Xiaopeng Song1, Bhaswati Roy2, Sadhana Singh1, Ashish Sahib1, Cristina Caberera-Mino2, Gregg C. Fonarow3, Mary A. Woo2, and Rajesh Kumar1,4,5
1Departments of Anesthesiology, University of California at Los Angeles, Los Angeles, CA, United States, 2UCLA School of Nursing, University of California at Los Angeles, Los Angeles, CA, United States, 3Division of Cardiology, University of California at Los Angeles, Los Angeles, CA, United States, 4Radiological Sciences, University of California at Los Angeles, Los Angeles, CA, United States, 5Brain Research Institute, University of California at Los Angeles, Los Angeles, CA, United States
Synopsis
Heart
failure (HF) patients show inability to regulate heart rate and blood pressure
in response to autonomic challenge. Using BOLD-fMRI
and DTI-MD procedures, we found that functional MRI responses during the
Valsalva maneuver in cerebellum and insular are delayed or reduced in
amplitude, and comparable areas showed structural injury in HF subjects. These
findings show that impaired functional responses during the Valsalva maneuver
have brain structural basis in HF condition.
Introduction
Heart failure (HF) patients show inability to
regulate autonomic functions (e.g. heart rate, blood pressure) in response to
autonomic challenges1,2,
in addition to mood and cognitive deficits. The autonomic deficits may stem
from brain tissue injury in central autonomic regulatory areas resulting from
ischemic and hypoxic processes accompanying the condition3,4.
However, the direct evaluation of correlations between structural injury and functional
timing and magnitude of neural signal patterns within affected areas, which
lead to impaired autonomic outflow, is unclear. In this study, we evaluate neural
responses to the Valsalva maneuver with blood oxygen level-dependent functional
magnetic resonance imaging (BOLD-fMRI) and structural changes using diffusion tensor
imaging (DTI)-based mean diffusivity (MD) in HF over control subjects. We
hypothesize that brain areas with structural impairment should also show
aberrant fMRI responses to the Valsalva challenge, and the severity of tissue changes
will be correlated with impaired functional responses in HF subjects.Materials and methods
We collected BOLD-fMRI
data (TR/TE=2000/30 ms; FA=90°; FOV=230×230 mm2; matrix=64×64; slice thickness=4.2mm; volumes=352) from 29 HF (54.2±8.0
years, 22 males, BMI 26.8±5.1 kg/m2) and 35 healthy controls (HC, 51.2±5.9 years, 22 males, BMI 25.4±3.0kg/m2) during the
Valsalva maneuver, which contained a sequence of four 16-second forceful exhalations
into a mouthpiece after 160s baseline period, spaced 120 seconds apart, to a
target expiratory pressure of 30 mmHg. DTI data (TR/TE=12,200/87ms; FA=90°; bandwidth=1,345Hz/pixel; matrix=128×128; FOV=230×230mm2;
slice thickness=1.7mm, diffusion values=0 and 800 s/mm2;
gradient directions=30) were collected from a subset of 19 HF (51.9±7.6
years, 14 males, BMI 27.5±5.2kg/m2) and 24 HC (50.3±6.4 years, 17
males, BMI 25.3±3.1kg/m2). After standard fMRI preprocessing steps,
activation maps from each subject were generated. MD maps were derived from each DTI series, realigned
and averaged, normalized to common space, and smoothed. We performed one-sample
t-tests (FDR corrected P<0.05) to examine brain areas that were activated by
the Valsalva maneuver in HF and HC. We compared brain areas with increased or
decreased neural changes during the Valsalva maneuver between HF and HC using
analysis of covariance (ANCOVA; covariates, age and sex; FDR corrected P<0.05).
We compared the smoothed MD maps between HF (n=19) and control (n=24) subjects
using ANCOVA (FDR corrected P<0.05). Using functional and structural maps
with changes, clusters common in both structural and functional deficits were
determined and overlaid onto background images. Four sites that showed altered MD and/or BOLD activation, including
bilateral cerebellum and anterior insular, were selected as regions of interest
(ROIs). The group-mean BOLD responses of each ROI were calculated by averaging
the standardized ROI time courses across 29 HF and 35 controls over the 4
repeated challenges. We further examined across-subjects correlations between
MD maps and BOLD activation maps in HF subjects (n=19, covariates: age, gender;
Alphasim corrected P < 0.05).Results
The
Valsalva challenge significantly showed increased neural response in multiple
sites, including the bilateral cerebellum, temporal poles, insular, brainstem,
lateral prefrontal, middle occipital, postcentral gyrus, and right inferior
parietal lobule in HC. Similar brain areas showed increased BOLD signal in HF, but
were less extensive. HF patients showed decreased neural activity in the bilateral
posterior cerebellar cortices, vermis, brainstem, postcentral gyrus, precuneus,
paracentral lobule, left anterior insular, and left putamen (Figure 1). Compared
with HC, HF patients showed increased MD (indicative of brain injury) in right posterior
cerebellar, bilateral anterior and posterior insula, ventral medial prefrontal
cortex, dorsal lateral prefrontal gyrus, left ventral lateral prefrontal, bilateral
middle occipital gyrus, cuneus, precuneus, angular, and right postcentral gyrus.
However, no sites emerged with either increased neural responses or decreased
MD values in HF over control subjects. Significant overlap emerged between
neural deficits and structural changes in areas, including the left cerebellum,
left insular, precuneus, and bilateral post-central gyrus in HF over controls
(Figure 2B). ROI analyses showed delayed
neural responses in bilateral cerebellar areas and reduced amplitude in left
insula (Figure 3). Correlation analyses showed that increased MD values are correlated
with lower neural responses in the bilateral cerebellum, insular cortices, and
left putamen in HF (Figure 4).Discussion
HF
showed decreased neural activation in multiple autonomic control areas. Structural
brain changes emerged in similar autonomic, as well as cognitive and mood
regulation areas, which may contribute to deficient autonomic functions in HF. Functional
MRI responses in cerebellum and insular of HF are delayed or decreased in
magnitude to the challenge indicating that neural control regions involved in
autonomic regulation are compromised. The impaired functional responses of insular
and cerebellar sites are correlated with brain structural injury, indicating that
autonomic deficits in those areas have brain structural basis for impaired
functions.Conclusion
Our
findings show that autonomic deficits may result from brain structural injury
in autonomic regulatory areas in HF subjects.Acknowledgements
This work was supported by National Institutes
of Health R01 NR-013625 and R01 NR-014669.References
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