4.62 ± 2.46 1.56 ± 1.84 2.00 ± 1.59 3.55 ± 3.58 1.94 ± 1.19Control VLF LF HFpMAP pCBFV pMAP pCBFV pMAP pCBFVC1 0.47 1.12 1.55 0.80 3.80 0.56C2 1.52 4.92 0.08 0.61 2.44 1.42C3 2.43 6.93 0.10 0.43 2.55 1.69C4 0.95 2.72 0.23 0.65 0.17 0.25C5 0.24 1.20 0.70 1.42 1.98 3.23Mean ± SD 1.12 ± 0.88 3.38 ± 2.51 0.53 ± 0.62 0.78 ± 0.38 2.19 ± 1.31 1.43 ± 1.17P 0.17 0.45 0.27 0.13 0.45 0.52VLF, very low frequency (0.02-0.07 Hz); LF, low frequency (0.07-0.2 Hz); HF, high frequency (0.2-0.35 Hz). pMAP (in mmHg2) and pCBFV (in (cm/s)2) are spectralpowers of MAP and mean CBFV respectively.*P < 0.05 from t-test between VAD and Control.Table 4 Transfer function analysis (TFA) of mean arterial pressure (MAP) and mean cerebral blood flow velocity (CBFV)in ventricular assist device (VAD) cases and controlsVAD VLF LF HFCoh Gain Phase Coh Gain Phase Coh Gain PhaseVAD1 0.67 1.35 1.00 0.65 1.20 -0.38 0.67 0.75 0.51VAD2 0.76 1.82 0.98 0.79 1.25 -0.08 0.68 1.96 0.30VAD3 0.20 0.95 0.32 0.45 1.52 0.27 0.54 1.13 0.21VAD4 0.44 0.89 0.90 0.82 0.83 0.51 0.74 0.79 0.16VAD5 0.45 0.63 1.04 0.56 1.18 0.72 0.77 0.72 0.00Mean ± SD 0.50 ± 0.22 1.13 ± 0.47 0.85 ± 0.30 0.65 ± 0.16 1.20 ± 0.25 0.21 ± 0.44 0.68 ± 0.09 1.07 ± 0.52 0.24 ± 0.19Control VLF LF HFCoh Gain Phase Coh Gain Phase Coh Gain PhaseC1 0.13 0.55 0.73 0.65 0.65 0.62 0.74 0.36 -0.09C2 0.61 1.43 0.63 0.21 1.71 -0.24 0.32 2.29 0.27C3 0.72 1.33 0.33 0.30 1.89 0.07 0.34 2.24 -0.15C4 0.46 1.12 -0.27 0.25 1.07 -0.40 0.28 1.02 -0.18C5 0.25 1.15 -1.71 0.51 1.18 0.76 0.91 1.28 0.21Mean ± SD 0.43 ± 0.25 1.12 ± 0.34 -0.06 ± 1.00 0.38 ± 0.19 1.30 ± 0.50 0.16 ± 0.51 0.52 ± 0.29 1.44 ± 0.83 0.01 ± 0.21P 0.65 0.96 0.089 0.039* 0.69 0.88 0.26 0.42 0.11VLF, very low frequency (0.02-0.07 Hz); LF, low frequency (0.07-0.2 Hz); HF, high frequency (0.2-0.35 Hz). Coh, gain (in cm/s/mmHg) and phase (in rad) are thetransfer function coherence, gain and phase from MAP to mean CBFV.*P < 0.05 from t-test between VAD and Control.Bellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 5 of 8cerebral autoregulation function by pathological condi-tions (such as stroke and autonomic failure [28,29]) aretypically associated with changes in gain and/or phase,which were not observed in the current study. Never-thelss, it appeared that the highpass filtering property ofthe cerebral circulation, characterised by smaller gain atthe lower frequencies (VLF) and an increase in gaintowards the higher frequencies (HF) [21,27], was moreapparent in the control group compared with the VADgroup. It would therefore still be possible that gain prop-erties of cerebral autoregulation might have changed inthe VAD patients, although the interpretation of the gainparameter would have been limited somewhat by the lowcoherences in the control patients.Methodological considerations and limitationsIn this study, direct assessment of CBF was not feasibleas the use of non-imaging TCD does not facilitate themeasurement of the cerebral vessel cross-sectional area.Instead, there is a global consensus supporting the useof CBFV as a surrogate for CBF, provided the vesseldiameter remains stable during the study [30]. Amongall factors intervening in changes of vessel diameter andtherefore determining CBF [23], pCO2 is directly relatedwith vessel diameter and was maintained stable andwithin normal values, during patient recruitment.For TCD recordings, only the MCA with better acous-tic properties was recorded and analyzed. Although spa-tial heterogeneity of cerebral perfusion as well asinterhemispheric differences has been described [30];the endpoint in this study was to ensure the best tran-scranial Doppler recordings in order to minimize thesignal-to-noise ratio and increase data reliability [30].No significant change in gain and phase was foundbetween the two groups in this study, but the smallpopulation recruited could have contributed to the lackof statistical significance, thus further studies with largersample size would be desirable.ConclusionThe use of pulsatile VAD affected the coherence but notthe gain or phase of the cerebral pressure-flow relationshipFigure 2 Transfer function analysis (TFA) of mean arterial pressure (MAP) and cerebral blood flow velocity (CBFV) in a patient withventricular