Jennifer M Watchmaker1, Meher R Juttukonda1, Larry T Davis1, Allison O Scott1, Carlos C Faraco1, Melissa C Gindville2, Lori C Jordan2, Petrice M Cogswell1, Angela L Jefferson3, Howard S Kirshner4, and Manus J Donahue1,4,5
1Radiology & Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States, 2Department of Pediatrics, Division of Pediatric Neurology, Vanderbilt University Medical Center, 3Vanderbilt Memory & Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, 4Department of Neurology, Vanderbilt University Medical Center, 5Department of Psychiatry, Vanderbilt University Medical Center
Synopsis
T2-relaxation-under-spin-tagging (TRUST-MRI) was performed in patients with intracranial stenosis due to
moyamoya for determination of whole-brain oxygen extraction fraction (OEF).
Elevated OEF was observed in this group compared to controls. In15O
PET studies in individuals with intracranial stenosis, it has been shown that
OEF increases regionally when cerebral blood volume (CBV) is inadequate to
maintain cerebral blood flow (CBF) over a normal range, and importantly that
regionally elevated OEF and CBV may be prognostic for recurrent stroke risk.
This work has motivated the development and application of TRUST-MRI for use in
patients with intracranial stenosis at risk for stroke.
Purpose
The overall purpose of this work is to apply
novel multi-modal MRI approaches in sequence to investigate mechanisms of hemodynamic
impairment and compensation adequacy in patients with cerebrovascular disease. More specifically, elevated oxygen extraction
fraction (OEF), is a well-known marker of hemo-metabolic impairment in patients
with cerebrovascular disease based on prior 15O-PET studies1 and MRI methods have more recently been
developed to assess OEF in vivo and without exogenous contrast. The
purpose of this study is to apply multi-modal metabolic (OEF-weighted) and hemodynamic
(cerebral blood flow (CBF)-and cerebrovascular reactivity (CVR)-weighted) MRI
to evaluate mechanisms of parenchymal impairment in patients with hypothesized globally
elevated OEF secondary to bilateral vasculopathy and moyamoya or reduced oxygen
carrying capacity and sickle cell anemia (SCA). The underlying hypothesis is that
OEF is elevated (i) secondary to reduced CBF in patients with moyamoya, and (ii) secondary to reduced blood oxygen carrying capacity in patients with SCA. Methods
All
volunteers provided informed, written consent and were scanned at 3T (Philips
Achieva). T2-relaxataion-under-spin-tagging (TRUST-MRI; Figure 1) was
applied in patients with intracranial stenosis due to moyamoya (n=18), a
population in which OEF is hypothesized to be elevated due to hypoperfusion,
and in patients with SCA (n=18), a population in which OEF is hypothesized to
be elevated due to reduced blood oxygen carrying capacity. Additionally, age-matched
control participants for both the moyamoya cohort (n=43) and SCA cohort (n=11)
were imaged. To determine OEF, CPMG-T2
was calculated in the sagittal sinus for each participant by performing
pair-wise subtraction of the label from the unlabeled control image at four
effective echo times (eTEs)=0, 40, 80, and 160ms. CPMG-T2 was then
converted to venous oxygenation (Yv) using knowledge of blood water T2,
and measured hematocrit2, 3. Arterial
oxygenation (Ya) was measured by pulse oximetry and used to calculate OEF=(Ya-Yv)/Ya.
For CBF determination, pseudo-continuous arterial spin labeling (pCASL) was
applied using ISMRM Perfusion Study Group guidelines4.
For cerebrovascular reactivity (CVR)
determination, BOLD data (spatial resolution: 3.5x3.5x3.5 mm3;
TE/TR=35/2000ms) were acquired during mild hypercapnia (5% CO2) and signal
changes normalized by end tidal CO2 change recorded. Non-parametric
tests were applied to compare study variables (significance: two-sided p<0.05).Results
Moyamoya. OEF values
(mean±s.d.) of moyamoya participants (OEF=0.419±0.083) were significantly (P<0.001)
elevated compared to age-matched controls (Figure 2A; OEF=0.343±0.061). Gray
matter (GM) CBF values (mean±s.d.) of age-matched controls (CBF=49.2±12.5
ml/100g/min) and moyamoya participants (Figure 2B; CBF=44.4±10.7 ml/100g/min)
were determined, and a trend for a reduction in mean GM CBF in moyamoya
participants compared to control participants was observed. SCA. OEF was
significantly elevated in participants with SCA (OEF=0.410±0.056) compared to
age-matched control participants (Figure 2C; OEF=0.359±0.052). GM CBF values in
SCA participants (CBF=85.3±19.4 ml/100g/min) were significantly elevated
compared to age-matched controls (Figure 2D; CBF=51.4±8.6 ml/100g/min). Figure
3 summarizes case examples of structural and functional imaging data from representative
controls and patients. Mean CBF maps for each participant group are shown in Figure 4. In subjects with moyamoya, BOLD-weighted CVR positively trended with CBF
(Figure 5A; ρ=0.43, P=0.073). A significant inverse relationship between OEF
and CBF was observed in patients with moyamoya (Figure 5B; ρ=-0.56, P=0.016), however there was only a weak
and non-significant inverse relationship between CVR and OEF in moyamoya
patients (Figure 5C; ρ=-0.13, P=0.082).Discussion
To our knowledge,
this is the first time elevated whole-brain OEF has been reported in
participants with moyamoya using TRUST-MRI. Inter-subject variation in this
parameter may provide a biomarker of hemodynamic compensation and possibly
stroke risk, which is a logical extension of these initial findings. While the
moyamoya participants as a group exhibited a strong inverse relationship
between CBF and OEF, group-level pCASL-measured CBF was only marginally reduced
in moyamoya subjects relative to control volunteers which may be due to
intravascular signal from delayed blood arrival5. Elevated OEF was only weakly related to
reductions in CVR, consistent with basal CBF level, rather than vascular
reserve capacity, being most closely associated with OEF. In the SCA cohort,
elevated OEF and elevated CBF was detected, consistent with prior studies6.Conclusion
Multi-modal
hemo-metabolic MRI methods were applied in patients with distinct origins of
elevated OEF. Acknowledgements
No acknowledgement found.References
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