Download Low Body Negative Pressure and Cardiac MRI

Low Body Negative Pressure and Cardiac MRI: Observations of global and regional left ventricular
changes.
S.J. Wilson’, SE. Rose’, F. Chen’, D. Rose’, C.J. Bennett3, K. McMahon’, G.J. Galloway’, D.M. DoddrelIt
‘Centre for Magnetic Resonance, University of Queensland, Brisbane 4072, ‘Saint Andrew War Memorial
Hospital, Brisbane, 3Div. Of Medicine, Royal Brisbane Hospital, Brisbane 4029.
Background
The application of negative pressure to the lower body (LBNP)
induces the pooling of venous blood and reducesvenous return. The
technique has an extensivehistory in its physiological simulation of
quiet standing, upright tilt and increasedg forces I.‘. Stroke volume,
cardiac output (CO) and pulse pressures (PP) have all been
observedto decreaseupon application of LBNF in normal humans.
Compensatory mechanisms to LBNP not sufficient to cause
reduction in mean arterial pressure (MAP) (subhypotensiveLBNP)
are of interest in the fields of vasovagal syncope and the study of
volume unloading in chronic heart failure ‘.
The aim of this study was to quantify the changesin left ventricular
end systolic, end diastolic and ejection volumes (ESV, EDV and EV
respectively)and thereby ejection fraction (EF) upon the application
of subhypotensive LBNP. Such measured volumes represented a
measureof global strain and were supplementedby quantification of
regional wall strain using tagged magnetic resonance imaging
(MRI).
Methods
LBNP: An MRI compatible LBNP device consisted of two rigid
tubes in communication coupled to flexible trousers and ankle
sealing collars. Such a device enabled comfortable application of up
to -50 mmHg vacuum from ankles to ischium whilst being
physically and electromagneticallycompatible with the MR system.
Vacuuum was applied and monitored remotely. Figure 1 below
shows.theI device applied.
Regional Strain Analysis: Representativetagged short axis images
from a subject acquired in the control state (a) and with LBNP (b)
are displayed below.
(a)
b)
Figure 2. (a) shows a tagged image at end diastole. Epi’and
endocardial contours are shown, as are the circumferential
locations of septal (S), anterior (A), lateral (L) and posterior (P)
segments. Fig. 2(b) is the identical slice with LBNP applied. A
volumetric change is clearly seen.
An extract of the regional strain vs. time plot for one subject is
presentedbelow in figure 3. Behaviour during the early filling phase
of diastole is shown in 50 ms epochs. Other myocardial regions
were found to exhibit similar behaviour.
Base
Mid
Apex
F
n
monitoring tube exit to the right.
Subjects: 8 normal healthy adults (7 male, 1 female) with mean age
of 26 years (23-37) were imaged with and without -30 mmHg
LBNP both for volumetric assessmentand tagged myocardial
imaging on two separateoccasions.
MR protocol: Experiments were performed on a Bruker Medspec
S200 whole-body 2T scanner.Images were acquired using R wave
triggered segmentedspoiled grass sequencein breath-hold. For each
experiment, a complete set of control data was acquired before
application of LBNP (-30mm Hg). For volumetric studies, 8 to 10
contiguous double oblique short axis images of the heart were
acquired from apex to base. For tagging experiments, 4 to 6
contiguous double oblique short axis images were acquired with
two seriesof 8 tag lines at anglesof 45’and 135’to the image plane.
Two long axis images were acquired with parallel tags for the
calculation of through plane motion.
Image Analysis: Volume analysis was performed by manual tracing.
Tagged imageswere processedusing a semi-automatedtag-tracking
algorithm based on a snake contour model and endoiepicardial
contours were traced manually. A spline fitting routine was then
employed to calculate 3D deformation fields. Regional strains vs.
time plots were generatedfor both control and LBNP experiments.
Results Volumetric Measurements:
EDV
ESV
EV
EF
Ws)
(mls)
(%)
(mls)
43.6
81.7
125
65.7
Control
(16.1)
(25.7)
(13.2)
(6.3
109
42.3
66.9
61.5
LBNP
(12.1)
(16.4)
(24.5)
(6.4)
p>.o5
p<.Ol
p<.o
p<.Ol
5
Table 1. Mean volumes (SD) for the 8 studies +I-LBNP.
Proc. Intl. Sot. Mag. Reson. Med. 8 (2000)
Time
Figure 3. Strain vs. time plots for control and LBNP
experiments. H denotes LBNP data. Time divisions are 50 ms.
Discussion I Conclusions
The changes in LV volumes with -3Omm Hg LBNP are in
agreement with measured parameters seen by others. The
combination of LBNP and volumetric assessmentby MRI permits
insight into the origin of CO and PP reductions. The reduction in
EDV and thereby EV is the principal contributing factor to PP
decrease. Given that observed heart rates did not increase
significantly during LBNP the CO falls are also likely to be due to
reduction in EV. The changesin EDV and EV observed with LBNP
are a manifestationof Starlings’s law.
In this experiment regional strain was seen to increasewith LBNP.
Possible mechanisms for this change and its relationship to
myocardial diseasestatesare the subject of ongoing work.
References
1 Ahn, B. et al. (1989) Circulatory and respiratory responsesto lower
body negative pressurein man. Jap. .I. Physiol. 39: 919-929.
2 White, DD. Montgomery, LD. (1996) Aviat. Space Environ.
Med.67:555-559.
3 Atherton JJ, etal. (1997) Diastolic ventricular interaction: a possible
mechanismfor abnormal vascularresponsesduring volume unloading
in heart failure. Circ. 96 (12): 4273-9.
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