assist device (VAD). The gain, phase and coherence spectra of a representative case with VAD were shown.Bellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 6 of 8in the low frequency range, thus whether there was anysignificant disruption of cerebral autoregulation mechan-ism was not clear. The augmentation of input pressurefluctuations might contribute in part to the higher coher-ence observed. Given the absence of all conditions thatdefine autoregulation, these results should be regarded aspreliminary data, and further studies, employing biggersamples, are warranted.AcknowledgementsWe acknowledge Dr Daniel Mullany for ensuring patients’ availability duringstudy recruitment.This research was supported by a research grant from the Royal BrisbaneHospital Research Foundation (Protocol 2007/076). Additional funding wasprovided by the Prince Charles Hospital Research Foundation.Author details1Department of Intensive Care, Royal Brisbane and Women’s Hospital.Butterfield Street, Herston (4029), QLD, Australia. 2Critical Care ResearchGroup and Department of Intensive Care Medicine, The Prince CharlesHospital and University of Queensland, Rode road, Brisbane, (4032), QLD,Australia. 3Biomedical Systems Laboratory, School of Electrical Engineeringand Telecommunications, University of New South Wales, Sydney, NSW,2052, Australia. 4Cardiovascular Systems Laboratory, Department of Surgeryand Anesthesia, University of Otago, 23 A Mein Street, Newtown, PO Box7343, Wellington, New Zealand. 5Department of Human Kinetics, Faculty ofHealth and Social Development, University of British Columbia Okanagan,Kelowna, Canada. 6Institute of Health and Biomedical Innovation & School ofPublic Health, Queensland University of Technology, 60 Musk Avenue,Brisbane, (4059), Australia. 7Critical Care Research Group, The Prince CharlesHospital. Medical Engineering Research Facility, Queensland University ofTechnology, Australia.Authors’ contributionsJB and JFF conceived and designed the study; JB undertook patient screenand data acquisition; JB drafted the manuscript which was reviewed andamended by all other authors. GC and Y-C T undertook data analysis andcontributed to its interpretation. AGB undertook statistical analysis. KRDconceived and designed the technical components of the study, alsoreviewed revised the manuscript. RB and PA reviewed and amended themanuscript. All authors read and approved the final manuscript.Competing interestsThe authors declare that they have no competing interests.Received: 25 September 2010 Accepted: 22 February 2011Published: 22 February 2011Figure 3 Transfer function analysis (TFA) of mean arterial pressure (MAP) and cerebral blood flow velocity (CBFV) in a control patient.The gain, phase and coherence spectra of a representative control were shown.Bellapart et al. 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Blaber AP, Bondar RL, Stein F, Dunphy PT, Moradshahi P: Transfer FunctionAnalysis of cerebral autoregulation dynamics in Autonomic failurepatients. Stroke 1997, 28:1686-1692.29. Reinhard M, Roth M, Guschlbauer B, Harloff A, Timmer J, Czosnyka M,Hetzel A: Dynamic cerebral autoregulation in acute ischemic strokeassessed from spontaneous blood pressure fluctuations. Stroke 2005,36:1684-1689.30. Lindegaard KF, Lundar T, Wiberg J, Sjoberg D, Aaslid R, Nornes H:Variations in middle cerebral artery blood flow investigated withnoninvasive Transcranial blood velocity measurements. Stroke 1987,18:1025-1030.Pre-publication historyThe pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2253/11/4/prepubdoi:10.1186/1471-2253-11-4Cite this article as: Bellapart et al.: The effect of Ventricular AssistDevices on cerebral autoregulation: A preliminary study. BMCAnesthesiology 2011 11:4.Submit your next manuscript to BioMed Centraland take full advantage of: • Convenient online submission• Thorough peer review• No space constraints or color figure charges• Immediate publication on acceptance• Inclusion in PubMed, CAS, Scopus and Google Scholar• Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submitBellapart et al. BMC Anesthesiology 2011, 11:4http://www.biomedcentral.com/1471-2253/11/4Page 8 of 8

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